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THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: G protein‐coupled receptors

Stephen P H Alexander, Arthur Christopoulos, Anthony P Davenport and 12 more

British Journal of Pharmacology · 2019 · Review

Abstract

The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands ( www.guidetopharmacology.org ), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point‐in‐time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.14748 . G protein‐coupled receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid‐2019, and supersedes data presented in the 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC‐IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 16, 2026. Paragraph numbers are ours, so an answer can point at one.

Conflict of interest

1The authors state that there are no conflicts of interest to disclose.

Overview

2G protein‐coupled receptors (GPCRs) are the largest class of membrane proteins in the human genome. The term "7TM receptor" is commonly used interchangeably with "GPCR", although there are some receptors with seven transmembrane domains that do not signal through G proteins. GPCRs share a common architecture, each consisting of a single polypeptide with an extracellular N‐terminus, an intracellular C‐terminus and seven hydrophobic transmembrane domains (TM1‐TM7) linked by three extracellular loops (ECL1‐ECL3) and three intracellular loops (ICL1‐ICL3). About 800 GPCRs have been identified in man, of which about half have sensory functions, mediating olfaction (˜400), taste (33), light perception (10) and pheromone signalling (5) [http://www.ncbi.nlm.nih.gov/pubmed/15034552?dopt=AbstractPlus]. The remaining 350 non‐sensory GPCRs mediate signalling by ligands that range in size from small molecules to peptides to large proteins; they are the targets for the majority of drugs in clinical usage [http://www.ncbi.nlm.nih.gov/pubmed/17139284?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24016212?dopt=AbstractPlus], although only a minority of these receptors are exploited therapeutically. The first classification scheme to be proposed for GPCRs [http://www.ncbi.nlm.nih.gov/pubmed/8081729?dopt=AbstractPlus] divided them, on the basic of sequence homology, into six classes. These classes and their prototype members were as follows: Class A (rhodopsin‐like), Class B (secretin receptor family), Class C (metabotropic glutamate), Class D (fungal mating pheromone receptors), Class E (cyclic AMP receptors) and Class F (frizzled/smoothened). Of these, classes D and E are not found in vertebrates. An alternative classification scheme "GRAFS" [http://www.ncbi.nlm.nih.gov/pubmed/15862553?dopt=AbstractPlus] divides vertebrate GPCRs into five classes, overlapping with the A‐F nomenclature, viz:

3Glutamate family (http://www.guidetopharmacology.org/GRAC/GPCRListForward?class=C), which includes metabotropic glutamate receptors, a calcium‐sensing receptor and GABAB receptors, as well as three taste type 1 receptors and a family of pheromone receptors (V2 receptors) that are abundant in rodents but absent in man [http://www.ncbi.nlm.nih.gov/pubmed/15034552?dopt=AbstractPlus].

4Rhodopsin family (http://www.guidetopharmacology.org/GRAC/GPCRListForward?class=A), which includes receptors for a wide variety of small molecules, neurotransmitters, peptides and hormones, together with olfactory receptors, visual pigments, taste type 2 receptors and five pheromone receptors (V1 receptors).

5http://www.guidetopharmacology.org/GRAC/GPCRListForward?class=Adhesion GPCRs are phylogenetically related to class B receptors, from which they differ by possessing large extracellular N‐termini that are autoproteolytically cleaved from their 7TM domains at a conserved "GPCR proteolysis site" (GPS) which lies within a much larger (320 residue) "GPCR autoproteolysis‐inducing" (GAIN) domain, an evolutionary ancient mofif also found in polycystic kidney disease 1 (PKD1)‐like proteins, which has been suggested to be both required and sufficient for autoproteolysis [http://www.ncbi.nlm.nih.gov/pubmed/23850273?dopt=AbstractPlus].

6http://www.guidetopharmacology.org/GRAC/GPCRListForward?class=Frizzled consists of 10 Frizzled proteins (FZD(1‐10)) and Smoothened (SMO). The FZDs are activated by secreted lipoglycoproteins of the WNT family, whereas SMO is indirectly activated by the Hedgehog (HH) family of proteins acting on the transmembrane protein Patched (PTCH).

7Secretin family, encoded by 15 genes in humans. The ligands for receptors in this family are polypeptide hormones of 27‐141 amino acid residues; nine of the mammalian receptors respond to ligands that are structurally related to one another (glucagon, glucagon‐like peptides (GLP‐1, GLP‐2), glucose‐dependent insulinotropic polypeptide (GIP), secretin, vasoactive intestinal peptide (VIP), pituitary adenylate cyclase‐activating polypeptide (PACAP) and growth‐hormone‐releasing hormone (GHRH)) [http://www.ncbi.nlm.nih.gov/pubmed/11790261?dopt=AbstractPlus].

GPCR families

8aNumbers in brackets refer to orphan receptors for which an endogenous ligand has been proposed in at least one publication, see [http://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus]; b[http://www.ncbi.nlm.nih.gov/pubmed/19129093?dopt=AbstractPlus]; c[http://www.ncbi.nlm.nih.gov/pubmed/15034552?dopt=AbstractPlus]; d[http://www.ncbi.nlm.nih.gov/pubmed/15774036?dopt=AbstractPlus].

9Much of our current understanding of the structure and function of GPCRs is the result of pioneering work on the visual pigment rhodopsin and on the β2 adrenoceptor, the latter culminating in the award of the 2012 Nobel Prize in chemistry to Robert Lefkowitz and Brian Kobilka [http://www.ncbi.nlm.nih.gov/pubmed/23650120?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23650015?dopt=AbstractPlus].

Pseudogenes

10Below is a curated list of pseudogenes that in humans are non‐coding for receptor protein. In some cases these have a shared ancestry with genes that encode functional receptors in rats and mice.

11https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:19240, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16341, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4529, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16291, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7959, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4513, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:31924, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:31925, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:19103, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:19106, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:19107, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:20615, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:20640, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:20641, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:20642, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:43898, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:43905, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:20616. A more detailed listing containg further information can be viewed http://www.guidetopharmacology.org/GRAC//DATA/GPCR_pseudogenes.xlsx.

Olfactory receptors

12Olfactory receptors are also seven‐transmembrane spanning G protein‐coupled receptors, responsible for the detection of odorants. These are not currently included as they are not yet associated with extensive pharmacological data but are curated in the following databases: The gene list of olfactory receptors at https://www.genenames.org/cgi‐bin/genefamilies/set/141, and curated by https://genome.weizmann.ac.il/horde/ and https://senselab.med.yale.edu/ordb/.

Family structure

17S23 Orphan and other 7TM receptors

18S24 Class A Orphans

19– http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=706

20S33 Class C Orphans

21–http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=975

22S33 Taste 1 receptors

23S34 Taste 2 receptors

24S35 Other 7TM proteins

25S36 5‐Hydroxytryptamine receptors

26S39 Acetylcholine receptors (muscarinic)

27S41 Adenosine receptors

28S42 Adhesion Class GPCRs

29S45 Adrenoceptors

30S48 Angiotensin receptors

31S50 Apelin receptor

32S51 Bile acid receptor

33S51 Bombesin receptors

34S53 Bradykinin receptors

35S54 Calcitonin receptors

36S56 Calcium‐sensing receptor

37S57 Cannabinoid receptors

38S58 Chemerin receptors

39S59 Chemokine receptors

40S63 Cholecystokinin receptors

41S64 Class Frizzled GPCRs

42S67 Complement peptide receptors

43S68 Corticotropin‐releasing factor receptors

44S69 Dopamine receptors

45S71 Endothelin receptors

46S72 G protein‐coupled estrogen receptor

47S73 Formylpeptide receptors

48S74 Free fatty acid receptors

49S76 GABAB receptors

50S78 Galanin receptors

51S79 Ghrelin receptor

52S80 Glucagon receptor family

53S81 Glycoprotein hormone receptors

54S82 Gonadotrophin‐releasing hormone receptors

55S83 GPR18, GPR55 and GPR119

56S84 Histamine receptors

57S86 Hydroxycarboxylic acid receptors

58S87 Kisspeptin receptor

59S88 Leukotriene receptors

60S89 Lysophospholipid (LPA) receptors

61S90 Lysophospholipid (S1P) receptors

62S92 Melanin‐concentrating hormone receptors

63S93 Melanocortin receptors

64S94 Melatonin receptors

65S95 Metabotropic glutamate receptors

66S97 Motilin receptor

67S98 Neuromedin U receptors

68S99 Neuropeptide FF/neuropeptide AF receptors

69S100 Neuropeptide S receptor

70S101 Neuropeptide W/neuropeptide B receptors

71S102 Neuropeptide Y receptors

72S103 Neurotensin receptors

73S104 Opioid receptors

74S106 Orexin receptors

75S107 Oxoglutarate receptor

76S108 P2Y receptors

77S110 Parathyroid hormone receptors

78S111 Platelet‐activating factor receptor

79S112 Prokineticin receptors

80S113 Prolactin‐releasing peptide receptor

81S114 Prostanoid receptors

82S116 Proteinase‐activated receptors

83S117 QRFP receptor

84S118 Relaxin family peptide receptors

85S120 Somatostatin receptors

86S121 Succinate receptor

87S122 Tachykinin receptors

88S123 Thyrotropin‐releasing hormone receptors

89S124 Trace amine receptor

90S125 Urotensin receptor

91S126 Vasopressin and oxytocin receptors

92S127 VIP and PACAP receptors

Overview

93This set contains ’orphan’ G protein coupled receptors where the endogenous ligand(s) is not known, and other 7TM receptors.

94Table 1 lists a number of putative GPCRs identified by NC‐IUPHAR[http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus], for which preliminary evidence for an endogenous ligand has been published, or for which there exists a potential link to a disease, or disorder. These GPCRs have recently been reviewed in detail [http://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus]. The GPCRs in Table 1 are all Class A, rhodopsin‐like GPCRs. Class A orphan GPCRs not listed in Table 1 are putative GPCRs with as‐yet unidentified endogenous ligands.

Table 1

95Class A orphan GPCRs with putative endogenous ligands

96In addition the orphan receptors http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=89, http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=109 and http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=126 which are reported to respond to endogenous agents analogous to the endogenous cannabinoid ligands have been grouped together (http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=114).

Overview

98This set contains class C ’orphan’ G protein coupled receptors where the endogenous ligand(s) is not known.

Overview

100Whilst the taste of acid and salty foods appear to be sensed by regulation of ion channel activity, bitter, sweet and umami tastes are sensed by specialised GPCR. Two classes of taste GPCR have been identified, T1R and T2R, which are similar in sequence and structure to Class C and Class A GPCR, respectively. Activation of taste receptors appears to involve gustducin‐ (Gαt3) and Gα14‐mediated signalling, although the precise mechanisms remain obscure. Gene disruption studies suggest the involvement of PLCβ2 [http://www.ncbi.nlm.nih.gov/pubmed/12581520?dopt=AbstractPlus], TRPM5 [http://www.ncbi.nlm.nih.gov/pubmed/12581520?dopt=AbstractPlus] and IP3 [http://www.ncbi.nlm.nih.gov/pubmed/17925404?dopt=AbstractPlus] receptors in postreceptor signalling of taste receptors. Although predominantly associated with the oral cavity, taste receptors are also located elsewhere, including further down the gastrointestinal system, in the lungs and in the brain.

Sweet/Umami

101T1R3 acts as an obligate partner in T1R1/T1R3 and T1R2/T1R3 heterodimers, which sense umami or sweet, respectively. T1R1/T1R3 heterodimers respond to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1369 and may be positively allosterically modulated by 5’‐nucleoside monophosphates, such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5123 [http://www.ncbi.nlm.nih.gov/pubmed/12013525?dopt=AbstractPlus]. T1R2/T1R3 heterodimers respond to sugars, such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5411, and artificial sweeteners, such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5432 [http://www.ncbi.nlm.nih.gov/pubmed/11509186?dopt=AbstractPlus].

Comments

102Positive allosteric modulators of T1R2/T1R3 have been reported [2363]. Such compounds enhance the sweet taste of sucrose mediated by these receptors, but are tasteless on their own.

http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=117

104G protein‐coupled receptors → Orphan and other 7TM receptors → Taste 2 receptors

Overview

105The composition and stoichiometry of bitter taste receptors is not yet established. Bitter receptors appear to separate into two groups, with very restricted ligand specificity or much broader responsiveness. For example, T2R5 responded to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5433, but not 10 other bitter compounds [http://www.ncbi.nlm.nih.gov/pubmed/10761935?dopt=AbstractPlus], while T2R14 responded to at least eight different bitter tastants, including (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5344‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5344 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2291 [http://www.ncbi.nlm.nih.gov/pubmed/15178431?dopt=AbstractPlus].

106Specialist database http://bitterdb.agri.huji.ac.il/dbbitter.php contains additional information on bitter compounds and receptors [http://www.ncbi.nlm.nih.gov/pubmed/21940398?dopt=AbstractPlus].

Overview

1145‐HT receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on 5‐HT receptors [http://www.ncbi.nlm.nih.gov/pubmed/7938165?dopt=AbstractPlus] and subsequently revised [http://www.ncbi.nlm.nih.gov/pubmed/8936345?dopt=AbstractPlus]) are, with the exception of the ionotropic 5‐HT3 class, GPCRs where the endogenous agonist is http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5. The diversity of metabotropic 5‐HT receptors is increased by alternative splicing that produces isoforms of the 5‐HT2A (non‐functional), 5‐HT2C (non‐functional), 5‐HT4, 5‐HT6 (non‐functional) and 5‐HT7 receptors. Unique amongst the GPCRs, RNA editing produces 5‐HT2C receptor isoforms that differ in function, such as efficiency and specificity of coupling to Gq/11 and also pharmacology [http://www.ncbi.nlm.nih.gov/pubmed/16896947?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18554725?dopt=AbstractPlus]. Most 5‐HT receptors (except 5‐ht1e and 5‐ht5b) play specific roles mediating functional responses in different tissues (reviewed by [http://www.ncbi.nlm.nih.gov/pubmed/19086344?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17703282?dopt=AbstractPlus]).

Comments

115Tabulated pK i and K D values refer to binding to human 5‐HT receptors unless indicated otherwise. The nomenclature of 5‐HT1B/5‐HT1D receptors has been revised [http://www.ncbi.nlm.nih.gov/pubmed/8936345?dopt=AbstractPlus]. Only the non‐rodent form of the receptor was previously called 5‐HT1D: the human 5‐HT1B receptor (tabulated) displays a different pharmacology to the rodent forms of the receptor due to Thr335 of the human sequence being replaced by Asn in rodent receptors [http://www.ncbi.nlm.nih.gov/pubmed/18571247?dopt=AbstractPlus]. Wang et al. (2013) report X‐ray structures which reveal the binding modality of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=149 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=121 (DHE) to the 5‐HT1B receptor in comparison with the structure of the 5HT2B receptor [http://www.ncbi.nlm.nih.gov/pubmed/23519210?dopt=AbstractPlus]; some of these drugs adopt rather different conformations depending on the target receptor [http://www.ncbi.nlm.nih.gov/pubmed/29398112?dopt=AbstractPlus]. Various 5‐HT receptors have multiple partners in addition to G proteins, which may affect function and pharmacology [http://www.ncbi.nlm.nih.gov/pubmed/21777185?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3226 is a selective antagonist of the rodent 5‐HT1B receptor. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5434 (LSD) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=88 bind with high affinity to dopamine D4 and histamine H1 receptors respectively, and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=88 is a potent α1 adrenoceptor antagonist, in addition to blocking 5‐HT2A receptors. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=139 (LSD) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=149 show a strong preference for arrestin recruitment over G protein coupling at the 5‐HT2B receptor, with no such preference evident at 5‐HT1B receptors, and they also antagonise 5‐HT7A receptors [http://www.ncbi.nlm.nih.gov/pubmed/23519215?dopt=AbstractPlus]. DHE (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=282), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=48 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=37 also show significant preference for arrestin recruitment over G protein coupling at 5‐HT2B receptors [http://www.ncbi.nlm.nih.gov/pubmed/23519215?dopt=AbstractPlus]. The 5‐HT2B (and other 5‐HT) receptors interact with immunocompetent cells [http://www.ncbi.nlm.nih.gov/pubmed/28265714?dopt=AbstractPlus]. The serotonin antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=206 was key to the discovery of the 5HT2C receptor [http://www.ncbi.nlm.nih.gov/pubmed/6519175?dopt=AbstractPlus], initially known as 5‐HT1C [http://www.ncbi.nlm.nih.gov/pubmed/28806488?dopt=AbstractPlus]. The human 5‐HT5A receptor may couple to several signal transduction pathways when stably expressed in C6 glioma cells [http://www.ncbi.nlm.nih.gov/pubmed/12558985?dopt=AbstractPlus] and rodent prefrontal cortex (layer V pyramidal neurons) [http://www.ncbi.nlm.nih.gov/pubmed/22539842?dopt=AbstractPlus]. The human orthologue of the mouse 5‐ht5b receptor is non‐functional (stop codons); the 5‐ht1e receptor has not been cloned from mouse, or rat, impeding definition of its function [http://www.ncbi.nlm.nih.gov/pubmed/18571247?dopt=AbstractPlus]. In addition to accepted receptors, an ’orphan’ receptor, unofficially termed5‐HT1P, has been described [http://www.ncbi.nlm.nih.gov/pubmed/10429737?dopt=AbstractPlus].

Overview

122Muscarinic acetylcholine receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Muscarinic Acetylcholine Receptors [http://www.ncbi.nlm.nih.gov/pubmed/9647869?dopt=AbstractPlus]) are GPCRs of the Class A, rhodopsin‐like family where the endogenous agonist is http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=294. In addition to the agents listed in the table, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=289, its structural analogues http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=334 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3271, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=333, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3258 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5435 have been described as functionally selective agonists of the M1 receptor subtype via binding in a mode distinct from that utilized by non‐selective agonists [http://www.ncbi.nlm.nih.gov/pubmed/20413650?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18842902?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18454168?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16207821?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17525129?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20684563?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16959945?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12021390?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/14595031?dopt=AbstractPlus]. There are two pharmacologically characterised allosteric sites on muscarinic receptors, one defined by it binding http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=356, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=347 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=342, and the other defined by the binding of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=337, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=340, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=339 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=346 [http://www.ncbi.nlm.nih.gov/pubmed/10860942?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12435818?dopt=AbstractPlus].

Comments

123The crystal structures of the M1‐M4 receptor subtypes have been reported [http://www.ncbi.nlm.nih.gov/pubmed/22278061?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26958838?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22358838?dopt=AbstractPlus]. Direct activation via an allosteric site has been reported for M1 receptors (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5436, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9228) and M4 receptors (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3262) [http://www.ncbi.nlm.nih.gov/pubmed/27275946?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21300722?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19940843?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19717450?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20406819?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18628403?dopt=AbstractPlus]. The allosteric site for http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=356 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=347 on M2 receptors can be labelled by [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=364 [http://www.ncbi.nlm.nih.gov/pubmed/12815174?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=290 is a functionally selective partial agonist that appears to interact in a bitopic mode with both the orthosteric and an allosteric site on the M2 muscarinic receptor [http://www.ncbi.nlm.nih.gov/pubmed/18723515?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3255, hybrid 1 and hybrid 2, are multivalent (bitopic) ligands that also achieve selectivity for M2 receptors by binding both to the orthosteric and a nearby allosteric site [http://www.ncbi.nlm.nih.gov/pubmed/18842964?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17478612?dopt=AbstractPlus].

124Although numerous ligands for muscarinic acetylcholine receptors have been described, relatively few selective antagonists have been described, so it is common to assess the rank order of affinity of a number of antagonists of limited selectivity (e.g. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=307, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=321, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=328) in order to identify the involvement of particular subtypes. It should be noted that the measured affinities of antagonists (and agonists) in radioligand binding studies are sensitive to ionic strength and can increase over 10‐fold at low ionic strength compared to their values at physiological ionic strengths [http://www.ncbi.nlm.nih.gov/pubmed/497538?dopt=AbstractPlus].

Overview

131Adenosine receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Adenosine Receptors [http://www.ncbi.nlm.nih.gov/pubmed/11734617?dopt=AbstractPlus]) are activated by the endogenous ligand http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2844 (potentially http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4554 also at A3 receptors). Crystal structures for the antagonist‐bound [http://www.ncbi.nlm.nih.gov/pubmed/22220592?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18832607?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22798613?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/27312113?dopt=AbstractPlus], agonist‐bound [http://www.ncbi.nlm.nih.gov/pubmed/25762024?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21593763?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21393508?dopt=AbstractPlus] and G protein‐bound A2A adenosine receptors [http://www.ncbi.nlm.nih.gov/pubmed/27462812?dopt=AbstractPlus] have been described. The structures of an antagonist‐bound A1 receptor [http://www.ncbi.nlm.nih.gov/pubmed/28235198?dopt=AbstractPlus] and an adenosine‐bound A1 receptor‐Gi complex [http://www.ncbi.nlm.nih.gov/pubmed/29925945?dopt=AbstractPlus] have been resolved by cryo‐electronmicroscopy. Another structure of an antagonist‐bound A1 receptor obtained with X‐ray crystallography has also been reported [http://www.ncbi.nlm.nih.gov/pubmed/28712806?dopt=AbstractPlus].

Comments

132Adenosine inhibits many intracellular ATP‐utilising enzymes, including adenylyl cyclase (P‐site). A pseudogene exists for the A2B adenosine receptor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:265) with 79% identity to the A2B adenosine receptor cDNA coding sequence, but which is unable to encode a functional receptor [http://www.ncbi.nlm.nih.gov/pubmed/7558011?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=386 also exhibits antagonism at A2B receptors (pKi ca. 7,[http://www.ncbi.nlm.nih.gov/pubmed/8937736?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9459566?dopt=AbstractPlus]). Antagonists at A3 receptors exhibit marked species differences, such that only http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=474 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=470 are selective at the rat A3 receptor. In the absence of other adenosine receptors, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=406 and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=455 can also be used to label A2B receptors (KD ca. 30 and 60 nM respectively). [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=436 also binds to A1 receptors [http://www.ncbi.nlm.nih.gov/pubmed/9459566?dopt=AbstractPlus]. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=424 is relatively selective for A2A receptors, but may also bind to other sites in cerebral cortex [http://www.ncbi.nlm.nih.gov/pubmed/8692280?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/7566470?dopt=AbstractPlus]. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=425 binds to other non‐receptor elements, which also recognise adenosine [http://www.ncbi.nlm.nih.gov/pubmed/8937447?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3279 has been described as a fluorescent antagonist for labelling A1 adenosine receptors in living cells, although activity at other adenosine receptors was not examined [http://www.ncbi.nlm.nih.gov/pubmed/15070776?dopt=AbstractPlus].

Overview

142Adhesion GPCRs are structurally identified on the basis of a large extracellular region, similar to the Class B GPCR, but which is linked to the 7TM region by a GPCR autoproteolysisinducing (GAIN) domain [http://www.ncbi.nlm.nih.gov/pubmed/22333914?dopt=AbstractPlus] containing a GPCR proteolytic site. The N‐terminus often shares structural homology with adhesive domains (e.g. cadherins, immunolobulin, lectins) facilitating inter‐ and matricellular interactions and leading to the term adhesion GPCR [http://www.ncbi.nlm.nih.gov/pubmed/12761335?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18789697?dopt=AbstractPlus]. Several receptors have been suggested to function as mechanosensors [http://www.ncbi.nlm.nih.gov/pubmed/26841242?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25695270?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25937282?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26499266?dopt=AbstractPlus]. The nomenclature of these receptors was revised in 2015 as recommended by NC‐IUPHAR and the Adhesion GPCR Consortium [http://www.ncbi.nlm.nih.gov/pubmed/25713288?dopt=AbstractPlus].

Overview

148The nomenclature of the Adrenoceptors has been agreed by the NC‐IUPHAR Subcommittee on Adrenoceptors [http://www.ncbi.nlm.nih.gov/pubmed/7938162?dopt=AbstractPlus], see also [http://www.ncbi.nlm.nih.gov/pubmed/7568329?dopt=AbstractPlus].

Adrenoceptors, α1

149α1‐Adrenoceptors are activated by the endogenous agonists (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=479 and (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=505. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=485, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=483 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=515 are agonists and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=503 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=515 antagonists considered selective for α1‐ relative to α2‐adrenoceptors. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5385 and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=482 (BE2254) are relatively selective radioligands. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=487 also has high affinity for L‐type Ca2+ channels. Fluorescent derivatives of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=503 (Bodipy PLprazosin‐ QAPB) are used to examine cellular localisation of α1‐adrenoceptors. Selective α1‐adrenoceptor agonists are used as nasal decongestants; antagonists to treat hypertension (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7170, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7170) and benign prostatic hyperplasia (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7109, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=488). The α1‐ and β2‐adrenoceptor antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=551 is used to treat congestive heart failure, although the contribution of α1‐adrenoceptor blockade to the therapeutic effect is unclear. Several anti‐depressants and anti‐psychotic drugs are α1‐adrenoceptor antagonists contributing to side effects such as orthostatic hypotension and extrapyramidal effects.

Comments

150The α1C‐adrenoceptor corresponds to the pharmacologically defined α1A‐adrenoceptor [http://www.ncbi.nlm.nih.gov/pubmed/7568329?dopt=AbstractPlus]. Some tissues possess α1A‐adrenoceptors (α1L‐adrenoceptors [http://www.ncbi.nlm.nih.gov/pubmed/9249248?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17162094?dopt=AbstractPlus]) that display relatively low affinity in functional and binding assays for http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=503 indicative of different receptor states or locations. α1A‐adrenoceptor C‐terminal splice variants form homo‐ and heterodimers, but fail to generate a functional α1L‐adrenoceptor [http://www.ncbi.nlm.nih.gov/pubmed/15266013?dopt=AbstractPlus]. α1D‐Adrenoceptors form heterodimers with α1B‐ or β2‐adrenoceptors that show increased cell‐surface expression [http://www.ncbi.nlm.nih.gov/pubmed/15615865?dopt=AbstractPlus]. Recombinant α1D‐adrenoceptors have been shown in some heterologous systems to be mainly located intracellularly but cell‐surface localization is encouraged by truncation of the Nterminus, or by co‐expression of α1B‐ or β2‐adrenoceptors [http://www.ncbi.nlm.nih.gov/pubmed/14718583?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/14718583?dopt=AbstractPlus]. In blood vessels all three α1‐adrenoceptor subtypes are located on the surface and intracellularly [http://www.ncbi.nlm.nih.gov/pubmed/19572943?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19888965?dopt=AbstractPlus]. Signalling is predominantly via Gq/11 butα1‐adrenoceptors also couple toGi/o, Gs and G12/13. Several α1A‐adrenoceptor agonists display ligand directed signalling bias relative to noradrenaline [http://www.ncbi.nlm.nih.gov/pubmed/20978120?dopt=AbstractPlus]. There are also differences between subtypes in coupling efficiency to different pathways. In vascular smooth muscle, the potency of agonists is related to the predominant subtype, α1D‐ conveying greater agonist sensitivity than α1A‐adrenoceptors [http://www.ncbi.nlm.nih.gov/pubmed/23373597?dopt=AbstractPlus].

Adrenoceptors, α2

151α2‐Adrenoceptors are activated by (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=479 and with lower potency by (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=505. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=520 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5442 are agonists and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=136 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=102 antagonists selective for α2‐ relative to α1‐adrenoceptors. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=223, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5386 and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=528 are relatively selective radioligands. There is species variation in the pharmacology of the α2A‐adrenoceptor. Multiple mutations of α2‐adrenoceptors have been described, some associated with alterations in function. Presynaptic α2‐adrenoceptors regulate many functions in the nervous system. The α2‐adrenoceptor agonists http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=516, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5443 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=520 affect central baroreflex control (hypotension and bradycardia), induce hypnotic effects and analgesia, and modulate seizure activity and platelet aggregation. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=516 is an anti‐hypertensive and counteracts opioid withdrawal. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=521 (also http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=523) is used as a sedative and analgesic in human and veterinary medicine with sympatholytic and anxiolytic properties. The α2‐adrenoceptor antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=102 has been used to treat erectile dysfunction and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7241 as an anti‐depressant. The α2B subtype appears to be involved in neurotransmission in the spinal cord and α2C in regulating catecholamine release from adrenal chromaffin cells.

Comments

152http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=524 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=503 show selectivity for α2B‐ and α2C‐adrenoceptors over α2A‐adrenoceptors.http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=124 is a reduced efficacy imidazoline agonist but also binds to non‐GPCR binding sites for imidazolines, classified as I1, I2 and I3 sites [http://www.ncbi.nlm.nih.gov/pubmed/15224384?dopt=AbstractPlus]; catecholamines have a low affinity, while rilmenidine and moxonidine are selective ligands evoking hypotensive effects in vivo. I1‐imidazoline receptors cause central inhibition of sympathetic tone, I2‐imidazoline receptors are an allosteric binding site on monoamine oxidase B, and I3‐imidazoline receptors regulate insulin secretion from pancreatic β‐cells. α2A‐adrenoceptor stimulation reduces insulin secretion from β‐islets [http://www.ncbi.nlm.nih.gov/pubmed/22645144?dopt=AbstractPlus], with a polymorphism in the 5’‐UTR of the ADRA2A gene being associated with increased receptor expression in β‐islets and heightened susceptibility to diabetes [http://www.ncbi.nlm.nih.gov/pubmed/19965390?dopt=AbstractPlus]. α2A‐ and α2C‐adrenoceptors form homodimers [http://www.ncbi.nlm.nih.gov/pubmed/16605244?dopt=AbstractPlus]. Heterodimers between α2A‐ and either the α2C‐adrenoceptor or μ opioid peptide receptor exhibit altered signalling and trafficking properties compared to the individual receptors [http://www.ncbi.nlm.nih.gov/pubmed/16605244?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19126537?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18193048?dopt=AbstractPlus]. Signalling by α2‐adrenoceptors is primarily via Gi/o, although the α2A‐adrenoceptor also couples to Gs [http://www.ncbi.nlm.nih.gov/pubmed/7559592?dopt=AbstractPlus]. Imidazoline compounds display bias relative to each other at the α2A‐adrenoceptor [http://www.ncbi.nlm.nih.gov/pubmed/12649300?dopt=AbstractPlus]. The noradrenaline reuptake inhibitor desipramine acts directly on the α2A‐adrenoceptor to promote internalisation via recruitment of arrestin [http://www.ncbi.nlm.nih.gov/pubmed/21859713?dopt=AbstractPlus].

Adrenoceptors, β

153β‐Adrenoceptors are activated by the endogenous agonists (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=479 and (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=505. Isoprenaline is selective for β‐adrenoceptors relative to α1‐ and α2‐adrenoceptors, while http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=564 (pKi 8.2‐9.2) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=132 (pKi 10.011.0) are relatively β1 and β2 adrenoceptor‐selective antagonists. (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=505, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=538 and (‐)‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5571 show selectivity for β1‐ relative to β2‐adrenoceptors. Pharmacological differences exist between human and mouse β3‐adrenoceptors, and the ’rodent selective’ agonists http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=567 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3462 have low efficacy at the human β3‐adrenoceptor whereas http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=532 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3931 activate human β3‐adrenoceptors [88]. β3‐Adrenoceptors are resistant to blockade by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=564, but can be blocked by high concentrations of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=550. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=547 has reasonably high affinity at β3‐adrenoceptors, but does not discriminate well between the three β‐ subtypes whereas http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3931 is more selective. [125I]‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=132, [125I]‐hydroxy benzylpindolol and [3H]‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=563 are high affinity radioligands that label β1‐ and β2‐ adrenoceptors and β3‐adrenoceptors can be labelled with higher concentrations (nM) of [125I]‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=132 together with β1‐ and β2‐adrenoceptor antagonists. [3H]‐L748337 is a β3‐selective radioligand [http://www.ncbi.nlm.nih.gov/pubmed/24183974?dopt=AbstractPlus]. Fluorescent ligands such as BODIPY‐TMR‐CGP12177 can be used to track βadrenoceptors at the cellular level [8]. Somewhat selective β1adrenoceptor agonists (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=534, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=535) are used short term to treat cardiogenic shock but, chronically, reduce survival. β1‐Adrenoceptor‐preferring antagonists areused totreathypertension (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=548, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=549, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7129, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=553 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7246), cardiac arrhythmias (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=548, bisoprolol, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7178) and cardiac failure (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=553, nebivolol). Cardiac failure is also treated with carvedilol that blocks β1‐ and β2‐adrenoceptors, as well as α1‐adrenoceptors. Short (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=558, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=560) and long (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3465, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=559) acting β2‐adrenoceptor‐selective agonists are powerful bronchodilators used to treat respiratory disorders. Many first generation β‐adrenoceptor antagonists (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=564) block both β1‐ and β2‐adrenoceptors and there are no β2adrenoceptor‐selective antagonists used therapeutically. The β3‐adrenoceptor agonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7445 is used to control overactive bladder syndrome.

Comments

154[http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=562 can be used to define β1‐ or β2adrenoceptors when conducted in the presence of a β1‐ or β2adrenoceptor‐selective antagonist. A fluorescent analogue of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=532 can be used to study β2‐adrenoceptors in living cells [http://www.ncbi.nlm.nih.gov/pubmed/12770928?dopt=AbstractPlus]. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=562 at higher (nM) concentrations can be used to label β3‐adrenoceptors in systems with few if any other β‐adrenoceptor subtypes. The β3‐adrenoceptor has an intron in the coding region, but splice variants have only been described for the mouse [http://www.ncbi.nlm.nih.gov/pubmed/10455305?dopt=AbstractPlus], where the isoforms display different signalling characteristics [http://www.ncbi.nlm.nih.gov/pubmed/11959793?dopt=AbstractPlus]. There are 3 β‐adrenoceptors in turkey (termed the tβ, tβ3c and tβ4c) that have a pharmacology that differs from the human β‐adrenoceptors [http://www.ncbi.nlm.nih.gov/pubmed/21152092?dopt=AbstractPlus]. Numerous polymorphisms have been described for the β‐adrenoceptors; some are associated with signalling and trafficking, altered susceptibility to disease and/or altered responses to pharmacotherapy [http://www.ncbi.nlm.nih.gov/pubmed/15090197?dopt=AbstractPlus]. All β‐adrenoceptors couple to Gs (activating adenylyl cyclase and elevating cAMP levels), but also activate Gi and β‐arrestin‐mediated signalling. Many β1‐ and β2‐adrenoceptor antagonists are agonists at β3adrenoceptors (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3462 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=569). Many ‘antagonists’ of cAMP accumulation, for example http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=551 and bucindolol, weakly activate MAP kinase pathways [http://www.ncbi.nlm.nih.gov/pubmed/14645666?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20132209?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16901982?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18403719?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17717109?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18684840?dopt=AbstractPlus] and thus display ’protean agonism’. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=550 acts as a neutral antagonist in most systems so far examined. Agonists also display biased signalling at the β2‐adrenoceptor via Gs or arrestins [http://www.ncbi.nlm.nih.gov/pubmed/18086673?dopt=AbstractPlus]. X‐ray crystal structures have been described of the agonist bound [http://www.ncbi.nlm.nih.gov/pubmed/21228877?dopt=AbstractPlus] and antagonist bound forms of the β1[http://www.ncbi.nlm.nih.gov/pubmed/18594507?dopt=AbstractPlus], agonist‐bound [http://www.ncbi.nlm.nih.gov/pubmed/17962520?dopt=AbstractPlus] and antagonist‐bound forms of the β2‐adrenoceptor [http://www.ncbi.nlm.nih.gov/pubmed/21228869?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21228876?dopt=AbstractPlus], as well as a fully active agonistbound, Gs protein‐coupled β2‐adrenoceptor [http://www.ncbi.nlm.nih.gov/pubmed/21772288?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=551 and bucindolol bind to a site on the β1‐adrenoceptor involving contacts in TM2, 3, and 7 and extracellular loop 2 that may facilitate coupling to arrestins [http://www.ncbi.nlm.nih.gov/pubmed/18594507?dopt=AbstractPlus]. Compounds displaying arrestinbiased signalling at the β2‐adrenoceptor have a greater effect on the conformation of TM7, whereas full agonists for Gs coupling promote movement of TM5 and TM6 [http://www.ncbi.nlm.nih.gov/pubmed/22267580?dopt=AbstractPlus]. Recent studies using NMR spectroscopy demonstrate significant conformational flexibility in the β2‐adrenoceptor that is stabilized by both agonist and G proteins highlighting the dynamic nature of interactions with both ligand and downstreamsignalling partners [http://www.ncbi.nlm.nih.gov/pubmed/23721409?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25981665?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23374348?dopt=AbstractPlus]. Such flexibility likely has consequences for our understanding of biased agonism, and for the future therapeutic exploitation of this phenomenon.

Overview

162The actions of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2504 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:333, http://www.uniprot.org/uniprot/P01019) (Ang II) are mediated by AT1 and AT2 receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Angiotensin receptors [http://www.ncbi.nlm.nih.gov/pubmed/10977869?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26315714?dopt=AbstractPlus]), which have around 30% sequence similarity. The decapeptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=583, http://www.uniprot.org/uniprot/P01019), the octapeptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2504, http://www.uniprot.org/uniprot/P01019) and the heptapeptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=585, http://www.uniprot.org/uniprot/P01019) are endogenous ligands. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=590, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=587, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=592, etc. are clinically used AT1 receptor blockers.

Comments

163AT1 receptors are predominantly coupled to Gq/11, however they are also linked to arrestin recruitment and stimulate G protein‐independent arrestin signalling [http://www.ncbi.nlm.nih.gov/pubmed/20427692?dopt=AbstractPlus]. Most species express a single AGTR1 gene, but two related agtr1a and agtr1b receptor genes are expressed in rodents. The AT2 receptor counteracts several of the growth responses initiated by the AT1 receptors. The AT2 receptor is much less abundant than the AT1 receptor in adult tissues and is upregulated in pathological conditions. AT1 receptor antagonists bearing substituted 4‐phenylquinoline moieties have been synthesized, which bind to AT1 receptors with nanomolar affinity and are slightly more potent than http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=590 in functional studies [http://www.ncbi.nlm.nih.gov/pubmed/15115399?dopt=AbstractPlus]. The antagonist activity of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3944 at the AT2 receptor has also been reported [http://www.ncbi.nlm.nih.gov/pubmed/3071214?dopt=AbstractPlus]. The AT1 and bradykinin B2 receptors have been proposed to form a heterodimeric complex [http://www.ncbi.nlm.nih.gov/pubmed/10993080?dopt=AbstractPlus]. β‐Arrestin1 prevents AT1‐B2 receptor heteromerization[http://www.ncbi.nlm.nih.gov/pubmed/30503206?dopt=AbstractPlus]. There is also evidence for an AT4 receptor that specifically binds http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5368 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:333, http://www.uniprot.org/uniprot/P01019) and is located in the brain and kidney. An additional putative endogenous ligand for the AT4 receptor has been described (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5353 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4827, http://www.uniprot.org/uniprot/P68871), a globin decapeptide) [http://www.ncbi.nlm.nih.gov/pubmed/9166749?dopt=AbstractPlus].

Overview

170The apelin receptor (nomenclature as agreed by the NC‐IUPHAR Subcommittee on the apelin receptor [http://www.ncbi.nlm.nih.gov/pubmed/20605969?dopt=AbstractPlus]) responds to apelin, a 36 amino‐acid peptide derived initially from bovine stomach. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=606 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16665, http://www.uniprot.org/uniprot/Q9ULZ1), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=605, http://www.uniprot.org/uniprot/Q9ULZ1) and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=599]http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=599 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16665, http://www.uniprot.org/uniprot/Q9ULZ1) are the predominant endogenous ligands which are cleaved from a 77 amino‐acid precursor peptide (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16665 http://www.uniprot.org/uniprot/Q9ULZ1) by a so far unidentified enzymatic pathway [http://www.ncbi.nlm.nih.gov/pubmed/9792798?dopt=AbstractPlus]. A second family of peptides discovered independently and named Elabela [http://www.ncbi.nlm.nih.gov/pubmed/24316148?dopt=AbstractPlus] or Toddler, that has little sequence similarity to apelin, is present, and functional at the apelin receptor in the adult cardiovascular system [http://www.ncbi.nlm.nih.gov/pubmed/24407481?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/28137936?dopt=AbstractPlus]. Structure‐activity relationship Elabela analogues have been described [http://www.ncbi.nlm.nih.gov/pubmed/26986036?dopt=AbstractPlus].

Comments

171Potency order determined for heterologously expressed human apelin receptor (pD 2 values range from 9.5 to 8.6). The apelin receptor may also act as a co‐receptor with CD4 for isolates of human immunodeficiency virus, with apelin blocking this function [http://www.ncbi.nlm.nih.gov/pubmed/11090199?dopt=AbstractPlus]. A modified apelin‐13 peptide, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5354) was reported to block the hypotensive response to apelin in rat in vivo [http://www.ncbi.nlm.nih.gov/pubmed/15486224?dopt=AbstractPlus], however, this peptide exhibits agonist activity in HEK293 cells stably expressing the recombinant apelin receptor [http://www.ncbi.nlm.nih.gov/pubmed/12939143?dopt=AbstractPlus]. The apelin receptor antagonist, MM54, was reported to suppress tumour growth and increase survival in an intracranial xenograft mouse model of glioblastoma [http://www.ncbi.nlm.nih.gov/pubmed/29053791?dopt=AbstractPlus].

Overview

178The bile acid receptor (GPBA) responds to bile acids produced during the liver metabolism of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2718. Selective agonists are promising drugs for the treatment of metabolic disorders, such as type II diabetes, obesity and atherosclerosis.

Comments

179The triterpenoid natural product http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3945 has also been reported to inhibit inflammatory signalling through the NFκB pathway [http://www.ncbi.nlm.nih.gov/pubmed/12960358?dopt=AbstractPlus]. Disruption of GPBA expression is reported to protect from cholesterol gallstone formation [http://www.ncbi.nlm.nih.gov/pubmed/16724960?dopt=AbstractPlus]. A new series of 5‐phenoxy‐1,3‐dimethyl‐1H‐pyrazole‐4‐carboxamides have been reported as highly potent agonists [http://www.ncbi.nlm.nih.gov/pubmed/23337601?dopt=AbstractPlus].

Overview

184Mammalian bombesin (Bn) receptors comprise 3 subtypes: BB1, BB2, BB3 (nomenclature recommended by the NC‐IUPHAR Subcommittee on bombesin receptors, [http://www.ncbi.nlm.nih.gov/pubmed/18055507?dopt=AbstractPlus]). BB1 and BB2 are activated by the endogenous ligands http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=612 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4605, http://www.uniprot.org/uniprot/P07492) (GRP), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=613 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7842, http://www.uniprot.org/uniprot/P08949) (NMB) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3582) (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4605, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4605). http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=616 is a tetradecapeptide, originally derived from amphibians. The three Bn receptor subtypes couple primarily to the Gq/11 and G12/13 family of G proteins [http://www.ncbi.nlm.nih.gov/pubmed/18055507?dopt=AbstractPlus]. Each of these receptors is widely distributed in the CNS and peripheral tissues [http://www.ncbi.nlm.nih.gov/pubmed/26066663?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18055507?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15726424?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25976083?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15203211?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22911445?dopt=AbstractPlus]. Activation of BB1 and BB2 receptors causes a wide range of physiological/pathophysiogical actions, including the stimulation of normal and neoplastic tissue growth, smoothmuscle contraction, feeding behavior, secretion and many central nervous system effects including regulation of circadian rhythm and mediation of pruritus [http://www.ncbi.nlm.nih.gov/pubmed/18055507?dopt=AbstractPlus, 991, 992, http://www.ncbi.nlm.nih.gov/pubmed/21042212?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15134870?dopt=AbstractPlus,http://www.ncbi.nlm.nih.gov/pubmed/25976083?dopt=AbstractPlus]. A physiological role for the BB3 receptor has yet to be fully defined although recently studies suggest an important role in glucose and insulin regulation, metabolic homeostasis, feeding, regulation of body temperature, obesity, diabetes mellitus and growth of normal/neoplastic tissues [http://www.ncbi.nlm.nih.gov/pubmed/26066663?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22157398?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9367152?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/27055378?dopt=AbstractPlus].

Comments

185All three human subtypes may be activated by [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=632,http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=632‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=632,http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=632,http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=632]http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=632) [http://www.ncbi.nlm.nih.gov/pubmed/9325344?dopt=AbstractPlus]. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3946,http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3946,http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3946,http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3946]http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3946) has more than 200‐fold selectivity for BB3 receptors over BB1 and BB2 [http://www.ncbi.nlm.nih.gov/pubmed/15102928?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15102928?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25976083?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26524625?dopt=AbstractPlus].

Overview

192Bradykinin (or kinin) receptors (nomenclature as agreed by the NC‐IUPHAR subcommittee on Bradykinin (kinin) Receptors [http://www.ncbi.nlm.nih.gov/pubmed/15734727?dopt=AbstractPlus]) are activated by the endogenous peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=649 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6383, http://www.uniprot.org/uniprot/P01042) (BK), [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=646]http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=646, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6383), Lys‐BK (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=650, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6383)), [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=644]http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=644, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6383), [Phospho‐Ser6]‐Bradykinin, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=639, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6383) (Ile‐SerBK), [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3578]http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3578, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6383) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3580]‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3580, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6383). Variation in pharmacology and activity of B1 and B2 receptor antagonists at species orthologs has been documented. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=667 (Hoe140, Firazir) is approved in North America and Europe for the treatment of acute attacks of hereditary angioedema.

Overview

199This receptor family comprises a group of receptors for the calcitonin/CGRP family of peptides. The calcitonin (CT), amylin (AMY), calcitonin gene‐related peptide (CGRP) and adrenomedullin (AM) receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on CGRP, AM, AMY, and CT receptors [http://www.ncbi.nlm.nih.gov/pubmed/18552275?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12037140?dopt=AbstractPlus]) are generated by the genes https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1440 (which codes for the CT receptor) and https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16709 (which codes for the calcitonin receptor‐like receptor, CLR, previously known as CRLR). Their function and pharmacology are altered in the presence of RAMPs (receptor activity‐modifying proteins), which are single TM domain proteins of ca. 130 amino acids, identified as a family of three members; RAMP1, RAMP2 and RAMP3. There are splice variants of the CT receptor; these in turn produce variants of the AMY receptor [http://www.ncbi.nlm.nih.gov/pubmed/12037140?dopt=AbstractPlus], some of which can be potently activated by CGRP. The endogenous agonists are the peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=685 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1437, http://www.uniprot.org/uniprot/P01258), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=681‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=681, http://www.uniprot.org/uniprot/P06881) (formerly known as CGRP‐I), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=682 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1438, http://www.uniprot.org/uniprot/P10092) (formerly known as CGRP‐II), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=687 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:5329, http://www.uniprot.org/uniprot/P10997) (occasionally called islet‐amyloid polypeptide, diabetes‐associated polypeptide), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=683 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:259, http://www.uniprot.org/uniprot/P35318) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=684 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:28898, http://www.uniprot.org/uniprot/Q7Z4H4). There are species differences in peptide sequences, particularly for the CTs. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5369 {Pig} (CRSP) is another member of the family with selectivity for the CT receptor but it is not expressed in humans [http://www.ncbi.nlm.nih.gov/pubmed/12556539?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=702 (also known as BIBN4096BS, pKi10.5) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=703 (also known as MK0974, pKi9) are the most selective antagonists available, showing selectivity for CGRP receptors, with a particular preference for those of primate origin. CLR (calcitonin receptor‐like receptor) by itself binds no known endogenous ligand, but in the presence of RAMPs it gives receptors for CGRP, adrenomedullin and adrenomedullin 2/intermedin.

Comments

200It is important to note that a complication with the interpretation of pharmacological studies with AMY receptors in transfected cells is that most of this work has likely used a mixed population of receptors, encompassing RAMP‐coupled CTR as well as CTR alone. This means that although in binding assays human http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=685 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1437, http://www.uniprot.org/uniprot/P01258) has low affinity for 125I‐AMY binding sites, cells transfected with CTR and RAMPs can display potent CT functional responses. Transfection of human CTR with any RAMP can generate receptors with a high affinity for both salmon CT and AMY and varying affinity for different antagonists [http://www.ncbi.nlm.nih.gov/pubmed/10385705?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15692146?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16959943?dopt=AbstractPlus]. The major human CTR splice variant (hCT(a), which does not contain an insert) with RAMP1 (i.e. the AMY1(a) receptor) has a high affinity for CGRP [http://www.ncbi.nlm.nih.gov/pubmed/26125036?dopt=AbstractPlus], unlike hCT(a)‐RAMP3 (i.e. AMY3(a) receptor) [http://www.ncbi.nlm.nih.gov/pubmed/10385705?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15692146?dopt=AbstractPlus]. However, the AMY receptor phenotype is RAMP‐type, splice variant and cell‐line‐dependent [http://www.ncbi.nlm.nih.gov/pubmed/18599553?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22946511?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10871296?dopt=AbstractPlus]. Emerging data suggests that AMY1 could be a second CGRP receptor [http://www.ncbi.nlm.nih.gov/pubmed/29797087?dopt=AbstractPlus].

201The ligands described have limited selectivity. Adrenomedullin has appreciable affinity for CGRP receptors. CGRP can show significant cross‐reactivity at AMY receptors and AM2 receptors. Adrenomedullin 2/intermedin also has high affinity for the AM2 receptor [http://www.ncbi.nlm.nih.gov/pubmed/21658025?dopt=AbstractPlus]. CGRP‐(8‐37) acts as an antagonist of CGRP (pKi 8) and inhibits some AM and AMY responses (pKi 6‐7). It is weak at CT receptors. HumanAM‐(22‐52)has some selectivity towardsAM receptors, but with modest potency (pKi 7), limiting its use [http://www.ncbi.nlm.nih.gov/pubmed/12970090?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=702 shows the greatest selectivity between receptors but still has significant affinity for AMY1 receptors [http://www.ncbi.nlm.nih.gov/pubmed/26125036?dopt=AbstractPlus].

202Gs is a prominent route for effector coupling for CLR and CTR but other pathways (e.g. Ca2+, ERK, Akt), and G proteins can be activated [http://www.ncbi.nlm.nih.gov/pubmed/20633935?dopt=AbstractPlus]. There is evidence that CGRP‐RCP (a 148 amino‐acid hydrophilic protein, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:746 (http://www.uniprot.org/uniprot/P04424) is important for the coupling of CLR to adenylyl cyclase [http://www.ncbi.nlm.nih.gov/pubmed/10903324?dopt=AbstractPlus].

203[125I]‐Salmon CT is the most common radioligand for CT receptors but it has high affinity for AMY receptors and is also poorly reversible.

Overview

209The calcium‐sensing receptor (CaS, provisional nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) responds to multiple endogenous ligands, including extracellular calcium and other divalent/trivalent cations, polyamines and polycationic peptides, L‐amino acids (particularly L‐Trp and L‐Phe), glutathione and various peptide analogues, ionic strength and extracellular pH (reviewed in [http://www.ncbi.nlm.nih.gov/pubmed/24111791?dopt=AbstractPlus]). While divalent/trivalent cations, polyamines and polycations are CaS receptor agonists [http://www.ncbi.nlm.nih.gov/pubmed/8255296?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9357776?dopt=AbstractPlus], L‐amino acids, glutamyl peptides, ionic strength and pH are allosteric modulators of agonist function [http://www.ncbi.nlm.nih.gov/pubmed/10781086?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10781086?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/7493018?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15201280?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9677383?dopt=AbstractPlus]. Indeed, L‐amino acids have been identified as "co‐agonists", with both concomitant calcium and L‐amino acid binding required for full receptor activation [http://www.ncbi.nlm.nih.gov/pubmed/27434672?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/27746744?dopt=AbstractPlus]. The sensitivity of the CaS receptor to primary agonists is increased by elevated extracellular pH [http://www.ncbi.nlm.nih.gov/pubmed/25556167?dopt=AbstractPlus] or decreased extracellular ionic strength [http://www.ncbi.nlm.nih.gov/pubmed/9677383?dopt=AbstractPlus]. This receptor bears no sequence or structural relation to the plant calcium receptor, also called CaS.

Comments

210The CaS receptor has a number of physiological functions, but it is best known for its central role in parathyroid and renal regulation of extracellular calcium homeostasis [http://www.ncbi.nlm.nih.gov/pubmed/27647839?dopt=AbstractPlus]. This is seen most clearly in patients with loss‐of‐function CaS receptor mutations who develop familial hypocalciuric hypercalcaemia (heterozygous mutations) or neonatal severe hyperparathyroidism (heterozygous, compound heterozygous or homozygous mutations) [http://www.ncbi.nlm.nih.gov/pubmed/27647839?dopt=AbstractPlus] and in Casr null mice [http://www.ncbi.nlm.nih.gov/pubmed/18765830?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/7493018?dopt=AbstractPlus], which exhibit similar increases in PTH secretion and blood calcium levels. Gain‐of‐function CaS mutations are associated with autosomal dominant hypocalcaemia and Bartter syndrome type V [http://www.ncbi.nlm.nih.gov/pubmed/27647839?dopt=AbstractPlus].

211The CaS receptor primarily couples to Gq/11, G12/13 and Gi/o [http://www.ncbi.nlm.nih.gov/pubmed/22210744?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16247029?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12954603?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22192592?dopt=AbstractPlus], but in some cell types can couple to Gs [http://www.ncbi.nlm.nih.gov/pubmed/20032198?dopt=AbstractPlus]. However, the CaS receptor can form heteromers with Class C GABAB [http://www.ncbi.nlm.nih.gov/pubmed/17591780?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17615148?dopt=AbstractPlus] and mGlu1/5 receptors [http://www.ncbi.nlm.nih.gov/pubmed/11489900?dopt=AbstractPlus], which may introduce further complexity in its signalling capabilities.

212Multiple other small molecule chemotypes are positive and negative allosteric modulators of the CaS receptor [http://www.ncbi.nlm.nih.gov/pubmed/21406038?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24050279?dopt=AbstractPlus]. Further, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=8375 is a novel peptide positive allosteric modulator of the receptor [http://www.ncbi.nlm.nih.gov/pubmed/23674604?dopt=AbstractPlus]. Agonists and positive allosteric modulators of the CaS receptor are termed Type I and II calcimimetics, respectively, and can suppress parathyroid hormone (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1785 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9606, http://www.uniprot.org/uniprot/P01270)) secretion [http://www.ncbi.nlm.nih.gov/pubmed/9520489?dopt=AbstractPlus]. Negative allosteric modulators are called calcilytics and can act to increase http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1785, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9606) secretion [http://www.ncbi.nlm.nih.gov/pubmed/11561095?dopt=AbstractPlus].

213Where functional pKB values are provided for allosteric modulators, this refers to ligand affinity determined in an assay that measures a functional readout of receptor activity (i.e. a receptor signalling assay), as opposed to affinity determined in a radioligand binding assay. The functional pKB may differ depending on the signalling pathway studied. Consult the http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=54&familyId=12&familyType=GPCR#Allosterics for the assay description, as well as other functional readouts.

Overview

218Cannabinoid receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Cannabinoid Receptors [http://www.ncbi.nlm.nih.gov/pubmed/21079038?dopt=AbstractPlus]) are activated by endogenous ligands that include N‐arachidonoylethanolamine (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2364), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5444‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5444, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5445 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=729. Potency determinations of endogenous agonists at these receptors are complicated by the possibility of differential susceptibility of endogenous ligands to enzymatic conversion [http://www.ncbi.nlm.nih.gov/pubmed/17876303?dopt=AbstractPlus].

219There are currently three licenced cannabinoid medicines each of which contains a compound that can activate CB1 and CB2 receptors [http://www.ncbi.nlm.nih.gov/pubmed/23108552?dopt=AbstractPlus]. Two of these medicines were developed to suppress nausea and vomiting produced by chemotherapy. These are http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9071 (Cesamet®), a synthetic CB1/CB2 receptor agonist, and synthetic http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2424 (Marinol®; dronabinol), which can also be used as an appetite stimulant. The third medicine, Sativex®, contains mainly http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2424 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4150, both extracted from cannabis, and is used to treat multiple sclerosis and cancer pain.

Comments

220Both CB1 and CB2 receptors may be labelled with [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=734 (0.5 nM;[http://www.ncbi.nlm.nih.gov/pubmed/8819477?dopt=AbstractPlus]) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=736 (2‐2.4 nM; [http://www.ncbi.nlm.nih.gov/pubmed/7651369?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8622639?dopt=AbstractPlus]). http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2364 is also an agonist at vanilloid receptors (http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=78%23show_object_507)and http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=86 [http://www.ncbi.nlm.nih.gov/pubmed/17704824?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10440374?dopt=AbstractPlus]. There is evidence for an allosteric site on the CB1 receptor [http://www.ncbi.nlm.nih.gov/pubmed/16113085?dopt=AbstractPlus]. All of the compounds listed as antagonists behave as inverse agonists in some bioassay systems [http://www.ncbi.nlm.nih.gov/pubmed/21079038?dopt=AbstractPlus]. For some cannabinoid receptor ligands, additional pharmacological targets that include GPR55 and GPR119 have been identified [http://www.ncbi.nlm.nih.gov/pubmed/21079038?dopt=AbstractPlus]. Moreover, http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=114 although showing little structural similarity to CB1 and CB2 receptors, respond to endogenous agents that are structurally similar to the endogenous cannabinoid ligands [http://www.ncbi.nlm.nih.gov/pubmed/21079038?dopt=AbstractPlus].

Overview

224Nomenclature for the chemerin receptors is presented as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/29279348?dopt=AbstractPlus]). The chemoattractant protein and adipokine, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2945 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9868, http://www.uniprot.org/uniprot/Q99969), has been shown to be the endogenous ligand for both chemerin family receptors. Chemerin1 was the founding family member, and when GPR1 was de‐orphanised it was re‐named Chermerin2 [http://www.ncbi.nlm.nih.gov/pubmed/29279348?dopt=AbstractPlus]. Chemerin1 is also activated by the lipid‐derived, antiinflammatory ligand http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3333 (RvE1), which is formed via the sequential metabolism of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3362 by aspirin‐modified cyclooxygenase and lipoxygenase [http://www.ncbi.nlm.nih.gov/pubmed/15753205?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17339491?dopt=AbstractPlus]. In addition, two GPCRs for http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3934 (RvD1) have been identified: FPR2/ALX, the lipoxin A4 receptor, and GPR32, an orphan receptor [http://www.ncbi.nlm.nih.gov/pubmed/20080636?dopt=AbstractPlus].

Comments

225CCX832 (structure not disclosed) is a selective antagonist, pKi=9.2 [http://www.ncbi.nlm.nih.gov/pubmed/27742615?dopt=AbstractPlus].

Overview

228Chemokine receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Chemokine Receptors [http://www.ncbi.nlm.nih.gov/pubmed/24218476?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12037138?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10699158?dopt=AbstractPlus]) comprise a large subfamily of 7TM proteins that bind one or more chemokines, a large family of small cytokines typically possessing chemotactic activity for leukocytes. Additional hematopoietic and non‐hematopoietic roles have been identified for many chemokines in the areas of embryonic development, immune cell proliferation, activation and death, viral infection, and as antibiotics, among others. Chemokine receptors can be divided by function into two main groups: G protein‐coupled chemokine receptors, which mediate leukocyte trafficking, and "Atypical chemokine receptors", which may signal through non‐G protein‐coupled mechanisms and act as chemokine scavengers to downregulate inflammation or shape chemokine gradients [http://www.ncbi.nlm.nih.gov/pubmed/24218476?dopt=AbstractPlus].

229Chemokines in turn can be divided by structure into four subclasses by the number and arrangement of conserved cysteines. CC (also known as β‐chemokines; n= 28), CXC (also known as α‐chemokines; n= 17) and CX3C (n= 1) chemokines all have four conserved cysteines, with zero, one and three amino acids separating the first two cysteines respectively. C chemokines (n= 2) have only the second and fourth cysteines found in other chemokines. Chemokines can also be classified by function into homeostatic and inflammatory subgroups. Most chemokine receptors are able to bind multiple high‐affinity chemokine ligands, but the ligands for a given receptor are almost always restricted to the same structural subclass. Most chemokines bind to more than one receptor subtype. Receptors for inflammatory chemokines are typically highly promiscuous with regard to ligand specificity, and may lack a selective endogenous ligand. G protein‐coupled chemokine receptors are named acccording to the class of chemokines bound, whereas ACKR is the root acronym for atypical chemokine receptors [http://www.ncbi.nlm.nih.gov/pubmed/25958743?dopt=AbstractPlus]. There can be substantial cross‐species differences in the sequences of both chemokines and chemokine receptors, and in the pharmacology and biology of chemokine receptors. Endogenous and microbial non‐chemokine ligands have also been identified for chemokine receptors. Many chemokine receptors function as HIV co‐receptors, but CCR5 is the only one demonstrated to play an essential role in HIV/AIDS pathogenesis. The tables include bothstandard chemokine receptor names [http://www.ncbi.nlm.nih.gov/pubmed/10714678?dopt=AbstractPlus] and aliases.

Comments

230Specific chemokine receptors facilitate cell entry by microbes, such as ACKR1 for Plasmodium vivax, and CCR5 and CXCR4 for HIV‐1. Virally encoded chemokine receptors are known (e.g. US28, a homologue of CCR1 from human cytomegalovirus and ORF74, which encodes a homolog of CXCR2 in Herpesvirus saimiri and gamma‐Herpesvirus‐68), but their role in viral life cycles is not established. Viruses can exploit or subvert the chemokine system by producing chemokine antagonists and scavengers. Three chemokine receptor antagonists have now been approved by the FDA: 1) the CCR5 antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=806 (Pfizer) for treatment of HIV/AIDS in patients with CCR5‐using strains; and 2) the CXCR4 antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=844 (Sanofi) for hematopoietic stem cell mobilization with http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4934 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2438, http://www.uniprot.org/uniprot/P09919) in patients undergoing transplantation in the context of chemotherapy for Hodgkins’ Disease and multiple myeloma; and 3) the CCR4 blocking antibody Poteligeo (mogamulizumab‐kpkc, Kyowa Kirin, Inc.) for mycosis fungoides or Sezary syndrome.

Overview

236Cholecystokinin receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on CCK receptors [http://www.ncbi.nlm.nih.gov/pubmed/10581329?dopt=AbstractPlus) are activated by the endogenous peptides cholecystokinin‐8 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=864 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1569, http://www.uniprot.org/uniprot/P06307)), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=860, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1569), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3552, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1569) and gastrin (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3559 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4164, http://www.uniprot.org/uniprot/P01350)). There are only two distinct subtypes of CCK receptors, CCK1 and CCK2 receptors [http://www.ncbi.nlm.nih.gov/pubmed/1373504?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/1313582?dopt=AbstractPlus], with some alternatively spliced forms most often identified in neoplastic cells. The CCK receptor subtypes are distinguished by their peptide selectivity, with the CCK1 receptor requiring the carboxyl‐terminal heptapeptide‐amide that includes a sulfated tyrosine for high affinity and potency, while the CCK2 receptor requires only the carboxyl‐terminal tetrapeptide shared by each CCK and gastrin peptides. These receptors have characteristic and distinct distributions, with both present in both the central nervous system and peripheral tissues.

Comments

237While a cancer‐specific CCK receptor has been postulated to exist, which also might be responsive to incompletely processed forms of CCK (Gly‐extended forms), this has never been isolated. An alternatively spliced form of the CCK2 receptor in which intron 4 is retained, adding 69 amino acids to the intracellular loop 3 (ICL3) region, has been described to be present particularly in certain neoplasms where mRNA mis‐splicing has been commonly observed [http://www.ncbi.nlm.nih.gov/pubmed/12429993?dopt=AbstractPlus], but it is not clear that this receptor splice form plays a special role in carcinogenesis. Another alternative splicing event for the CCK2 receptor was reported [http://www.ncbi.nlm.nih.gov/pubmed/8415658?dopt=AbstractPlus], with alternative donor sites in exon 4 resulting in long (452 amino acids) and short (447 amino acids) forms of the receptor differing by five residues in ICL3, however, no clear functional differences have been observed.

Overview

242Receptors of the Class Frizzled (FZD, nomenclature as agreed by the NC‐IUPHAR subcommittee on the Class Frizzled GPCRs [http://www.ncbi.nlm.nih.gov/pubmed/21079039?dopt=AbstractPlus]), are GPCRs originally identified in Drosophila [http://www.ncbi.nlm.nih.gov/pubmed/1334084?dopt=AbstractPlus], which are highly conserved across species. While SMO shows structural resemblance to the 10 FZDs, it is functionally separated as it mediates effects in the Hedgehog signaling pathway [http://www.ncbi.nlm.nih.gov/pubmed/21079039?dopt=AbstractPlus]. FZDs are activated by WNTs, which are cysteine‐rich lipoglycoproteins withfundamentalfunctions inontogeny and tissue homeostasis. FZD signalling was initially divided into two pathways, being either dependent on the accumulation of the transcription regulator http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5371 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2514, http://www.uniprot.org/uniprot/P35222) or being β‐catenin‐independent (often referred to as canonical vs. non‐canonical WNT/FZD signalling, respectively). WNT stimulation of FZDs can, in cooperation with the low density lipoprotein receptors https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6697 (http://www.uniprot.org/uniprot/O75197) and https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6698 (http://www.uniprot.org/uniprot/O75581), lead to the inhibition of a constitutively active destruction complex, which results in the accumulation of β‐catenin and subsequently its translocation to the nucleus. β‐Catenin, in turn, modifies gene transcription by interacting with TCF/LEF transcription factors. βCatenin‐independent FZD signalling is far more complex with regard to the diversity of the activated pathways. WNT/FZD signalling can lead to the activation of heterotrimeric G proteins [http://www.ncbi.nlm.nih.gov/pubmed/24032637?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/28790300?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30049420?dopt=AbstractPlus], the elevation of intracellular calcium [http://www.ncbi.nlm.nih.gov/pubmed/9389482?dopt=AbstractPlus], activation of cGMP‐specific PDE6 [http://www.ncbi.nlm.nih.gov/pubmed/12471263?dopt=AbstractPlus] and elevation of cAMP as well as RAC‐1, JNK, Rho and Rho kinase signalling [http://www.ncbi.nlm.nih.gov/pubmed/19651774?dopt=AbstractPlus]. Novel resonance energy transfer‐based tools have allowed the study of the GPCR‐like nature of FZDs in greater detail. Upon ligand stimulation, FZDs undergo conformational changes and signal via heterotrimeric G proteins [http://www.ncbi.nlm.nih.gov/pubmed/30514810?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30737406?dopt=AbstractPlus]. Furthermore, the phosphoprotein Dishevelled constitutes a key player in WNT/FZD signalling. Importantly, FZDs exist in at least two distinct conformational states that regulate the pathway selection [http://www.ncbi.nlm.nih.gov/pubmed/30737406?dopt=AbstractPlus]. As with other GPCRs, members of the Frizzled family are functionally dependent on the arrestin scaffolding protein for internalization [http://www.ncbi.nlm.nih.gov/pubmed/12958365?dopt=AbstractPlus], as well as for β‐catenin‐dependent [http://www.ncbi.nlm.nih.gov/pubmed/17426148?dopt=AbstractPlus] and ‐independent [http://www.ncbi.nlm.nih.gov/pubmed/18953287?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17476309?dopt=AbstractPlus] signalling. The pattern of cell signalling is complicated by the presence of additional ligands, which can enhance or inhibit FZD signalling (secreted Frizzled‐related proteins (sFRP), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5372 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18081, http://www.uniprot.org/uniprot/Q9Y5W5) (WIF), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3704 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:13771, http://www.uniprot.org/uniprot/Q9BQB4) or Dickkopf (DKK)), as well as modulatory (co)‐receptors with http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=304#Type XV RTKs: RYK, http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=304#Type VIII RTKs: ROR1, http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=304#Type VIII RTKs: ROR2 and Kremen, which may also function as independent signalling proteins.

Comments

243There is limited knowledge about WNT/FZD specificity and which molecular entities determine the signalling outcome of a specific WNT/FZD pair. Understanding of theFZD and SMO coupling to G proteins is incomplete, but progress have been made [http://www.ncbi.nlm.nih.gov/pubmed/27458145?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24032637?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24873871?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26179037?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16885213?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23292797?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22179044?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30514810?dopt=AbstractPlus]. There is also a scarcity of information on basic pharmacological characteristics of FZDs, such as binding constants, ligand specificity or concentration‐response relationships [http://www.ncbi.nlm.nih.gov/pubmed/19208479?dopt=AbstractPlus]. Development of pharmacological tools for SMO has been faciliated by successful crystalization of several SMO structures [http://www.ncbi.nlm.nih.gov/pubmed/27437577?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/29804838?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25008467?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23636324?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24525480?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/28513578?dopt=AbstractPlus]. The recently solved FZD4 in apo state has provided first insight into FZD transmembranous organization [http://www.ncbi.nlm.nih.gov/pubmed/30135577?dopt=AbstractPlus].

Ligands associated with FZD signalling

244WNTs: http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3672 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12774, http://www.uniprot.org/uniprot/P04628), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3673 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12780, http://www.uniprot.org/uniprot/P09544) (also known as Int‐1‐related protein), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3674 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12781, http://www.uniprot.org/uniprot/Q93097) (also known as WNT‐13), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3675 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12782, http://www.uniprot.org/uniprot/P56703), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3549 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:15983, http://www.uniprot.org/uniprot/P56704), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3547 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12783, http://www.uniprot.org/uniprot/P56705), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3548 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12784, http://www.uniprot.org/uniprot/P41221) (pEC50 7.7‐8.9 [http://www.ncbi.nlm.nih.gov/pubmed/30514810?dopt=AbstractPlus]), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3676 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16265, http://www.uniprot.org/uniprot/Q9H1J7), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3678 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12785, http://www.uniprot.org/uniprot/Q9Y6F9), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3679 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12786, http://www.uniprot.org/uniprot/O00755), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3681 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12787, http://www.uniprot.org/uniprot/P56706), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3682 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12788, http://www.uniprot.org/uniprot/Q9H1J5), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3683 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12789, http://www.uniprot.org/uniprot/Q93098), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3684 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12778, http://www.uniprot.org/uniprot/O14904) (also known as WNT‐14), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3686 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12779, http://www.uniprot.org/uniprot/O14905) (also known as WNT‐15 or WNT14b), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3687(https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:13829, http://www.uniprot.org/uniprot/Q9GZT5), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3688 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12775, http://www.uniprot.org/uniprot/O00744) (also known as WNT‐12), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3689 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12776, http://www.uniprot.org/uniprot/O96014) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3690 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16267, http://www.uniprot.org/uniprot/Q9UBV4).

245Extracellular proteins that interact with FZDs: http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1063 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7678, http://www.uniprot.org/uniprot/Q00604), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3700 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:16175, http://www.uniprot.org/uniprot/Q2I0M5), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3691 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10776, http://www.uniprot.org/uniprot/Q8N474), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3692 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10777, http://www.uniprot.org/uniprot/Q96HF1), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3693 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3959,http://www.uniprot.org/uniprot/Q92765), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3694 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10778, http://www.uniprot.org/uniprot/Q6FHJ7), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3695 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10779, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10779).

246Extracellular proteins that interact with WNTs or LRPs: http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3701 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2891, http://www.uniprot.org/uniprot/O94907), https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18081 (http://www.uniprot.org/uniprot/Q9Y5W5), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3704 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:13771, http://www.uniprot.org/uniprot/Q9BQB4), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3702 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:17550, http://www.uniprot.org/uniprot/Q96MU8) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3703 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18797, http://www.uniprot.org/uniprot/Q8NCW0)

247Small exogenous ligands: Foxy‐5 [http://www.ncbi.nlm.nih.gov/pubmed/18927296?dopt=AbstractPlus], Box‐5 [http://www.ncbi.nlm.nih.gov/pubmed/19901340?dopt=AbstractPlus], UM206 [http://www.ncbi.nlm.nih.gov/pubmed/21931076?dopt=AbstractPlus], and XWnt8 (http://www.uniprot.org/uniprot/P28026) also known as mini‐Wnt8.

248Ligands associated with SMO signalling: http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2718, oxysterols [http://www.ncbi.nlm.nih.gov/pubmed/27437577?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/27705744?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30340023?dopt=AbstractPlus].

Overview

254Complement peptide receptors (nomenclature as agreed by the NC‐IUPHAR subcommittee on Complement peptide receptors [http://www.ncbi.nlm.nih.gov/pubmed/23383423?dopt=AbstractPlus]) are activated by the endogenous 75 amino‐acid anaphylatoxin polypeptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3640 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1318, http://www.uniprot.org/uniprot/P01024) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=573 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1331, http://www.uniprot.org/uniprot/P01031), generated upon stimulation of the complement cascade. C3a and C5a exert their functions through binding to their receptors (C3aR and C5aR), causing cell activation and triggering cellular degranulation that contributes to the local inflammation.

Comments

255http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3529 has also been reported to have agonist properties at the C3a receptor [http://www.ncbi.nlm.nih.gov/pubmed/16154494?dopt=AbstractPlus]. The putative chemoattractant receptor termed C5a2 (also known as GPR77, C5L2) binds [125I]C5a with no clear signalling function, but has a putative role opposing inflammatory responses [http://www.ncbi.nlm.nih.gov/pubmed/11773063?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15784721?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15715664?dopt=AbstractPlus]. Binding to this site may be displaced with the rank order http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=574 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1331)> http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=573 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1331, http://www.uniprot.org/uniprot/P01031[http://www.ncbi.nlm.nih.gov/pubmed/11773063?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12899627?dopt=AbstractPlus] while there is controversy over the ability of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3640 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1318, http://www.uniprot.org/uniprot/P01024) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5367 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1318, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1318) to compete [http://www.ncbi.nlm.nih.gov/pubmed/15990859?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12540846?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15833747?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12899627?dopt=AbstractPlus]. C5a2 appears to lack G protein signalling and has been termed a decoy receptor [http://www.ncbi.nlm.nih.gov/pubmed/19100624?dopt=AbstractPlus]. However, C5a2 does recruit arrestin after ligand binding, which might provide a signaling pathway for this receptor [http://www.ncbi.nlm.nih.gov/pubmed/20044484?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19641221?dopt=AbstractPlus], and forms heteromers with C5a1. C5a, but not C5a‐des Arg, induces upregulation of heteromer formation between complement C5a receptors C5a1 and C5a2 [http://www.ncbi.nlm.nih.gov/pubmed/24060963?dopt=AbstractPlus]. There are also reports of pro‐inflammatory activity of C5a2, mediated by HMGB1, but the signaling pathway that underlies this is currently unclear (reviewed in [http://www.ncbi.nlm.nih.gov/pubmed/23239822?dopt=AbstractPlus]). More recently, work in T cells has shown that C5a1 and C5a2 act in opposition to each other and that altering the equilibrium between the two receptors, by differential expression or production of C5a‐des Arg (which favours C5a2), can affect the final cellular response [http://www.ncbi.nlm.nih.gov/pubmed/27313051?dopt=AbstractPlus].

Overview

262Corticotropin‐releasing factor (CRF, nomenclature as agreed by the NC‐IUPHAR subcommittee on Corticotropin‐releasing Factor Receptors [http://www.ncbi.nlm.nih.gov/pubmed/12615952?dopt=AbstractPlus]) receptors are activated by the endogenous peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=912 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2355, http://www.uniprot.org/uniprot/P06850), a 41 aminoacid peptide, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=919 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12516, http://www.uniprot.org/uniprot/P55089), 40 amino‐acids, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=921 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18414, http://www.uniprot.org/uniprot/Q96RP3), 38 amino‐acids and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=928 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:17781, http://www.uniprot.org/uniprot/Q969E3), 38 amino‐acids. CRF1 and CRF2 receptors are activated non‐selectively by CRH and UCN. CRF2 receptors are selectively activated by UCN2 and UCN3. Binding to CRF receptors can be conducted using radioligands [125I]Tyr0‐CRF or [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5389‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5389 with K d values of 0.1‐0.4 nM. CRF1 and CRF2 receptors are non‐selectively antagonized by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=923, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3865) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=925. CRF1 receptors are selectively antagonized by small molecules http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3512, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3520, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3489, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3495, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3496. CRF2 receptors are selectively antagonized by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=931 and astressin 2B.

Comments

263A CRF binding protein has been identified (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2356, http://www.uniprot.org/uniprot/P24387) to which both http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=912 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2355, http://www.uniprot.org/uniprot/P06850) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=919 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12516, http://www.uniprot.org/uniprot/P55089) bind with high affinities, which has been suggested to bind and inactivate circulating http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=912, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2355) [http://www.ncbi.nlm.nih.gov/pubmed/7595134?dopt=AbstractPlus].

Overview

270Dopamine receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Dopamine Receptors [1906]) are commonly divided into D1‐like (D1 and D5) and D2‐like (D2, D3 and D4) families, where the endogenous agonist is http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=940.

Comments

271The selectivity of many of these agents is less than two orders of magnitude. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3299 exhibits similar high affinity for D2 and D3 receptors (low affinity for D4), but has been used to label D2 receptors in the presence of a D3‐selective antagonist. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3296 has similar affinity for D2 and D3 receptors, but labels only D3 receptors in the absence of divalent cations. The pharmacological profile of the D5 receptor is similar to, yet distinct from, that of the D1 receptor. The splice variants of the D2 receptor are commonly termed D2S and D2L (short and long). The DRD4 gene encoding the D4 receptor is highly polymorphic in humans, with allelic variations of the protein from amino acid 387 to 515.

Overview

279Endothelin receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Endothelin Receptors [http://www.ncbi.nlm.nih.gov/pubmed/12037137?dopt=AbstractPlus]) are activated by the endogenous 21 amino‐acid peptides endothelins 1‐3 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=989 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3176, http://www.uniprot.org/uniprot/P05305), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=990 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3177, http://www.uniprot.org/uniprot/P20800) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1004 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3178, http://www.uniprot.org/uniprot/P14138)).

Comments

280Splice variants of the ETA receptor have been identified in rat pituitary cells; one of these, ETAR‐C13, appeared to show loss of function with comparable plasma membrane expression to wild type receptor [http://www.ncbi.nlm.nih.gov/pubmed/17312275?dopt=AbstractPlus]. Subtypes of the ETB receptor have been proposed, although gene disruption studies in mice suggest that only a single gene product exists [http://www.ncbi.nlm.nih.gov/pubmed/9113361?dopt=AbstractPlus]. Crystal structures of the ETB receptor bound to the antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3494 and ETB selective analogue http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9651 [http://www.ncbi.nlm.nih.gov/pubmed/28805809?dopt=AbstractPlus] and selective ETB agonists http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1004 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3178, http://www.uniprot.org/uniprot/P14138) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3886 [http://www.ncbi.nlm.nih.gov/pubmed/30413709?dopt=AbstractPlus] have been reported.

Overview

286The G protein‐coupled estrogen receptor (GPER, nomenclature as agreed by the NC‐IUPHAR Subcommittee on the G protein‐coupled estrogen receptor [http://www.ncbi.nlm.nih.gov/pubmed/26023144?dopt=AbstractPlus]) was identified following observations of estrogen‐evoked http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2352 signalling in breast cancer cells [http://www.ncbi.nlm.nih.gov/pubmed/8078914?dopt=AbstractPlus], which mirrored the differential expression of an orphan 7‐transmembrane receptor GPR30 [http://www.ncbi.nlm.nih.gov/pubmed/9367686?dopt=AbstractPlus]. There are observations of both cell‐surface and intracellular expression of the GPER receptor [http://www.ncbi.nlm.nih.gov/pubmed/15705806?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15539556?dopt=AbstractPlus]. Selective agonist/ antagonists for GPER have been characterized [http://www.ncbi.nlm.nih.gov/pubmed/26023144?dopt=AbstractPlus]. Antagonists of the nuclear estrogen receptor, such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1015 [http://www.ncbi.nlm.nih.gov/pubmed/11043579?dopt=AbstractPlus], http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1016 [http://www.ncbi.nlm.nih.gov/pubmed/15705806?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15539556?dopt=AbstractPlus] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2820 [http://www.ncbi.nlm.nih.gov/pubmed/24379833?dopt=AbstractPlus], as well as the flavonoid ’phytoestrogens’ http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2826 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5346 [http://www.ncbi.nlm.nih.gov/pubmed/15090535?dopt=AbstractPlus], are agonists of GPER. A complete review of GPER pharmacology has been recently published [http://www.ncbi.nlm.nih.gov/pubmed/26023144?dopt=AbstractPlus]. The roles of GPER in physiological systems throughout the body (cardiovascular, metabolic, endocrine, immune, reproductive) and in cancer have also been reviewed [http://www.ncbi.nlm.nih.gov/pubmed/28595943?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/28249728?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/28343901?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26023144?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26189910?dopt=AbstractPlus].

Comments

287Antagonists at the nuclear estrogen receptor, such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1015, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1016 [http://www.ncbi.nlm.nih.gov/pubmed/11043579?dopt=AbstractPlus] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2820 [http://www.ncbi.nlm.nih.gov/pubmed/24379833?dopt=AbstractPlus], as well as the flavonoid ‘phytoestrogens’ http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2826 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5346 [http://www.ncbi.nlm.nih.gov/pubmed/15090535?dopt=AbstractPlus], are agonists at GPER receptors. A complete review of GPER pharmacology has been recently published [http://www.ncbi.nlm.nih.gov/pubmed/26023144?dopt=AbstractPlus].

Overview

292The http://www.ensembl.org/Homo_sapiens/Gene/Family/Genes?family=ENSFM00510000502765 (nomenclature agreed by the NC‐IUPHAR Subcommittee on the formylpeptide receptor family [http://www.ncbi.nlm.nih.gov/pubmed/19498085?dopt=AbstractPlus]) respond to exogenous ligands such as the bacterial product http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1022 (fMLP) and endogenous ligands such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1031 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:533, http://www.uniprot.org/uniprot/P04083), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3570 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2532, http://www.uniprot.org/uniprot/P08311), amyloid β42, serum amyloid A and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1026, derived from http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5370 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4827, http://www.uniprot.org/uniprot/P68871).

Comments

293Note that the data for FPR2/ALX are also reproduced on the http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=35 receptor page.

Overview

300Free fatty acid receptors (FFA, nomenclature as agreed by the NC‐IUPHAR Subcommittee on free fatty acid receptors [http://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19047536?dopt=AbstractPlus]) are activated by free fatty acids. Long‐chain saturated and unsaturated fatty acids (including C14.0 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2806), C16:0 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1055), C18:1 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1054), C18:2 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1052), C18:3, (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1049), C20:4 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2391), C20:5,n‐3 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3362) and C22:6,n‐3 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1051)) activate FFA1 [http://www.ncbi.nlm.nih.gov/pubmed/12496284?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12629551?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12565875?dopt=AbstractPlus] and FFA4 receptors [http://www.ncbi.nlm.nih.gov/pubmed/15619630?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22343897?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20813258?dopt=AbstractPlus], while short chain fatty acids (C2 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1058), C3 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1062), C4 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1059) and C5 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1061)) activate FFA2 [http://www.ncbi.nlm.nih.gov/pubmed/12496283?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12711604?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12684041?dopt=AbstractPlus] and FFA3 [http://www.ncbi.nlm.nih.gov/pubmed/12496283?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12711604?dopt=AbstractPlus] receptors. The crystal structure for agonist bound FFA1 has been described [http://www.ncbi.nlm.nih.gov/pubmed/25043059?dopt=AbstractPlus].

Comments

301Short (361 amino acids) and long (377 amino acids) splice variants of human FFA4 have been reported [http://www.ncbi.nlm.nih.gov/pubmed/19723586?dopt=AbstractPlus], which differ by a 16 amino acid insertion in intracellular loop 3, and exhibit differences in intracellular signalling properties in recombinant systems [http://www.ncbi.nlm.nih.gov/pubmed/22282525?dopt=AbstractPlus]. The long FFA4 splice variant has not been identified in other primates or rodents to date [http://www.ncbi.nlm.nih.gov/pubmed/15619630?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19723586?dopt=AbstractPlus].

302https://www.genenames.org/data/gene‐symbol‐report/%23!/hgnc_id/HGNC:4500 was originally described as a pseudogene within the family (http://www.ensembl.org/Homo_sapiens/Gene/Family/Genes?family=ENSFM00250000002583), but the discovery of several polymorphisms suggests that some versions of GPR42 may be functional [http://www.ncbi.nlm.nih.gov/pubmed/19630535?dopt=AbstractPlus]. https://www.genenames.org/data/gene‐symbol‐report/%23!/hgnc_id/HGNC:4535 is a structurally‐unrelated G protein‐coupled receptor which has been found to respond to medium chain fatty acids [http://www.ncbi.nlm.nih.gov/pubmed/16966319?dopt=AbstractPlus].

Overview

309Functional GABAB receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on GABAB receptors [http://www.ncbi.nlm.nih.gov/pubmed/12037141?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17329545?dopt=AbstractPlus]) are formed from the heterodimerization of two similar 7TM subunits termed GABAB1 and GABAB2 [http://www.ncbi.nlm.nih.gov/pubmed/12037141?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17499108?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15451400?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17329545?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17433877?dopt=AbstractPlus]. GABAB receptors are widespread in the CNS and regulate both pre‐ and postsynaptic activity. The GABAB1 subunit, when expressed alone, binds both antagonists and agonists, but the affinity of the latter is generally 10‐100fold less than for the native receptor. Co‐expression of GABAB1 and GABAB2 subunits allows transport of GABAB1 to the cell surface and generates a functional receptor that can couple to signal transduction pathways such as high‐voltage‐activated Ca2+ channels (Cav2.1, Cav2.2), or inwardly rectifying potassium channels (Kir3) [http://www.ncbi.nlm.nih.gov/pubmed/15269338?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12037141?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10604925?dopt=AbstractPlus]. The GABAB1 subunit harbours the GABA (orthosteric)‐binding site within an extracellular domain (ECD) venus flytrap module (VTM), whereas the GABAB2 subunit mediates G protein‐coupled signalling [http://www.ncbi.nlm.nih.gov/pubmed/12037141?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24305054?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22660477?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15451400?dopt=AbstractPlus]. The two subunits interact by direct allosteric coupling [http://www.ncbi.nlm.nih.gov/pubmed/21063387?dopt=AbstractPlus], such that GABAB2 increases the affinity of GABAB1 for agonists and reciprocally GABAB1 facilitates the coupling of GABAB2 to G proteins [http://www.ncbi.nlm.nih.gov/pubmed/24305054?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15922585?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15451400?dopt=AbstractPlus]. GABAB1 and GABAB2 subunits assemble in a 1:1 stoichiometry by means of a coiled‐coil interaction between α‐helices within their carboxy‐termini that masks an endoplasmic reticulum retention motif (RXRR) within the GABAB1 subunit but other domains of the proteins also contribute to their heteromerization [http://www.ncbi.nlm.nih.gov/pubmed/15269338?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24778228?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15451400?dopt=AbstractPlus]. Recent evidence indicates that higher order assemblies of GABAB receptor comprising dimers of heterodimers occur in recombinant expression systems and in vivo and that such complexes exhibit negative functional cooperativity between heterodimers [http://www.ncbi.nlm.nih.gov/pubmed/21552208?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19723778?dopt=AbstractPlus]. Adding further complexity, KCTD (potassium channel tetramerization proteins) 8, 12, 12b and 16 associate as tetramers with the carboxy terminus of the GABAB2 subunit to impart altered signalling kinetics and agonist potency to the receptor complex [http://www.ncbi.nlm.nih.gov/pubmed/20406808?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20400944?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24836506?dopt=AbstractPlus] and are reviewed by [http://www.ncbi.nlm.nih.gov/pubmed/20655485?dopt=AbstractPlus]. The molecular complexity of GABAB receptors is further increased through association with trafficking and effector proteins [Schwenk et al., 2016, Nature Neuroscience 19(2): 233‐42] and reviewed by [http://www.ncbi.nlm.nih.gov/pubmed/27905440?dopt=AbstractPlus]. Four isoforms of the human GABAB1 subunit have been cloned. The predominant GABAB1a and GABAB1b isoforms, which are most prevalent in neonatal and adult brain tissue respectively, differ in their ECD sequences as a result of the use of alternative transcription initiation sites. GABAB1a‐containing heterodimers localise todistal axonsand mediate inhibition of glutamate release in the CA3‐CA1 terminals, and GABA release onto the layer 5 pyramidal neurons, whereas GABAB1b‐containing receptors occur within dendritic spines and mediate slow postsynaptic inhibition [http://www.ncbi.nlm.nih.gov/pubmed/16701210?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16701209?dopt=AbstractPlus]. Only the 1a and 1b variants are identified as components of native receptors [http://www.ncbi.nlm.nih.gov/pubmed/12037141?dopt=AbstractPlus]. Additional GABAB1 subunit isoforms have been described in rodents and humans [http://www.ncbi.nlm.nih.gov/pubmed/21124972?dopt=AbstractPlus] and reviewed by [http://www.ncbi.nlm.nih.gov/pubmed/15269338?dopt=AbstractPlus].

310Subunits

Comments

311Potencies of agonists and antagonists listed in the table, quantified as IC50 values for the inhibition of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5381 binding to rat cerebral cortex membranes, are from [http://www.ncbi.nlm.nih.gov/pubmed/12037141?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21428811?dopt=AbstractPlus, 635]. Radioligand K D values relate to binding to rat brain membranes. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1074 is a photoaffinity ligand for the GABAB1 subunit [http://www.ncbi.nlm.nih.gov/pubmed/10658574?dopt=AbstractPlus]. CGP27492 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1081), CGP35024 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1080) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1082 act as antagonists at human GABAA ρ1 receptors, with potencies in the low micromolar range [http://www.ncbi.nlm.nih.gov/pubmed/21428811?dopt=AbstractPlus]. In addition to the ligands listed in the table, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=707 binds to the VTM of the GABAB1 subunit to act as a positive allosteric modulator of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1067 [http://www.ncbi.nlm.nih.gov/pubmed/10692480?dopt=AbstractPlus]. Synthetic positive allosteric modulators with low, or no, intrinsic activity include http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1079, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5446, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5503 [http://www.ncbi.nlm.nih.gov/pubmed/21181127?dopt=AbstractPlus] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5504 [http://www.ncbi.nlm.nih.gov/pubmed/17894647?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15269338?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15126507?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21428811?dopt=AbstractPlus]. The site of action of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1079 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5446 appears to be on the heptahelical domain of the GABAB2 subunit [http://www.ncbi.nlm.nih.gov/pubmed/16966477?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15451400?dopt=AbstractPlus]. In the presence of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1079 or http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5446, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1069 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1068 behave as partial agonists [http://www.ncbi.nlm.nih.gov/pubmed/21428811?dopt=AbstractPlus]. A negative allosteric modulator of GABAB activity has been reported [http://www.ncbi.nlm.nih.gov/pubmed/25050158?dopt=AbstractPlus]. Knock‐out of the GABAB1 subunit in C57B mice causes the development of severe tonic‐clonic convulsions that prove fatal within a month of birth, whereas GABAB1 ‐/‐ BALB/c mice, although also displaying spontaneous epileptiform activity, are viable. The phenotype of the latter animals additionally includes hyperalgesia, hyperlocomotion (in a novel, but not familiar, environment), hyperdopaminergia, memory impairment and behaviours indicative of anxiety [http://www.ncbi.nlm.nih.gov/pubmed/15451397?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16606363?dopt=AbstractPlus]. A similar phenotype has been found for GABAB2 ‐/‐ BALB/c mice [http://www.ncbi.nlm.nih.gov/pubmed/15240800?dopt=AbstractPlus].

Overview

316Galanin receptors (provisional nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by the endogenous peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3592 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4114, http://www.uniprot.org/uniprot/P22466) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3594 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:24840, http://www.uniprot.org/uniprot/Q9UBC7). Human http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3592 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4114, http://www.uniprot.org/uniprot/P22466) is a 30 amino‐acid non‐amidated peptide [http://www.ncbi.nlm.nih.gov/pubmed/1714839?dopt=AbstractPlus]; in other species, it is 29 amino acids long and C‐terminally amidated. Amino acids 1–14 of galanin are highly conserved in mammals, birds, reptiles, amphibia and fish. Shorter peptide species (e.g. human galanin‐1–19 [http://www.ncbi.nlm.nih.gov/pubmed/1710578?dopt=AbstractPlus] and porcine galanin‐5–29 [http://www.ncbi.nlm.nih.gov/pubmed/1283627?dopt=AbstractPlus]) and N‐terminally extended forms (e.g. N‐terminally seven and nine residue elongated forms of porcine galanin [http://www.ncbi.nlm.nih.gov/pubmed/1718731?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/1283627?dopt=AbstractPlus]) have been reported.

Comments

317http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5356) is a high‐affinity agonist at GAL1/GAL2 (pKi 9), and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5357) is selective for GAL2 and GAL3 compared with GAL1 [http://www.ncbi.nlm.nih.gov/pubmed/15944007?dopt=AbstractPlus]. [125I]‐[Tyr26]galanin binds to all three subtypes with K d values generally reported to range from 0.05 to 1 nM, depending on the assay conditions used [http://www.ncbi.nlm.nih.gov/pubmed/9808667?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/2436195?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9305929?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9722565?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9281594?dopt=AbstractPlus]. Porcine galanin‐(3‐29) does not bind to cloned GAL1, GAL2 or GAL3 receptors, but a receptor that is functionally activated by porcine galanin‐(3–29) has been reported in pituitary and gastric smooth muscle cells [http://www.ncbi.nlm.nih.gov/pubmed/7529309?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/7683428?dopt=AbstractPlus]. Additional galanin receptor subtypes are also suggested from studies with chimeric peptides (e.g. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3896, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3898 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3899), which act as antagonists in functional assays in the cardiovascular system [http://www.ncbi.nlm.nih.gov/pubmed/7693918?dopt=AbstractPlus], spinal cord [http://www.ncbi.nlm.nih.gov/pubmed/1373497?dopt=AbstractPlus], locus coeruleus, hippocampus [http://www.ncbi.nlm.nih.gov/pubmed/1720557?dopt=AbstractPlus] and hypothalamus [http://www.ncbi.nlm.nih.gov/pubmed/7504301?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/1283559?dopt=AbstractPlus], but exhibit agonist activity at some peripheral sites [http://www.ncbi.nlm.nih.gov/pubmed/7504301?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/7529309?dopt=AbstractPlus]. The chimeric peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3896, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3897, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3898, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3899 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3861 are agonists at GAL1 receptors expressed endogenously in Bowes human melanoma cells [http://www.ncbi.nlm.nih.gov/pubmed/10601261?dopt=AbstractPlus], and at heterologously expressed recombinant GAL1, GAL2 and GAL3 receptors [http://www.ncbi.nlm.nih.gov/pubmed/9808667?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9305929?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9722565?dopt=AbstractPlus]. Recent studies have described the synthesis of a series of novel, systemically‐active, galanin analogues, with modest preferential binding at the GAL2 receptor. Specific chemical modifications to the galanin backbone increased brain levels of these peptides after i.v. injection and several of these peptides exerted a potent antidepressant‐like effect in mouse models of depression [http://www.ncbi.nlm.nih.gov/pubmed/23600864?dopt=AbstractPlus].

Overview

323The ghrelin receptor (nomenclature as agreed by the NC‐IUPHAR Subcommittee for the Ghrelin receptor [http://www.ncbi.nlm.nih.gov/pubmed/16382107?dopt=AbstractPlus]) is activated by a 28 amino‐acid peptide originally isolated from rat stomach, where it is cleaved from a 117 aminoacid precursor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18129, http://www.uniprot.org/uniprot/Q9UBU3). The human gene encoding the precursor peptide has 83% sequence homology to rat preproghrelin, although the mature peptides from rat and human differ by only two amino acids [http://www.ncbi.nlm.nih.gov/pubmed/11549267?dopt=AbstractPlus]. Alternative splicing results in the formation of a second peptide, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3600 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18129, http://www.uniprot.org/uniprot/Q9UBU3) with equipotent biological activity [http://www.ncbi.nlm.nih.gov/pubmed/10801861?dopt=AbstractPlus]. A unique post‐translational modification (octanoylation of Ser3, catalysed by ghrelin O‐acyltransferase (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:32311, http://www.uniprot.org/uniprot/Q96T53) [http://www.ncbi.nlm.nih.gov/pubmed/18267071?dopt=AbstractPlus] occurs in both peptides, essential for full activity in binding to ghrelin receptors in the hypothalamus and pituitary, and for the release of growth hormone from the pituitary [http://www.ncbi.nlm.nih.gov/pubmed/10604470?dopt=AbstractPlus]. Structure activity studies showed the first five N‐terminal amino acids to be the minimum required for binding [http://www.ncbi.nlm.nih.gov/pubmed/11087562?dopt=AbstractPlus], and receptor mutagenesis has indicated overlap of the ghrelin binding site with those for small molecule agonists and allosteric modulators of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1099 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18129, http://www.uniprot.org/uniprot/Q9UBU3) function [http://www.ncbi.nlm.nih.gov/pubmed/18923064?dopt=AbstractPlus]. In cell systems, the ghrelin receptor is constitutively active [http://www.ncbi.nlm.nih.gov/pubmed/15383539?dopt=AbstractPlus], but this is abolished by a naturally occurring mutation (A204E) that results in decreased cell surface receptor expression and is associated with familial short stature [http://www.ncbi.nlm.nih.gov/pubmed/16511605?dopt=AbstractPlus].

Comments

324[http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1098 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18129, http://www.uniprot.org/uniprot/Q9UBU3) has been shown to bind (as [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3810) and have effects in the cardiovascular system [http://www.ncbi.nlm.nih.gov/pubmed/12969753?dopt=AbstractPlus], which raises the possible existence of different receptor subtypes in peripheral tissues and the central nervous system. A potent inverse agonist has been identified ([http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1102, pD 2 8.3; [http://www.ncbi.nlm.nih.gov/pubmed/12907757?dopt=AbstractPlus]). http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3535, described as a ghrelin receptor agonist (pKi 7.8 and pD 2 7.5 at human recombinant ghrelin receptors), has been shown to stimulate ghrelin receptor mediated food intake and gastric emptying but not elicit release of growth hormone, or modify ghrelin stimulated growth hormone release, thus pharmacologically discriminating the orexigenic and gastrointestinal actions of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1099 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18129, http://www.uniprot.org/uniprot/Q9UBU3) from the release of growth hormone [http://www.ncbi.nlm.nih.gov/pubmed/18719021?dopt=AbstractPlus]. A number of selective antagonists have been reported, including peptidomimetic [http://www.ncbi.nlm.nih.gov/pubmed/22798076?dopt=AbstractPlus] and non‐peptide small molecules including http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5870 [http://www.ncbi.nlm.nih.gov/pubmed/21034740?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20593439?dopt=AbstractPlus].

Overview

330The glucagon family of receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on the Glucagon receptor family [http://www.ncbi.nlm.nih.gov/pubmed/12615957?dopt=AbstractPlus]) are activated by the endogenous peptide (27‐44 aa) hormones http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1136 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4191, http://www.uniprot.org/uniprot/P01275), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5194 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4191, http://www.uniprot.org/uniprot/P01275), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1140 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4191, http://www.uniprot.org/uniprot/P01275), glucose‐dependent insulinotropic polypeptide (also known as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3542 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4270, http://www.uniprot.org/uniprot/P09681)), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2270 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4265, http://www.uniprot.org/uniprot/P01286) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3643 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10607, http://www.uniprot.org/uniprot/P09683). One common precursor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4191) generates http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1136 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4191, http://www.uniprot.org/uniprot/P01275), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5194 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4191, http://www.uniprot.org/uniprot/P01275) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1140 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4191, http://www.uniprot.org/uniprot/P01275) peptides [http://www.ncbi.nlm.nih.gov/pubmed/11179772?dopt=AbstractPlus]. For a recent review on review the current understanding of the structures of GLP‐1 and GLP‐1R, the molecular basis of their interaction, and the signaling events associated with it, see de Graaf et al., 2016 [http://www.ncbi.nlm.nih.gov/pubmed/27630114?dopt=AbstractPlus].

Comments

331The glucagon receptor has been reported to interact with receptor activity modifying proteins (RAMPs), specifically http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=52, in heterologous expression systems [http://www.ncbi.nlm.nih.gov/pubmed/12446722?dopt=AbstractPlus], although the physiological significance of this has yet to be established.

Overview

339Glycoprotein hormone receptors (provisional nomenclature [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by a non‐covalent heterodimeric glycoprotein made up of a common α chain

340(http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3731 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1885, http://www.uniprot.org/uniprot/P01215) https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1885, http://www.uniprot.org/uniprot/P01215), with a unique β chain that confers the biological specificity to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1157 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1885 https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3964, http://www.uniprot.org/uniprot/P01215 http://www.uniprot.org/uniprot/P01225), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1159 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1885 https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6584, http://www.uniprot.org/uniprot/P01215 http://www.uniprot.org/uniprot/P01229), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1160 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1885 https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1886, http://www.uniprot.org/uniprot/P01215 http://www.uniprot.org/uniprot/P01233) or http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3920 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:1885 https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12372, http://www.uniprot.org/uniprot/P01215 http://www.uniprot.org/uniprot/P01222). There is binding cross‐reactivity across the endogenous agonists for each of the glycoprotein hormone receptors. The deglycosylated hormones appear to exhibit reduced efficacy at these receptors [http://www.ncbi.nlm.nih.gov/pubmed/2542111?dopt=AbstractPlus].

Overview

345GnRH1 and GnRH2 receptors (provisonal nomenclature [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus], also called Type I and Type II GnRH receptor, respectively [http://www.ncbi.nlm.nih.gov/pubmed/15082521?dopt=AbstractPlus]) have been cloned from numerous species, most of which express two or three types of GnRH receptor [http://www.ncbi.nlm.nih.gov/pubmed/16140177?dopt=AbstractPlus, http:http://www.ncbi.nlm.nih.gov/pubmed/15082521?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15878963?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1162 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4419, http://www.uniprot.org/uniprot/P01148) (p‐Glu‐His‐Trp‐Ser‐Tyr‐Gly‐LeuArg‐Pro‐Gly‐NH2) is a hypothalamic decapeptide also known as luteinizing hormone‐releasing hormone, gonadoliberin, luliberin, gonadorelin or simply as GnRH. It is a member of a family of similar peptides found in many species [http://www.ncbi.nlm.nih.gov/pubmed/16140177?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15082521?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15878963?dopt=AbstractPlus] including http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1164 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4420, http://www.uniprot.org/uniprot/O43555) (pGlu‐His‐Trp‐Ser‐His‐Gly‐Trp‐Tyr‐Pro‐Gly‐NH2 (which is also known as chicken GnRH‐II). Receptors for three forms of GnRH exist in some species but only GnRH I and GnRH II and their cognate receptors have been found in mammals [http://www.ncbi.nlm.nih.gov/pubmed/16140177?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15082521?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15878963?dopt=AbstractPlus]. GnRH1 receptors are expressed by pituitary gonadotrophs, where they mediate the effects of GnRH on gonadotropin hormone synthesis and secretion that underpin central control of mammalian reproduction. GnRH analogues are used in assisted reproduction and to treat steroid hormone‐dependent conditions [http://www.ncbi.nlm.nih.gov/pubmed/12072036?dopt=AbstractPlus]. Notably, agonists cause desensitization of GnRH‐stimulated gonadotropin secretion and the consequent reduction in circulating sex steroids is exploited to treat hormone‐dependent cancers of the breast, ovary and prostate [http://www.ncbi.nlm.nih.gov/pubmed/12072036?dopt=AbstractPlus]. GnRH1 receptors are selectively activated by GnRH I and all lack the COOH‐terminal tails found in other GPCRs. GnRH2 receptors do have COOH‐terminal tails and (where tested) are selective for GnRH II over GnRH I. GnRH2 receptors are expressed by some primates but not by humans [http://www.ncbi.nlm.nih.gov/pubmed/12538601?dopt=AbstractPlus]. Phylogenetic classifications divide GnRH receptors into three [http://www.ncbi.nlm.nih.gov/pubmed/15082521?dopt=AbstractPlus] or five groups [http://www.ncbi.nlm.nih.gov/pubmed/25344287?dopt=AbstractPlus] and highlight examples of gene loss through evolution, with humans retaining only one ancient gene.

Comments

346GnRH1 and GnRH2 receptors couple primarily to Gq/11 [http://www.ncbi.nlm.nih.gov/pubmed/10734055?dopt=AbstractPlus] but coupling to Gs and Gi is evident in some systems [http://www.ncbi.nlm.nih.gov/pubmed/12591945?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8013367?dopt=AbstractPlus]. GnRH2 receptors may also mediate (heterotrimeric) G protein‐independent signalling to protein kinases [http://www.ncbi.nlm.nih.gov/pubmed/15059960?dopt=AbstractPlus]. There is increasing evidence for expression of GnRH receptors on hormone‐dependent cancer cells where they can exert antiproliferative and/or proapoptotic effects and mediate effects of cytotoxins conjugated to GnRH analogues [http://www.ncbi.nlm.nih.gov/pubmed/15561800?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15613448?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/14726258?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15350601?dopt=AbstractPlus]. In some human cancer cell models http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1164 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4420, http://www.uniprot.org/uniprot/O43555) is more potent than http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1162 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4419, http://www.uniprot.org/uniprot/P01148), implying mediation by GnRH2 receptors [http://www.ncbi.nlm.nih.gov/pubmed/12237622?dopt=AbstractPlus], but GnRH2 receptors are not expressed by humans because the human GNRHR2 gene contains a frame shift and internal stop codon [http://www.ncbi.nlm.nih.gov/pubmed/12538601?dopt=AbstractPlus]. The possibility remains that this gene generates GnRH2 receptor‐related proteins (other than the full‐length receptor) that mediate responses to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1164 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4420, http://www.uniprot.org/uniprot/O43555) (see [http://www.ncbi.nlm.nih.gov/pubmed/11861490?dopt=AbstractPlus]). Alternatively, evidence for multiple active GnRH receptor conformations [http://www.ncbi.nlm.nih.gov/pubmed/15059960?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22808094?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20009083?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15492280?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15082521?dopt=AbstractPlus] raises the possibility that GnRH1 receptor‐mediated proliferation inhibition in hormone‐dependent cancer cells is dependent upon a conformation that couples to Gi rather than Gq/11 proteins as in pituitary cells [http://www.ncbi.nlm.nih.gov/pubmed/22808094?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15492280?dopt=AbstractPlus]. Loss‐of‐function mutations in the GnRH1 receptor and deficiency of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1162 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4419, http://www.uniprot.org/uniprot/P01148) are associated with hypogonadotropic hypogonadism although some ’loss of function’ mutations may actually prevent trafficking of ’functional’ GnRH1 receptors to the cell surface, as evidenced by recovery of function by nonpeptide antagonists [http://www.ncbi.nlm.nih.gov/pubmed/12843188?dopt=AbstractPlus]. Human GnRH1 receptors are poorly expressed at the cell surface because of failure to meet structural quality control criteria for endoplasmic reticulum exit [http://www.ncbi.nlm.nih.gov/pubmed/19888967?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12843188?dopt=AbstractPlus], and this increases susceptibility to point mutations that further impair trafficking [http://www.ncbi.nlm.nih.gov/pubmed/19888967?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12843188?dopt=AbstractPlus]. GnRH receptor signalling may require receptor oligomerisation [http://www.ncbi.nlm.nih.gov/pubmed/6282571?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11278883?dopt=AbstractPlus].

Overview

352GPR18, GPR55 and GPR119 (provisional nomenclature), although showing little structural similarity to CB1 and CB2 cannabinoid receptors, respond to endogenous agents analogous to the endogenous cannabinoid ligands, as well as some natural/synthetic cannabinoid receptor ligands [http://www.ncbi.nlm.nih.gov/pubmed/21079038?dopt=AbstractPlus]. Although there are multiple reports to indicate that GPR18, GPR55 and GPR119 can be activated in vitro by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3635, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4028 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2661, respectively, there is a lack of evidence for activation by these lipid messengers in vivo. As such, therefore, these receptors retain their orphan status.

Comments

353GPR18 failed to respond to a variety of lipid‐derived agents in an in vitro screen [http://www.ncbi.nlm.nih.gov/pubmed/19286662?dopt=AbstractPlus], but has been reported to be activated by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2424 [http://www.ncbi.nlm.nih.gov/pubmed/21595653?dopt=AbstractPlus]. GPR55 responds to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3317 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=743 at micromolar concentrations, compared to their nanomolar affinity as CB1 receptor antagonists/inverse agonists [http://www.ncbi.nlm.nih.gov/pubmed/21079038?dopt=AbstractPlus]. It has been reported that http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4028 acts at other sites in addition to GPR55 [http://www.ncbi.nlm.nih.gov/pubmed/23714700?dopt=AbstractPlus]. N‐Arachidonoylserine has been suggested to act as a low efficacy agonist/antagonist at GPR18 in vitro [http://www.ncbi.nlm.nih.gov/pubmed/20346144?dopt=AbstractPlus]. It has also been suggested http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3623 acts, at least in part, through GPR119 [http://www.ncbi.nlm.nih.gov/pubmed/18724386?dopt=AbstractPlus]. Although http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3318 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3319 produce GPR119‐dependent responses in heterologous expression systems, comparison with http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2661‐mediated responses suggests additional mechanisms of action [http://www.ncbi.nlm.nih.gov/pubmed/18724386?dopt=AbstractPlus].

Overview

359Histamine receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Histamine Receptors [http://www.ncbi.nlm.nih.gov/pubmed/9311023?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26084539?dopt=AbstractPlus]) are activated by the endogenous ligand http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1204. Marked species differences exist between histamine receptor orthologues [http://www.ncbi.nlm.nih.gov/pubmed/9311023?dopt=AbstractPlus]. The human and rat H3 receptor genes are subject to significant splice variance [http://www.ncbi.nlm.nih.gov/pubmed/16415177?dopt=AbstractPlus]. The potency order of histamine at histamine receptor subtypes is H3 = H4 > H2 > H1 [http://www.ncbi.nlm.nih.gov/pubmed/26084539?dopt=AbstractPlus]. Some agonists at the human H3 receptor display significant ligand bias [http://www.ncbi.nlm.nih.gov/pubmed/27864425?dopt=AbstractPlus]. Antagonists of all 4 histamine receptors have clinical uses: H1 antagonists for allergies (e.g. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1222), H2 antagonists for acid‐reflux diseases (e.g. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1234), H3 antagonists for narcolepsy (e.g. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=8924/WAKIX; Registered) and H4 antagonists for atopic dermatitis (e.g. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=8985; Phase IIa) [http://www.ncbi.nlm.nih.gov/pubmed/26084539?dopt=AbstractPlus] and vestibular neuritis (AUV) (SENS‐111 (Seliforant, previously UR‐63325), entered and completed vestibular neuritis (AUV) Phase IIa efficacy and safety trials, respectively) [http://www.ncbi.nlm.nih.gov/pubmed/27673668?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30152527?dopt=AbstractPlus].

Comments

360http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4026 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1205 are reduced efficacy agonists. The H4 receptor appears to exhibit broadly similar pharmacology to the H3 receptor for imidazole‐containing ligands, although http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1236 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1239 are less potent, while http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1223 acts as a reduced efficacy agonist at the H4 receptor and an antagonist at the H3 receptor [http://www.ncbi.nlm.nih.gov/pubmed/11179434?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11118334?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11179435?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10973974?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11179436?dopt=AbstractPlus]. Moreover, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1269 is identified as a high affinity, full agonist for the human H4 receptor [http://www.ncbi.nlm.nih.gov/pubmed/15947036?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1247 has been used to label the H4 receptor heterologous expression systems.

Overview

365The hydroxycarboxylic acid family of receptors (http://www.ensembl.org/Homo_sapiens/Gene/Family/Genes?family=ENSFM00500000271913, nomenclature as agreed by the NC‐IUPHAR Subcommittee on Hydroxycarboxylic acid receptors [http://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21454438?dopt=AbstractPlus]) respond to organic acids, including the endogenous hydroxy carboxylic acids 3‐hydroxy butyric acid and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2932, as well as the lipid lowering agents http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1588 (niacin), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1596 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1595 [http://www.ncbi.nlm.nih.gov/pubmed/12646212?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12563315?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12522134?dopt=AbstractPlus]. These receptors were provisionally described as nicotinic acid receptors, although nicotinic acid shows submicromolar potency at HCA2 receptors only and is unlikely to be the natural ligand [http://www.ncbi.nlm.nih.gov/pubmed/12563315?dopt=AbstractPlus, https://www.ncbi.nlm.nih.gov/pubmed/12522134?dopt=AbstractPlus].

Comments

366Further closely‐related GPCRs include the http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=35 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:24884, http://www.uniprot.org/uniprot/Q8TDS5)and https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4486 (http://www.uniprot.org/uniprot/O00270). Lactate activates HCA1 on adipocytes in an autocrine manner. It inhibits lipolysis and thereby promotes anabolic effects. HCA2 and HCA3 regulate adipocyte lipolysis and immune functions under conditions of increased FFA formation through lipolysis (e.g., during fasting). HCA2 agonists acting mainly through the receptor on immune cells exert antiatherogenic and anti‐inflammatory effects. HCA2 is also a receptor for butyrate and mediates some of the beneficial effects of short‐chain fatty acids produced by gut microbiota. HCA3 has been shown to be activated by aromatic D‐amino acids.

Overview

373The kisspeptin receptor (nomenclature as agreed by the NC‐IUPHAR Subcommittee on the kisspeptin receptor [http://www.ncbi.nlm.nih.gov/pubmed/21079036?dopt=AbstractPlus]), like neuropeptide FF (NPFF), prolactin‐releasing peptide (PrP) and QRFP receptors (provisional nomenclature) responds to endogenous peptides with an arginine‐phenylalanine amide (RFamide) motif. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1288 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6341, http://www.uniprot.org/uniprot/Q15726) (KP54, originally named metastin), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1284 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6341, http://www.uniprot.org/uniprot/Q15726) (KP13) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1283 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6341) (KP10) are biologically‐active peptides cleaved from the https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6341 (http://www.uniprot.org/uniprot/Q15726) gene product. Kisspeptins have roles in, for example, cancer metastasis, fertility/puberty regula tion and glucose homeostasis.

Comments

3742‐acylamino‐4,6‐diphenylpyridine derivatives have been described and are the first small molecule kisspeptin receptor antagonists reported with potential for treatment of sex‐hormone dependent diseases such as prostate cancer and endometriosis [http://www.ncbi.nlm.nih.gov/pubmed/20580563?dopt=AbstractPlus].

Overview

380The leukotriene receptors (nomenclature as agreed by the NC‐IUPHAR subcommittee on Leukotriene Receptors [http://www.ncbi.nlm.nih.gov/pubmed/21771892?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24588652?dopt=AbstractPlus]) are activated by the endogenous ligands leukotrienes (LT), synthesized from lipoxygenase metabolism of arachidonic acid. The human BLT1 receptor is the high affinity LTB4 receptor whereas the BLT2 receptor in addition to being a low‐affinity LTB4 receptor also binds several other lipoxygenase‐products, such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3404, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2481, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3401, and the thromboxane synthase product http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=6159. The BLT receptors mediate chemotaxis and immunomodulation in several leukocyte populations and are in addition expressed on non‐myeloid cells, such as vascular smooth muscle and endothelial cells. In addition to BLT receptors, LTB4 has been reported to bind to the peroxisome proliferator activated receptor (PPAR) α [http://www.ncbi.nlm.nih.gov/pubmed/9890897?dopt=AbstractPlus] and the vanilloid TRPV1 ligand‐gated nonselective cation channel [http://www.ncbi.nlm.nih.gov/pubmed/16207832?dopt=AbstractPlus]. The receptors for the cysteinyl‐leukotrienes (i.e. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3354, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3353 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3352) aretermed CysLT1 and CysLT2 and exhibit distinct expression patterns in human tissues, mediating for example smooth muscle cell contraction, regulation of vascular permeability, and leukocyte activation. There is also evidence in the literature for additional CysLT receptor subtypes, derived from functional in vitro studies, radioligand binding and in mice lacking both CysLT1 and CysLT2 receptors [http://www.ncbi.nlm.nih.gov/pubmed/24588652?dopt=AbstractPlus]. Cysteinyl‐leukotrienes have also been suggested to signal through the P2Y12 receptor [http://www.ncbi.nlm.nih.gov/pubmed/20702811?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16185654?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19822647?dopt=AbstractPlus], GPR17 [http://www.ncbi.nlm.nih.gov/pubmed/16990797?dopt=AbstractPlus] and GPR99 [http://www.ncbi.nlm.nih.gov/pubmed/23504326?dopt=AbstractPlus].

Comments

381The FPR2/ALX receptor (nomenclatureas agreed by the NC‐IUPHAR subcommittee on Leukotriene and Lipoxin Receptors [http://www.ncbi.nlm.nih.gov/pubmed/24588652?dopt=AbstractPlus]) is activated by the endogenous lipidderived, anti‐inflammatory ligands lipoxin A4 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1034) and 15‐epiLXA4 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3933, ATL). The FPR2/ALX receptor also interacts with endogenous peptide and protein ligands, such as MHC binding peptide [http://www.ncbi.nlm.nih.gov/pubmed/10748237?dopt=AbstractPlus] as well as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1031 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:533, http://www.uniprot.org/uniprot/P04083) (ANXA1) and its N‐terminal peptides [http://www.ncbi.nlm.nih.gov/pubmed/24108355?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12368905?dopt=AbstractPlus]. In addition, a soluble hydrolytic product of protease action on the urokinase‐type plasminogen activator receptor has been reported to activate the FPR2/ALX receptor [http://www.ncbi.nlm.nih.gov/pubmed/11818541?dopt=AbstractPlus]. Furthermore, FPR2/ALX has been suggested to act as a receptor mediating the proinflammatory actions of the acute‐phase reactant, serum amyloid A [http://www.ncbi.nlm.nih.gov/pubmed/15171815?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9892621?dopt=AbstractPlus]. The agonist activity of the lipid mediators described has been questioned [http://www.ncbi.nlm.nih.gov/pubmed/23643932?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23607720?dopt=AbstractPlus], which may derive from batchto‐batch differences, partial agonism or biased agonism. Results from Cooray et al. (2013) [http://www.ncbi.nlm.nih.gov/pubmed/24108355?dopt=AbstractPlus] have addressed this issue and the role of homodimers and heterodimers in intracellular signaling. A receptor selective for http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5216 has been suggested from functional studies [http://www.ncbi.nlm.nih.gov/pubmed/12794159?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8551217?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8757340?dopt=AbstractPlus]. Note that the data for FPR2/ALX are also reproduced on the http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=23.

382Oxoeicosanoid receptors (OXE, nomenclature agreed by the NC‐IUPHAR subcommittee on Oxoeicosanoid Receptors [http://www.ncbi.nlm.nih.gov/pubmed/15001665?dopt=AbstractPlus]) are activated by endogenous chemotactic eicosanoid ligands oxidised at the C‐5 position, with http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3391 the most potent agonist identified for this receptor. Initial characterization of the heterologously expressed OXE receptor suggested that polyunsaturated fatty acids, such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1051 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3362, acted as receptor antagonists [http://www.ncbi.nlm.nih.gov/pubmed/12065583?dopt=AbstractPlus].

Overview

388Lysophosphatidic acid (LPA) receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Lysophospholipid (LPA) receptors Lysophospholipid Receptors [http://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24602016?dopt=AbstractPlus]) are activated by the endogenous phospholipid http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2906. The first receptor, LPA1, was identified as ventricular zone gene‐1 (vzg‐1) [http://www.ncbi.nlm.nih.gov/pubmed/8922387?dopt=AbstractPlus], leading to deorphanisation of members of the endothelial differentiation gene (edg) family as other LPA receptors along with sphingosine 1phosphate (S1P) receptors. Additional LPA receptor GPCRs were later identified. Gene names have been codified as LPAR1, etc. to reflect the receptor function of proteins. The crystal structure of LPA1 was solved and demonstrates extracellular LPA access to the binding pocket, consistent with proposed delivery via autotaxin [http://www.ncbi.nlm.nih.gov/pubmed/26091040?dopt=AbstractPlus]. These studies have also implicated cross‐talk with endocannabinoids via phosphorylated intermediates that can also activate these receptors. The identified receptors can account for most, although not all, LPA‐induced phenomena in the literature, indicating that a majority of LPA‐dependent phenomena are receptor‐mediated. Binding affinities of unlabeled, natural LPA and AEApto LPA1 weremeasured using backscattering interferometry (pKd = 9) [http://www.ncbi.nlm.nih.gov/pubmed/30463988?dopt=AbstractPlus]. Binding affinities were 77‐fold lower than than values obtained using radioactivity [http://www.ncbi.nlm.nih.gov/pubmed/19386608?dopt=AbstractPlus]. Targeted deletion of LPA receptors has clarified signalling pathways and identified physiological and pathophysiological roles. Independent validation by multiple groups has been reported in the peer‐reviewed literature for all six LPA receptors described in the tables, including further validation using a distinct read‐out via a novel TGFα “shedding” assay [http://www.ncbi.nlm.nih.gov/pubmed/22983457?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2906 has also been described as an agonist for the transient receptor potential (Trp) ion channel TRPV1 [http://www.ncbi.nlm.nih.gov/pubmed/22101604?dopt=AbstractPlus] and TRPA1 [http://www.ncbi.nlm.nih.gov/pubmed/28176353?dopt=AbstractPlus]. LPA was originally proposed to be a ligand for GPCR35, but data show that in fact it is a receptor for http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=6479 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:19232, http://www.uniprot.org/uniprot/Q6UXB2) [http://www.ncbi.nlm.nih.gov/pubmed/25411203?dopt=AbstractPlus]. All of these proposed non‐GPCR receptor identities require confirmation and are not currently recognized as bona fide LPA receptors.

Comments

389http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2907 [http://www.ncbi.nlm.nih.gov/pubmed/14500756?dopt=AbstractPlus], http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2909 [http://www.ncbi.nlm.nih.gov/pubmed/11723223?dopt=AbstractPlus] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5450 [http://www.ncbi.nlm.nih.gov/pubmed/15125924?dopt=AbstractPlus] have dual antagonist activity at LPA1 and LPA3 receptors. There is growing evidence for in vivo efficacy of these chemical antagonists in several disorders, including fetal hydrocephalus [http://www.ncbi.nlm.nih.gov/pubmed/21900594?dopt=AbstractPlus], fetal hypoxia [http://www.ncbi.nlm.nih.gov/pubmed/21878565?dopt=AbstractPlus], lung fibrosis [http://www.ncbi.nlm.nih.gov/pubmed/25959255?dopt=AbstractPlus], systemic sclerosis [http://www.ncbi.nlm.nih.gov/pubmed/25959255?dopt=AbstractPlus] and atherosclerosis progression [http://www.ncbi.nlm.nih.gov/pubmed/27883026?dopt=AbstractPlus]. The LPA2 selective agonist, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=6580, also shows efficacy in an animal model of multiple sclerosis [http://www.ncbi.nlm.nih.gov/pubmed/28578681?dopt=AbstractPlus]. The LPA5 selective antagonist, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=10230, is effective in pain models [http://www.ncbi.nlm.nih.gov/pubmed/29208511?dopt=AbstractPlus].

Overview

393Sphingosine 1‐phosphate (S1P) receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Lysophospholipid receptors [http://www.ncbi.nlm.nih.gov/pubmed/24602016?dopt=AbstractPlus]) are activated by the endogenous lipid http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=911 (S1P). Originally cloned as orphan members of the endothelial differentiation gene (edg) family, current gene names have been designated as S1P1R through S1P5R [http://www.ncbi.nlm.nih.gov/pubmed/2160972?dopt=AbstractPlus]. S1PRs, particularly S1P1, are expressed throughout all mammalian organ systems. Ligand delivery occurs via two known carriers (or “chaperones”): albumin and HDLbound apolipoprotein M (ApoM), the latter of which elicits biased agonist signaling by S1P1 in multiple cell types [http://www.ncbi.nlm.nih.gov/pubmed/26053123?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26268607?dopt=AbstractPlus]. The five S1PRs, two chaperones, and active cellular metabolism have complicated analyses of receptor ligand binding in native systems. Signaling pathways and physiological roles have been characterized through radioligand binding in heterologous expression systems, targeted deletion of the different S1PRs, and most recently, mouse models that report in vivo S1P1R activation [http://www.ncbi.nlm.nih.gov/pubmed/29079828?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24667638?dopt=AbstractPlus]. A crystal structure of an S1P1‐T4 fusion protein confirmed aspects and binding, specificity, and receptor activation determined previously through biochemical and genetic studies [http://www.ncbi.nlm.nih.gov/pubmed/30343728?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22344443?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2407 (FTY720), the first drug to target any of the lysophospholipid receptors, binds to four of the five S1PRs, and was the first oral therapy for multiple sclerosis [http://www.ncbi.nlm.nih.gov/pubmed/30625282?dopt=AbstractPlus]. The mechanisms of action of fingolimod and other S1PR modulating drugs in development include binding S1PRs in multiple organ systems, e.g., immune and nervous systems, although the precise nature of their receptor interactions requires clarification [http://www.ncbi.nlm.nih.gov/pubmed/21520239?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23518370?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30255127?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25831442?dopt=AbstractPlus].

Comments

394The FDA‐approved immunomodulator http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2407 (FTY720) is phosphorylated in vivo [http://www.ncbi.nlm.nih.gov/pubmed/16078855?dopt=AbstractPlus] to generatean agonist with activity at S1P1, S1P3, S1P4 and S1P5 receptors [http://www.ncbi.nlm.nih.gov/pubmed/11967257?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11923495?dopt=AbstractPlus]. Many of the physiological consequences of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2924 administration, as well as those of other currently described S1P1 agonists, may involve functional antagonism via ubiquitination and subsequent degradation of S1P1 [http://www.ncbi.nlm.nih.gov/pubmed/17237497?dopt=AbstractPlus]. Additionally, receptor specificities of the different compounds may depend on the functional assay system utilized and from which species the receptor sequence originated.

Overview

401Melanin‐concentrating hormone (MCH) receptors (provisional nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by an endogenous nonadecameric cyclic peptide identical in humans and rats (DFDMLRCMLGRVYRPCWQV; mammalian MCH) generated from a precursor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9109, http://www.uniprot.org/uniprot/P20382), which also produces http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5374 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9109, http://www.uniprot.org/uniprot/P20382) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5375 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9109, http://www.uniprot.org/uniprot/P20382).

Comments

402The MCH2 receptor appears to be a non‐functional pseudogene in rodents [http://www.ncbi.nlm.nih.gov/pubmed/12036292?dopt=AbstractPlus].

Overview

407Melanocortin receptors (provisional nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by members of the melanocortin family (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1320 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9201, http://www.uniprot.org/uniprot/P01189), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3606‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3606, http://www.uniprot.org/uniprot/P01189) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1333‐http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1333, http://www.uniprot.org/uniprot/P01189) forms; δ form is not found in mammals) and adrenocorticotrophin (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3633, http://www.uniprot.org/uniprot/P01189)). Endogenous antagonists include http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3609 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:745, http://www.uniprot.org/uniprot/P42127) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1335 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:330, http://www.uniprot.org/uniprot/O00253). ACTH(1‐24) was approved by the US FDA as a diagnostic agent for adrenal function test, whilst NDP‐MSH was approved by EMA for the treatment of erythropoietic protoporphyria. Several synthetic melanocortin receptor agonists are under clinical development.

Comments

408Polymorphisms of the MC1 receptor have been linked to variations in skin pigmentation. Defects of the MC2 receptor underlie familial glucocorticoid deficiency. Polymorphisms of the MC4 receptor have been linked to obesity [http://www.ncbi.nlm.nih.gov/pubmed/9392003?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/18779842?dopt=AbstractPlus].

Overview

412Melatonin receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Melatonin Receptors [http://www.ncbi.nlm.nih.gov/pubmed/20605968?dopt=AbstractPlus]) are activated by the endogenous ligands http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=224 and clinically used drugs like http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1356, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=198 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7393.

Comments

413http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=224, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1343, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=198, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1349, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1351 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1356 [http://www.ncbi.nlm.nih.gov/pubmed/15695169?dopt=AbstractPlus] are nonselective agonists for MT1 and MT2 receptors. (‐)‐AMMTC displays an ˜400‐fold greater agonist potency than (+)‐AMMTC at rat MT1 receptors (see http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3385 for structure) [http://www.ncbi.nlm.nih.gov/pubmed/10433507?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1363 is an MT1/MT2 non‐selective competitive melatonin receptor antagonist with about 15‐25 fold selectivity for the MT2 receptor [http://www.ncbi.nlm.nih.gov/pubmed/9737724?dopt=AbstractPlus]. MT1/MT2 heterodimers present differentpharmacological profiles from MT1 and MT2 receptors [http://www.ncbi.nlm.nih.gov/pubmed/15266022?dopt=AbstractPlus]. The MT3 binding site of hamster brain and peripheral tissues such as kidney and testis, also termed the ML2 receptor, binds selectively http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5396 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5396 [http://www.ncbi.nlm.nih.gov/pubmed/8773460?dopt=AbstractPlus]. Pharmacological investigations of MT3 binding sites have primarily been conducted in hamster tissues. At this site, The endogenous ligand http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5451 [http://www.ncbi.nlm.nih.gov/pubmed/8246675?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9283717?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/9283717?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/7798906?dopt=AbstractPlus] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3393 [http://www.ncbi.nlm.nih.gov/pubmed/7798906?dopt=AbstractPlus] appear to function as agonists, while http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=503 [http://www.ncbi.nlm.nih.gov/pubmed/9283717?dopt=AbstractPlus] functions as an antagonist. The MT3 binding site of hamster kidney was also identified as the hamster homologue of human quinone reductase 2 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7856, http://www.uniprot.org/uniprot/P16083 [http://www.ncbi.nlm.nih.gov/pubmed/10913150?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11331072?dopt=AbstractPlus]). The MT3 binding site activated by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3393 in eye ciliary body is positively coupled to adenylyl cyclase and regulates chloride secretion [http://www.ncbi.nlm.nih.gov/pubmed/25344385?dopt=AbstractPlus]. Xenopus melanophores and chick brain express a distinct receptor (x420, P49219; c346, P49288, initially termed Mel1C) coupled to the Gi/o family of G proteins, for which GPR50 has recently been suggested to be a mammalian counterpart [http://www.ncbi.nlm.nih.gov/pubmed/18400093?dopt=AbstractPlus] although http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=224 does not bind to GPR50 receptors. Several variants of the MTNR1B gene have been associated with increased type 2 diabetes risk [http://www.ncbi.nlm.nih.gov/pubmed/30531911?dopt=AbstractPlus].

Overview

420Metabotropic glutamate (mGlu) receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Metabotropic Glutamate Receptors[1899]) area family of G protein‐coupled receptors activated by the neurotransmitter glutamate. The mGlu family is composed of eight members (named mGlu1 to mGlu8) which are divided in three groups based on similarities of agonist pharmacology, primary sequence and G protein coupling to effector: Group‐I (mGlu1 and mGlu5), Group‐II (mGlu2 and mGlu3) and Group‐III (mGlu4, mGlu6, mGlu7 and mGlu8) (see Further reading).

421Structurally, mGlu are composed of three juxtaposed domains: a core G protein‐activating seven‐transmembrane domain (TM), common to all GPCRs, is linked via a rigid cysteine‐rich domain (CRD) to the Venus Flytrap domain (VFTD), a large bi‐lobed extracellular domain where glutamate binds. The structures of the VFTD of mGlu1, mGlu2, mGlu3, mGlu5 and mGlu7 have been solved [http://www.ncbi.nlm.nih.gov/pubmed/11069170?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25602126?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17360426?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11867751?dopt=AbstractPlus]. The structure of the 7 transmembrane (TM) domains of both mGlu1 and mGlu5 have been solved, and confirm a general helical organization similar to that of other GPCRs, although the helices appear more compacted [http://www.ncbi.nlm.nih.gov/pubmed/29455526?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25042998?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24603153?dopt=AbstractPlus]. mGlu form constitutive dimers crosslinked by a disulfide bridge. Recent studies revealed the possible formation of heterodimers between either group‐I receptors, or within and between group‐II and ‐III receptors [http://www.ncbi.nlm.nih.gov/pubmed/20826542?dopt=AbstractPlus]. Although well characterized in transfected cells, co‐localization and specific pharmacological properties also suggest the existence of such heterodimers in the brain [http://www.ncbi.nlm.nih.gov/pubmed/28661401?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24381270?dopt=AbstractPlus].

422The endogenous ligands of mGlu are http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1369, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1411, N‐acetylaspartylglutamate (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1405) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5447. Group‐I mGlu receptors may be activated by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1367 and (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1366)http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1366 [http://www.ncbi.nlm.nih.gov/pubmed/8532171?dopt=AbstractPlus] and antagonized by (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5448 [http://www.ncbi.nlm.nih.gov/pubmed/15996690?dopt=AbstractPlus]. Group‐II mGlu receptors may be activated by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3349 [http://www.ncbi.nlm.nih.gov/pubmed/10090786?dopt=AbstractPlus], http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1394], http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1393 [http://www.ncbi.nlm.nih.gov/pubmed/9144636?dopt=AbstractPlus http://www.ncbi.nlm.nih.gov/pubmed/9473604?dopt=AbstractPlus], http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1377 and (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1392,http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1392)http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1392 [http://www.ncbi.nlm.nih.gov/pubmed/9076745?dopt=AbstractPlus, and antagonised by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1400 [http://www.ncbi.nlm.nih.gov/pubmed/9121605?dopt=AbstractPlus] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3350 [http://www.ncbi.nlm.nih.gov/pubmed/9871538?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8632404?dopt=AbstractPlus]. Group‐III mGlu receptors may be activated by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1410 and (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1406)http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1406 [http://www.ncbi.nlm.nih.gov/pubmed/10336568?dopt=AbstractPlus]. An example of an antagonist selective for mGlu receptors is http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1378, which blocks mGlu2 and mGlu3 at low nanomolar concentrations, mGlu8 at high nanomolar concentrations, and mGlu4, mGlu5, and mGlu7 in the micromolar range [http://www.ncbi.nlm.nih.gov/pubmed/9680254?dopt=AbstractPlus]. In addition to orthosteric ligands that directly interact with the glutamate recognition site, allosteric modulators that bind within the TM domain have been described. Negative allosteric modulators are listed separately. The positive allosteric modulators most often act as ‘potentiators’ of an orthosteric agonist response, without significantly activating the receptor in the absence of agonist.

Comments

423The activity of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1405 as an agonist at mGlu3 receptors was questioned on the basis of contamination with glutamate [http://www.ncbi.nlm.nih.gov/pubmed/19389924?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19285517?dopt=AbstractPlus], but this has been refuted [http://www.ncbi.nlm.nih.gov/pubmed/21740441?dopt=AbstractPlus].

424Radioligand binding using a variety of radioligands has been conducted on recombinant receptors (for example, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1391 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1391 [http://www.ncbi.nlm.nih.gov/pubmed/12695537?dopt=AbstractPlus] and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5392 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5392 [http://www.ncbi.nlm.nih.gov/pubmed/15976016?dopt=AbstractPlus] at mGlu1 receptors and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1425 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1425 [http://www.ncbi.nlm.nih.gov/pubmed/11814808?dopt=AbstractPlus] and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5394 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5394 [http://www.ncbi.nlm.nih.gov/pubmed/12438526?dopt=AbstractPlus] at mGlu5 receptors; [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1399 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1399 and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1396 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1396 for mGlu2 and mGlu3 receptors [http://www.ncbi.nlm.nih.gov/pubmed/10530814?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10884552?dopt=AbstractPlus]). Although a number of radioligands have been used to examine binding in native tissues, correlation with individual subtypes is limited. Many pharmacological agents have not been fully tested across all known subtypes of mGlu receptors and may have unappreciated biased or neutral activity at other subtypes [http://www.ncbi.nlm.nih.gov/pubmed/29514854?dopt=AbstractPlus]. Potential differences linked to the species (e.g. human versus rat or mouse) of the receptors and the receptor splice variants are generally not known. The influence of receptor expression level on pharmacology and selectivity has not been controlled for in most studies, particularly those involving functional assays of receptor coupling.

425(http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3421 is an antagonist at mGlu1, but is an agonist (albeit of reduced efficacy) at mGlu5 receptors. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1377 also exhibits agonist activity at NMDA glutamate receptors [http://www.ncbi.nlm.nih.gov/pubmed/9106476?dopt=AbstractPlus], and is an antagonist at all Group‐III mGluRs with an IC50 of 30μM. A potential novel metabotropic glutamate receptor coupled to phosphoinositide turnover has been observed in rat brain; it is activated by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5449 (ineffective as an agonist at recombinant Group I metabotropic glutamate receptors), but is resistant to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1378 [http://www.ncbi.nlm.nih.gov/pubmed/9353394?dopt=AbstractPlus]. There are also reports of a distinct metabotropic glutamatereceptor coupled tophospholipase D in ratbrain, which does not readily fit into the current classification [http://www.ncbi.nlm.nih.gov/pubmed/9175608?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8799579?dopt=AbstractPlus]

426A related class C receptor composed of two distinct subunits, T1R1 + T1R3 is also activated by glutamate and is responsible for umami taste detection.

427All selective antagonists at metabotropic glutamate receptors are competitive.

Overview

434Motilin receptors (provisional nomenclature) are activated by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1458 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7141, http://www.uniprot.org/uniprot/P12872), a 22 amino‐acid peptide derived from a precursor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7141, http://www.uniprot.org/uniprot/P12872), which may also generate a http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5376 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7141, http://www.uniprot.org/uniprot/P12872). These receptors promote gastrointestinal motility and are suggested to be responsible for the gastrointestinal prokinetic effects of certain macrolide antibiotics (often called motilides; e.g. erythromycin), although for many of these molecules the evidence is sparse.

Comments

435In terms of structure, the motilin receptor has closest homology with the ghrelin receptor. Thus, the human motilin receptor shares 52% overall amino acid identity with the ghrelin receptor and 86% in the transmembrane regions [http://www.ncbi.nlm.nih.gov/pubmed/19696113?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17183187?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15764739?dopt=AbstractPlus]. However, differences between the N‐terminus regions of these receptors means that their cognate peptide ligands do not readily activate each other [http://www.ncbi.nlm.nih.gov/pubmed/14504130?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19374732?dopt=AbstractPlus]. In laboratory rodents, the gene encoding the motilin percursor appears to be absent, while the receptor appears to be a pseudogene [http://www.ncbi.nlm.nih.gov/pubmed/19696113?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21531468?dopt=AbstractPlus]. Functions of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1458 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7141, http://www.uniprot.org/uniprot/P12872) are not usually detected in rodents, although brain and other responses to motilin and the macrolide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1444 have been reported and the mechanism of these actions is obscure [http://www.ncbi.nlm.nih.gov/pubmed/9441746?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10092986?dopt=AbstractPlus]. Notably, in some non‐laboratory rodents (e.g. the North American kangaroo rat (Dipodomys) and mouse (Microdipodops) a functional form of motilin may exist but the motilin receptor is non‐functional [http://www.ncbi.nlm.nih.gov/pubmed/15027861?dopt=AbstractPlus]. Marked differences in ligand affinities for the motilin receptor in dogs and humans may be explained by significant differences in receptor structure [http://www.ncbi.nlm.nih.gov/pubmed/23189978?dopt=AbstractPlus]. Note that for the complex macrolide structures, selectivity of action has often not been rigorously examined and other actions are possible (e.g. P2X inhibition by erythromycin; [http://www.ncbi.nlm.nih.gov/pubmed/10749750?dopt=AbstractPlus]). Small molecule motilin receptor agonists are now described [http://www.ncbi.nlm.nih.gov/pubmed/15027861?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/19374732?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21544957?dopt=AbstractPlus]. The motilin receptor does not appear to have constitutive activity [http://www.ncbi.nlm.nih.gov/pubmed/12907757?dopt=AbstractPlus]. Although not proven, the existence of biased agonism at the receptor has been suggested [http://www.ncbi.nlm.nih.gov/pubmed/16531413?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17074305?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24438586?dopt=AbstractPlus]. A truncated 5‐transmembrane structure has been identified but this is without activity when transfected into a host cell [http://www.ncbi.nlm.nih.gov/pubmed/10381885?dopt=AbstractPlus]. Receptor dimerisation has not been reported.

Overview

439Neuromedin U receptors (provisional nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by the endogenous 25 amino acid peptide neuromedin U (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1470 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7859, http://www.uniprot.org/uniprot/P48645), NmU‐25), a peptide originally isolated from pig spinal cord [http://www.ncbi.nlm.nih.gov/pubmed/3839674?dopt=AbstractPlus]. In humans, NmU‐25 appears to be the sole product of a precursor gene (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7859, http://www.uniprot.org/uniprot/P48645) showing a broad tissue distribution, but which is expressed at highest levels in the upper gastrointestinal tract, CNS, bone marrow and fetal liver. Much shorter versions of NmU are found in some species, but not in human, and are derived at least in some instances from the proteolytic cleavage of the longer NmU. Despite species differences in NmU structure, the C‐terminal region (particularly the C‐terminal pentapeptide) is highly conserved and contains biological activity. Neuromedin S (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1468 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:32203, http://www.uniprot.org/uniprot/Q5H8A3)) has also been identified as an endogenous agonist [http://www.ncbi.nlm.nih.gov/pubmed/15635449?dopt=AbstractPlus]. NmS33 is, as its name suggests, a 33 amino‐acid product of a precursor protein derived from a single gene and contains an amidated Cterminal heptapeptide identical to NmU. NmS‐33 appears to activate NMU receptors with equivalent potency to NmU‐25.

Comments

440NMU1 and NMU2 couple predominantly to Gq/11 although there is evidence of good coupling to Gi/o [http://www.ncbi.nlm.nih.gov/pubmed/15331768?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10887190?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17652154?dopt=AbstractPlus]. NMU1 and NMU2 can be labelled with [125I]‐NmU and [125I]‐NmS (of various species, e.g. [http://www.ncbi.nlm.nih.gov/pubmed/18358099?dopt=AbstractPlus]), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3858 or http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3863 [http://www.ncbi.nlm.nih.gov/pubmed/15331768?dopt=AbstractPlus]. A range of radiolabelled ( 125I‐), fluorescently labelled (e.g. Cy3, Cy5, rhodamine and FAM) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4787 labelled versions of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1470 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7859, http://www.uniprot.org/uniprot/P48645) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1468 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:32203, http://www.uniprot.org/uniprot/Q5H8A3) are now commercially available.

Overview

445The Neuropeptide FF receptor family contains two subtypes, NPFF1 and NPFF2 (provisional nomenclature [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]), which exhibit high affinities for neuropeptide FF (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7901, http://www.uniprot.org/uniprot/O15130) and RFamide related peptides (RFRP: precursor genesymbol https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:13782, http://www.uniprot.org/uniprot/Q9HCQ7). NPFF1 is broadly distributed in the central nervous system with the highest levels found in the limbic system and the hypothalamus. NPFF2 is present in high density in the superficial layers of the mammalian spinal cord where it is involved in nociception and modulation of opioid functions.

Comments

446An orphan receptor https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4523 (http://www.uniprot.org/uniprot/Q9NYM4) shows sequence similarities with NPFF1, NPFF2, PrRP and QRFP receptors. The antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1486 is selective for NPFF receptors, but does not distinguish between the NPFF1 and NPFF2 subtypes (pKi 7.1 and 7.2, respectively, [http://www.ncbi.nlm.nih.gov/pubmed/16407169?dopt=AbstractPlus]).

Overview

450The neuropeptide S receptor (NPS, provisional nomenclature [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) responds to the 20 amino‐acid peptide neuropeptide S derived from a precursor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:33940, http://www.uniprot.org/uniprot/P0C0P6).

Comments

451Multiple single‐nucleotide polymorphisms (SNP) and several splice variants have been identified in the human NPS receptor. The most interesting of these is an Asn‐Ile exchange at position 107 (Asn107Ile). The human NPS receptor Asn107Ile displayed similar binding affinity buthigher NPSpotency (by approx. 10‐fold) than human NPS receptor Asn107 [http://www.ncbi.nlm.nih.gov/pubmed/16144971?dopt=AbstractPlus]. Several epidemiological studies reported an association between Asn107Ile receptor variant and susceptibility to panic disorders [http://www.ncbi.nlm.nih.gov/pubmed/20603625?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20705147?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/17669576?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20628342?dopt=AbstractPlus]. The SNP Asn107Ile has also been linked to sleep behavior [http://www.ncbi.nlm.nih.gov/pubmed/17903308?dopt=AbstractPlus], inflammatory bowel disease [http://www.ncbi.nlm.nih.gov/pubmed/17854592?dopt=AbstractPlus], schizophrenia [http://www.ncbi.nlm.nih.gov/pubmed/22078257?dopt=AbstractPlus], increased impulsivity and ADHD symptoms [http://www.ncbi.nlm.nih.gov/pubmed/23325374?dopt=AbstractPlus]. Interestingly, a carboxy‐terminal splice variant of human NPS receptor was found to be overexpressed in asthmatic patients [http://www.ncbi.nlm.nih.gov/pubmed/15073379?dopt=AbstractPlus].

Overview

456The neuropeptide BW receptor 1 (NPBW1, provisional nomenclature [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) is activated by two 23‐amino‐acid peptides, neuropeptide W (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1495 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30509, http://www.uniprot.org/uniprot/Q8N729)) and neuropeptide B (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1501 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30099, http://www.uniprot.org/uniprot/Q8NG41)) [http://www.ncbi.nlm.nih.gov/pubmed/12118011?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12130646?dopt=AbstractPlus]. C‐terminally extended forms of the peptides (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1496 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30509, http://www.uniprot.org/uniprot/Q8N729) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1502 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30099, http://www.uniprot.org/uniprot/Q8NG41)) also activate NPBW1[http://www.ncbi.nlm.nih.gov/pubmed/12401809?dopt=AbstractPlus]. Unique to both forms of neuropeptide B is the N‐terminal bromination of the first tryptophan residue, and it is from this post‐translational modification that the nomenclature NPB is derived. These peptides were first identified from bovine hypothalamus and therefore are classed as neuropeptides. Endogenous variants of the peptides without the N‐terminal bromination, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1499 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30099, http://www.uniprot.org/uniprot/Q8NG41) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1500 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30099, http://www.uniprot.org/uniprot/Q8NG41), were not found to be major components of bovine hypothalamic tissue extracts. The NPBW2 receptor is activated by the short and C‐terminal extended forms of neuropeptide W and neuropeptide B [http://www.ncbi.nlm.nih.gov/pubmed/12401809?dopt=AbstractPlus].

Comments

457Potency measurements were conducted with heterologously‐expressed receptors with a range of 0.14‐0.57 nM (NPBW1) and 0.98‐21 nM (NPBW2).

458NPBW1‐/‐ mice show changes in social behavior, suggesting that the NPBW1pathway may have animportant role in theemotional responses of social interaction [http://www.ncbi.nlm.nih.gov/pubmed/21390312?dopt=AbstractPlus].

459For a review of the contribution of neuropeptide B/W to social dominance, see Watanabe and Yamamoto, 2015 [http://www.ncbi.nlm.nih.gov/pubmed/26136644?dopt=AbstractPlus]. It has been reported that neuropeptide W may have a key role in the gating of stressful stimuli when mice are exposed to novel environments [http://www.ncbi.nlm.nih.gov/pubmed/27140610?dopt=AbstractPlus].

460Two antagonists have been discovered and reported to have affinity for NPBW1, ML181 and ML250, the latter exhibiting improved selectivity (100 fold) for NPBW1 compared to MCH1 receptors [http://www.ncbi.nlm.nih.gov/pubmed/23762933?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22834040?dopt=AbstractPlus]. Computational insights into the binding of antagonists to this receptor have also been described [http://www.ncbi.nlm.nih.gov/pubmed/24938207?dopt=AbstractPlus].

Overview

463Neuropeptide Y (NPY) receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Neuropeptide Y Receptors [http://www.ncbi.nlm.nih.gov/pubmed/9549761?dopt=AbstractPlus]) are activated by the endogenous peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1504 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7955, http://www.uniprot.org/uniprot/P01303), neuropeptide Y‐(3‐36), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1514 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9748, http://www.uniprot.org/uniprot/P10082), PYY‐(3‐36) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1512 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9327, http://www.uniprot.org/uniprot/P01298) (PP). The receptor originally identified as the Y3 receptor has been identified as the http://www.guidetopharmacology.org/GRAC/ObjectDisplayForward?objectId=71 (originally named LESTR, [http://www.ncbi.nlm.nih.gov/pubmed/8276799?dopt=AbstractPlus]). The y6 receptor is a functional gene product in mouse, absent in rat, but contains a frame‐shift mutation in primates producing a truncated non‐functional gene [http://www.ncbi.nlm.nih.gov/pubmed/8641440?dopt=AbstractPlus]. Many of the agonists exhibit differing degrees of selectivity dependent on the species examined. For example, the potency of PP is greater at the rat Y4 receptor than at the human receptor [http://www.ncbi.nlm.nih.gov/pubmed/9802391?dopt=AbstractPlus]. In addition, many agonists lack selectivity for individual subtypes, but can exhibit comparable potency against pairs of NPY receptor subtypes, or have not been examined for activity at all subtypes. [125I]‐PYY or [125I]‐NPY can be used to label Y1, Y2, Y5 and y6 subtypes non‐selectively, while [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3921 may be used to label Y5 receptors preferentially (note that cPP denotes chicken peptide sequence and hPP is the human sequence).

Comments

464The Y1 agonists indicated are selective relative to Y2 receptors. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1485 is selective relative to Y2, Y4 and Y5 receptors [http://www.ncbi.nlm.nih.gov/pubmed/8700207?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3903) is Y2 selective relative to Y1 and Y5 receptors. PYY‐(3‐36) is Y2 selective relative to Y1 receptors. Note that Pro34‐containing NPY and PYY can also bind Y4 and Y5, thus they are selective only relative to Y2. The y6 receptor is a pseudogene in humans, but is functional in mouse, rabbit and some other mammals.

Overview

469Neurotensin receptors (nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by the endogenous tridecapeptide neurotensin (pGlu‐Leu‐Tyr‐Glu‐Asn‐Lys‐Pro‐Arg‐Arg‐Pro‐Tyr‐Ile‐Leu) derived from a precursor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8038, http://www.uniprot.org/uniprot/30990), which also generates neuromedin N, an agonist at the NTS2 receptor. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3830) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1574) may be used to label NTS1 and NTS2 receptors at 0.1‐0.3 and 3‐5 nM concentrations respectively.

Comments

470http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1579 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8038, http://www.uniprot.org/uniprot/P30990) appears to be a lowefficacy agonist at the NTS2 receptor [http://www.ncbi.nlm.nih.gov/pubmed/9851594?dopt=AbstractPlus], while the NTS1 receptor antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1582 is an agonist at NTS2 receptors [http://www.ncbi.nlm.nih.gov/pubmed/9851594?dopt=AbstractPlus]. An additional protein, provisionally termed NTS3 (also known as NTR3, gp95 and sortilin; http://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000134243;r=1:109852192‐109940573), has been suggested to bind lipoprotein lipase and mediate its degradation [http://www.ncbi.nlm.nih.gov/pubmed/10085125?dopt=AbstractPlus]. It has been reported to interact with the NTS1 receptor [http://www.ncbi.nlm.nih.gov/pubmed/12360476?dopt=AbstractPlus] and the NTS2 receptor [http://www.ncbi.nlm.nih.gov/pubmed/19891061?dopt=AbstractPlus], and has beenimplicated in hormone trafficking and/or neurotensin uptake. A splice variant of the NTS2 receptor bearing 5 transmembrane domains has been identified in mouse [http://www.ncbi.nlm.nih.gov/pubmed/9001400?dopt=AbstractPlus] and later in rat [http://www.ncbi.nlm.nih.gov/pubmed/15637074?dopt=AbstractPlus].

Overview

475Opioid and opioid‐like receptors are activated by a variety of endogenous peptides including [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1614 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8831, http://www.uniprot.org/uniprot/P01210) (met), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1613 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8831, http://www.uniprot.org/uniprot/P01210) (leu), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1643 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9201, http://www.uniprot.org/uniprot/P01189) (β‐end), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3737 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8820, http://www.uniprot.org/uniprot/P01213), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1620 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8820, http://www.uniprot.org/uniprot/P01213) (dynA), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1622 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8820, http://www.uniprot.org/uniprot/P01213) (dynB), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3669 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8820, http://www.uniprot.org/uniprot/P01213) (Big dyn), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1681 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9163, http://www.uniprot.org/uniprot/Q13519) (N/OFQ); http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1623 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3668 are also potential endogenous peptides. The Greek letter nomenclature for the opioid receptors, μ, δ and κ, is well established, and NC‐IUPHAR considers this nomenclature appropriate, along with the symbols spelled out (mu, delta, and kappa), and the acronyms, MOP, DOP, and KOP. [http://www.ncbi.nlm.nih.gov/pubmed/24528283?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8981566?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]. The human N/OFQ receptor, NOP, is considered ’opioid‐related’ rather than opioid because, while it exhibits a high degree of structural homology with the conventional opioid receptors [http://www.ncbi.nlm.nih.gov/pubmed/8137918?dopt=AbstractPlus], it displays a distinct pharmacology. Currently there are numerous clinically used drugs, such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1627 and many other opioid analgesics, as well as antagonists such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1638, however only for the μ receptor.

Comments

476Three naloxone‐sensitive opioid receptor genes havebeen identified in humans, and while the μ‐receptor in particular may be subject to extensive alternative splicing [http://www.ncbi.nlm.nih.gov/pubmed/24076545?dopt=AbstractPlus], these putative isoforms have not been correlated with any of the subtypesof receptor proposed inyears past. Opioid receptors may heterodimerize with each other or with other 7TM receptors [http://www.ncbi.nlm.nih.gov/pubmed/10385123?dopt=AbstractPlus], and give rise to complexes with a unique pharmacology, however, evidence for such heterodimers in native cells is equivocal and the consequences of this heterodimerization for signalling remains largely unknown. For μ‐opioid receptors at least, dimerization does not seem to be required for signalling [http://www.ncbi.nlm.nih.gov/pubmed/19542234?dopt=AbstractPlus]. A distinct met‐enkephalin receptor lacking structural resemblance to the opioid receptors listed has been identified (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:15768, http://www.uniprot.org/uniprot/9NZT2) and termed an opioid growth factor receptor [http://www.ncbi.nlm.nih.gov/pubmed/11890982?dopt=AbstractPlus].

477http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1623 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3668 have been identified as highly selective, putative endogenous agonists for the μ‐opioid receptor. At present, however, the mechanisms for endomorphin synthesis in vivo have not been established, and there is no gene identified that encodes for either. Thus, the status of these peptides as endogenous ligands remains unproven.

478Two areas of increasing importance in defining opioid receptor function are the presence of functionally relevant single nucleotide polymorphisms in human μ‐receptors [http://www.ncbi.nlm.nih.gov/pubmed/19116204?dopt=AbstractPlus] and the identification of biased signalling by opioid receptor ligands, in particular, compounds previously characterized as antagonists [http://www.ncbi.nlm.nih.gov/pubmed/17702750?dopt=AbstractPlus]. Pathway bias for agonists makes general rank orders of potency and efficacy somewhat obsolete, so these do not appear in the table. As ever, the mechanisms underlying the acute and long term regulation of opiod receptor function are the subject of intense investigation and debate.

479The richness of opioid receptor pharmacology has been enhanced with the recent discovery of allosteric modulators of μ and δ receptors, notably thepositive allosteric modulators and silent allosteric “antagonists” outlined in [http://www.ncbi.nlm.nih.gov/pubmed/23754417?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25901762?dopt=AbstractPlus]. Negative allosteric modulation of opioid receptors has been previously suggested [http://www.ncbi.nlm.nih.gov/pubmed/16489449?dopt=AbstractPlus], whether all compounds are acting at a similar site remains to be established.

Overview

484Orexin receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Orexin receptors [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by the endogenous polypeptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1697 (https://www.genenames.org/data/gene‐symbol‐report/%23!/hgnc_id/HGNC:4847, http://www.uniprot.org/uniprot/O43612)and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1699 (https://www.genenames.org/data/gene‐symbol‐report/%23!/hgnc_id/HGNC:4847,http://www.uniprot.org/uniprot/O43612) (also known as hypocretin‐1 and ‐2; 33 and 28 aa) derived from a common precursor, https://www.genenames.org/data/gene‐symbol‐report/%23!/hgnc_id/HGNC:4847, by proteolytic cleavage and some typical peptide modifications [http://www.ncbi.nlm.nih.gov/pubmed/9491897?dopt=AbstractPlus]. Currently the only orexin receptor ligand in clinical use is http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2890,whichisused as a hypnotic. Orexin receptor crystal structures have been solved [http://www.ncbi.nlm.nih.gov/pubmed/26950369?dopt=AbstractPlus,http://www.ncbi.nlm.nih.gov/pubmed/25533960?dopt=AbstractPlus].

Comments

485The primary coupling of orexin receptors to Gq/11 proteins is rather speculative and based on the strong activation of phospholipase C, though recent studies in recombinant cells also stress the importance of Gq/11 [http://www.ncbi.nlm.nih.gov/pubmed/27237973?dopt=AbstractPlus]. Coupling of both receptors to Gi/o and Gs has also been reported [http://www.ncbi.nlm.nih.gov/pubmed/15687100?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23902572?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23848055?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11600545?dopt=AbstractPlus]. For most native cellular responses observed, the G protein pathway is unknown. The relative potency order of endogenous ligands depends on the cellular signal transduction machinery [http://www.ncbi.nlm.nih.gov/pubmed/23034387?dopt=AbstractPlus]. Similarly, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1700, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1700]http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1700, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9305 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=10277 may show variable selectivity for OX2 receptors and are also likely to activate OX1 receptors [http://www.ncbi.nlm.nih.gov/pubmed/21362456?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30194937?dopt=AbstractPlus]. Many antagonists and radioligands are not well‐characterized, and thus the affinities are uncertain. Among radioligands, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1706 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1706, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9467 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9467 and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9465 http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=9465 are commercially available. [3H]‐TCS 1102 (pKd/OX1 8.2, pKd/OX2 9.0) [http://www.ncbi.nlm.nih.gov/pubmed/24376396?dopt=AbstractPlus] and Rhodamine Green‐orexinA [http://www.ncbi.nlm.nih.gov/pubmed/11266181?dopt=AbstractPlus] are also useful radioligand tools. Orexin receptors have been reported to be able to form complexes with each other and some other GPCRs as well as σ1 receptors, which might affect the signaling and pharmacology [http://www.ncbi.nlm.nih.gov/pubmed/27909990?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25926444?dopt=AbstractPlus]. Loss‐of‐function mutations in the gene encoding the OX2 receptor underlie canine hereditary narcolepsy [http://www.ncbi.nlm.nih.gov/pubmed/10458611?dopt=AbstractPlus]. Antagonists of the orexin receptors are the focus of major drug discovery efforts for their potential to treat insomnia and other disorders of wakefulness [http://www.ncbi.nlm.nih.gov/pubmed/26317591?dopt=AbstractPlus], while agonists would likely be useful in human narcolepsy.

Overview

491Nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus].

Overview

494P2Y receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on P2Y Receptors [http://www.ncbi.nlm.nih.gov/pubmed/12559763?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/16968944?dopt=AbstractPlus]) are activated by the endogenous ligands http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1713, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1712, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1734, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1749 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1783. The relationship of many of the cloned receptors to endogenously expressed receptors is not yet established and so it might be appropriate to use wording such as ’http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1734‐preferring (or http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1713‐, etc.) P2Y receptor’ or ’P2Y1‐like’, etc., until further, as yet undefined, corroborative criteria can be applied [271, http://www.ncbi.nlm.nih.gov/pubmed/21586366?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23597047?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21586365?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22963441?dopt=AbstractPlus]. Clinically used drugs acting on these receptors include the dinucleoside polyphosphate http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1736, agonist of the P2Y2 receptor subtype, approved in Japan for the management of dry eye disease [http://www.ncbi.nlm.nih.gov/pubmed/24511227?dopt=AbstractPlus], and the P2Y12 receptor antagonists http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7562, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1765 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1776, all approved as antiplatelet drugs [http://www.ncbi.nlm.nih.gov/pubmed/23809135?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/27886821?dopt=AbstractPlus].

Comments

495A series of 4‐alkyloxyimino derivatives of uridine5’‐triphosphate which could be useful for derivatization as fluorescent P2Y2/4/6 receptor probes has been recently synthesized [http://www.ncbi.nlm.nih.gov/pubmed/24712832?dopt=AbstractPlus].

496Single nucleotide polymorphisms of the P2YR1 gene have been associated to different platelet reactivity to ADP http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1712 [http://www.ncbi.nlm.nih.gov/pubmed/15514209?dopt=AbstractPlus]. Three frequent nonsynonymous P2Y2 receptor polymorphisms have been identified, one of which was significantly more common in cystic fibrosis patients. This polymorphism is linked to increases in Ca2+ influx in transfected cells, and might therefore play a role in disease development [http://www.ncbi.nlm.nih.gov/pubmed/16495779?dopt=AbstractPlus]. Although http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1734 (UTP) was also shown to be a biased agonist at P2Y11, this is still under debate [http://www.ncbi.nlm.nih.gov/pubmed/25015314?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12761346?dopt=AbstractPlus]. A group of single nucleotide polymorphisms in the P2Y12 gene, forming the so called P2Y12 H2 haplotype, has been associated with increased platelet responsiveness to ADP, increased risk of peripheral arterial disease and with coronary artery disease [http://www.ncbi.nlm.nih.gov/pubmed/17803810?dopt=AbstractPlus]. The platelet‐type bleeding disorder due to P2Y12 receptor defects is an autosomal recessive condition characterized by mild to moderate mucocutaneous bleeding and excessive bleeding after surgery or trauma. The defect is due to the inability of ADP to induce platelet aggregation [http://www.ncbi.nlm.nih.gov/pubmed/12578987?dopt=AbstractPlus]. The P2Y13 receptor Met‐158‐Thr polymorphism, which is in linkage disequilibrium with the P2Y12 locus, is not associated with acute myocardial infarction, diabetes mellitus or related risk factors [http://www.ncbi.nlm.nih.gov/pubmed/18213371?dopt=AbstractPlus]. The P2Y14 receptor was previously considered to exclusively bind sugar nucleotides such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1783 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1782 [http://www.ncbi.nlm.nih.gov/pubmed/10753868?dopt=AbstractPlus]. However, more recent evidence with several cell lines has demonstrated that http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1749 (UDP) is 5‐fold more potent than http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1783 [http://www.ncbi.nlm.nih.gov/pubmed/19759354?dopt=AbstractPlus]. UDP was also shown to competitively antagonise the UDP‐glucose response at the human recombinant P2Y14 receptor [http://www.ncbi.nlm.nih.gov/pubmed/18252808?dopt=AbstractPlus].

Overview

500The parathyroid hormone receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Parathyroid Hormone Receptors [http://www.ncbi.nlm.nih.gov/pubmed/25713287?dopt=AbstractPlus]) are family B G protein‐coupled receptors. The parathyroid hormone (PTH)/parathyroid hormone‐related peptide (PTHrP) receptor (PTH1 receptor) is activated by precursor‐derived peptides: http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1785 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9606, http://www.uniprot.org/uniprot/P01270) (84 amino acids), and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3738 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9607, http://www.uniprot.org/uniprot/P12272) (141 amino‐acids) and related peptides (PTH‐(1‐34), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1790, http://www.uniprot.org/uniprot/P12272)). The parathyroid hormone 2 receptor (PTH2 receptor) is activated by the precursor‐derived peptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1815 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30828, http://www.uniprot.org/uniprot/Q96A98) (39 amino acids). [125I]PTH may be used to label both PTH1 and PTH2 receptors.

Comments

501The parathyroid hormone type 1 receptor (PTHR) is the canonical GPCR for PTH and PTHrP. It is coupled to Gs and Gq and regulates the development of bone, heart, mammary glands and other tissues in response to PTHrP, and blood concentrations of calcium and phosphate ions, as well as vitamin D, in response to PTH. Another important action of the PTH/PTHR system is to stimulate bone formation when the hormone is intermittently administrated (daily injection).

502Although http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1785 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9606, http://www.uniprot.org/uniprot/P01270) is an agonist at human PTH2 receptors, it fails to activate the rodent orthologues. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1815 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30828, http://www.uniprot.org/uniprot/Q96A98) is a weak antagonist at PTH1 receptors [http://www.ncbi.nlm.nih.gov/pubmed/11159842?dopt=AbstractPlus].

Overview

506Platelet‐activating factor (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1831, 1‐O‐alkyl‐2‐acetyl‐sn‐glycero‐3‐phosphocholine) is an ether phospholipid mediator associated with platelet coagulation, but also subserves inflammatory roles. The PAF receptor (provisional nomenclature recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) is activated by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1831 and other suggested endogenous ligands are oxidized phosphatidylcholine [http://www.ncbi.nlm.nih.gov/pubmed/10497200?dopt=AbstractPlus] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2508 [http://www.ncbi.nlm.nih.gov/pubmed/9038918?dopt=AbstractPlus]. It may also be activated by bacterial lipopolysaccharide [http://www.ncbi.nlm.nih.gov/pubmed/1333988?dopt=AbstractPlus].

Comments

507Note that a previously recommended radioligand (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1859 Kd 44.6 nM) is currently unavailable.

Overview

511Prokineticin receptors, PKR1 and PKR2 (provisional nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) respond to the cysteine‐rich 81‐86 amino‐acid peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1866 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18454, http://www.uniprot.org/uniprot/Q9HC23) (also known as endocrine glandderived vascular endothelial growth factor, mambakine) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1867 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18455, https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:18455) (protein Bv8 homologue). An orthologue of PROK1 from black mamba (Dendroaspis polylepis) venom, mamba intestinal toxin 1 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1865, [http://www.ncbi.nlm.nih.gov/pubmed/10567694?dopt=AbstractPlus]) is a potent, nonselective agonist at prokineticin receptors [http://www.ncbi.nlm.nih.gov/pubmed/12054613?dopt=AbstractPlus], while http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5362, an orthologue of PROK2 from amphibians (Bombina sp., [http://www.ncbi.nlm.nih.gov/pubmed/10422759?dopt=AbstractPlus]), is equipotent at recombinant PKR1 and PKR2 [http://www.ncbi.nlm.nih.gov/pubmed/16113687?dopt=AbstractPlus], and has high potency in macrophagechemotaxis assays, which arelost in PKR1null mice.

Comments

512Genetic mutations in PROKR1 are associated with Hirschsprung's disease [http://www.ncbi.nlm.nih.gov/pubmed/21858136?dopt=AbstractPlus], while genetic mutations in PROKR2 are associated with hypogonadotropic hypogonadism with anosmia [http://www.ncbi.nlm.nih.gov/pubmed/23596439?dopt=AbstractPlus], hypopituitarism with pituitary stalk interruption [http://www.ncbi.nlm.nih.gov/pubmed/22466334?dopt=AbstractPlus] and Hirschsprung's disease [http://www.ncbi.nlm.nih.gov/pubmed/21858136?dopt=AbstractPlus]. PKR2 has been recently identified as a receptor for T. cruzi natural infection [http://www.ncbi.nlm.nih.gov/pubmed/25324134?dopt=AbstractPlus].

Overview

518The precursor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:17945, http://www.uniprot.org/uniprot/P81277) for PrRP generates 31 and 20‐amino‐acid versions. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3665 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:29982, http://www.uniprot.org/uniprot/P83859) (named after a pyroglutamylated arginine‐phenylalanine‐amide peptide) is a 43 amino acid peptide derived from https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:29982 (http://www.uniprot.org/uniprot/P83859) and is also known as P518 or 26RFa. RFRP is an RF amide‐related peptide [http://www.ncbi.nlm.nih.gov/pubmed/11025660?dopt=AbstractPlus] derived from a FMRFamide‐related peptide precursor (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:13782, http://www.uniprot.org/uniprot/Q9HCQ7), which is cleaved to generate http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3736 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7901, http://www.uniprot.org/uniprot/O15130), neuropeptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5340 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:13782, http://www.uniprot.org/uniprot/Q9HCQ7), neuropeptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5373 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:13782, http://www.uniprot.org/uniprot/Q9HCQ7) and neuropeptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4016 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:13782, http://www.uniprot.org/uniprot/Q9HCQ7) (neuropeptide NPVF).

Comments

519The orphan receptor https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:4523 (http://www.uniprot.org/uniprot/Q9NYM4) shows sequence similarities with NPFF1, NPFF2, PrRP and QRFP receptors.

Overview

522Prostanoid receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Prostanoid Receptors [http://www.ncbi.nlm.nih.gov/pubmed/21752876?dopt=AbstractPlus]) are activated by the endogenous ligands prostaglandins http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1881, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1882, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1883, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1884, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4483, prostacyclin [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1915] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4482. Measurement of the potency of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1915 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4482 is hampered by their instability in physiological salt solution; they are often replaced by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1917 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1888, respectively, in receptor characterization studies.

Comments

523Whilst http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1917 is selective for IP receptors, it does exhibit moderate agonist potency at EP4 receptors [http://www.ncbi.nlm.nih.gov/pubmed/10634944?dopt=AbstractPlus]. Apart from IP receptors, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1895 also binds to EP1 receptors.

524The EP1 agonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1912 also shows agonist activity at EP3 and EP4 receptors [http://www.ncbi.nlm.nih.gov/pubmed/21323896?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/27664754?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3379 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3331 may require de‐esterification within tissues to attain full agonist potency. There is evidence for subtypes of FP [http://www.ncbi.nlm.nih.gov/pubmed/7830272?dopt=AbstractPlus] and TP receptors [http://www.ncbi.nlm.nih.gov/pubmed/8882612?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8034687?dopt=AbstractPlus]. mRNA for the EP3 receptor undergoes alternative splicing to produce variants which can interfere with signalling [http://www.ncbi.nlm.nih.gov/pubmed/8940129?dopt=AbstractPlus] or generate complex patterns of G‐protein (Gi/o, Gq/11, Gs and G12,13) coupling (e.g. [http://www.ncbi.nlm.nih.gov/pubmed/7476918?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/7608175?dopt=AbstractPlus]). The number of EP3 receptor (protein) variants are variable depending on species, with five in human, three in rat and three in mouse. Putative receptor(s) for prostamide F (which as yet lack molecular correlates) and which preferentially recognize http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5456 and its analogues (e.g. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1958) have been identified, together with moderate‐potency antagonists (e.g. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5455) [http://www.ncbi.nlm.nih.gov/pubmed/18700152?dopt=AbstractPlus].

525The free acid form of AL‐12182, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3386, used in in vitro studies, has a EC50 of 15nM which is the concentration of the compound giving half‐maximal stimulation of inositol phosphate turnover in HEK‐293 cells expressing the human FP receptor [http://www.ncbi.nlm.nih.gov/pubmed/17076623?dopt=AbstractPlus].

526References given alongside the TP receptor agonists I‐BOP [http://www.ncbi.nlm.nih.gov/pubmed/1830308?dopt=AbstractPlus] and STA2 [http://www.ncbi.nlm.nih.gov/pubmed/8242228?dopt=AbstractPlus] use human platelets as the source of TP receptors for competition radio‐ligand binding assays to determine the indicated activity values.

527Pharmacological evidence for a second IP receptor, denoted IP2, in the central nervous system [http://www.ncbi.nlm.nih.gov/pubmed/8621463?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10349870?dopt=AbstractPlus] and in the BEAS‐2B human airway epithelial cell line [http://www.ncbi.nlm.nih.gov/pubmed/21173040?dopt=AbstractPlus] is available. This receptor is selectively activated by 15R‐17,18,19,20‐tetranor‐16‐m‐tolylisocarbacyclin (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5864) and 15R‐Deoxy 17,18,19,20‐tetranor‐16m‐tolyl‐isocarbacyclin (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5865). However, molecular biological evidence for an IP2 subtype is currently lacking.

Overview

529Proteinase‐activated receptors (PARs, nomenclature as agreed by the NC‐IUPHAR Subcommittee on Proteinase‐activated Receptors [http://www.ncbi.nlm.nih.gov/pubmed/12037136?dopt=AbstractPlus]) are unique members of the GPCR superfamily activated by proteolytic cleavage of their amino terminal exodomains. Agonist proteinase‐induced hydrolysis unmasks a tethered ligand (TL) at the exposed amino terminus, which acts intramolecularly at the binding site in the body of the receptor to effect transmembrane signalling. TL sequences at human PAR1‐4 are http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5361, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3740, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5360 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3739, respectively. With the exception of PAR3, synthetic peptides with these sequences (as carboxyl terminal amides) are able to act as agonists at their respective receptors. Several proteinases, including neutrophil elastase, cathepsin G and chymotrypsin can have inhibitory effects at PAR1 and PAR2 such that they cleave the exodomain of the receptor without inducing activation of Gαq‐coupled calcium signalling, thereby preventing activation by activating proteinases but not by agonist peptides. Neutrophil elastase (NE) cleavage of PAR1 and PAR2 can however activate MAP kinase signaling by exposing a TL that is different from the one revealed by trypsin [http://www.ncbi.nlm.nih.gov/pubmed/22212680?dopt=AbstractPlus]. PAR2 ectivation by NE regulates inflammation and pain responses [http://www.ncbi.nlm.nih.gov/pubmed/26140667?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25878251?dopt=AbstractPlus] and triggers mucin secretion from airway epithelial cells [http://www.ncbi.nlm.nih.gov/pubmed/23392769?dopt=AbstractPlus].

Comments

530Endogenous serine proteases (EC 3.4.21.) active at the proteinase‐activated receptors include: http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4453 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3535, http://www.uniprot.org/uniprot/P00734), generated by the action of Factor X (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3528, http://www.uniprot.org/uniprot/P00742) on liver‐derived prothrombin (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3535, http://www.uniprot.org/uniprot/P00734); trypsin, generated by the action of enterokinase (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9490, http://www.uniprot.org/uniprot/P98073) on pancreatic‐derived trypsinogen (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9475, http://www.uniprot.org/uniprot/P07477); tryptase, a family of enzymes (α/β1 https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12019, http://www.uniprot.org/uniprot/Q15661; γ1 https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:14134, http://www.uniprot.org/uniprot/Q9NRR2 δ1 https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:14118, http://www.uniprot.org/uniprot/Q9BZJ3) secreted from mast cells; cathepsin G (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:2532, http://www.uniprot.org/uniprot/P08311) generated from leukocytes; liver‐derived protein C (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:9451, http://www.uniprot.org/uniprot/P04070) generated in plasma by http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4453 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:3535, http://www.uniprot.org/uniprot/P00734) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=6655 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:7155, http://www.uniprot.org/uniprot/P45452).

Overview

537The human gene encoding the QRFP receptor (nomenclature as agreed by the NC‐IUPHAR Subcommittee on the QRFP receptor [http://www.ncbi.nlm.nih.gov/pubmed/28613414?dopt=AbstractPlus]; QRFPR, formerly known as the Peptide P518 receptor), previously designated as an orphan GPCR receptor was identified in 2001 by Lee et al. from a hypothalamus cDNA library [http://www.ncbi.nlm.nih.gov/pubmed/11574155?dopt=AbstractPlus]. However, the reported cDNA (AF411117) is a chimera with bases 1‐127 derived from chromosome 1 and bases 155‐1368 derived from chromosome 4. When corrected, QRFPR (also referred to as SP9155 or AQ27) encodes a 431 amino acid protein that shares sequence similarities in the transmembrane spanning regions with other peptide receptors. These include neuropeptide FF2 (38%), neuropeptide Y2 (37%) and galanin Gal1 (35%) receptors.

Comments

538The orphan receptor http://www.guidetopharmacology.org/GRAC/ (http://www.uniprot.org/uniprot/9NYM4) shows sequence similarities with the QRFP receptor, as well as with the NPFF1, NPFF2, and PrRP receptors.

Overview

542Relaxin family peptide receptors (RXFP, nomenclature as agreed by the NC‐IUPHAR Subcommittee on Relaxin family peptide receptors [http://www.ncbi.nlm.nih.gov/pubmed/16507880?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25761609?dopt=AbstractPlus]) may be divided into two pairs, RXFP1/2 and RXFP3/4. Endogenous agonists at these receptors are heterodimeric peptide hormones structurally related to insulin: http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1988 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10026, http://www.uniprot.org/uniprot/P04808), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1989 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10027, http://www.uniprot.org/uniprot/P04090), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1990 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:17135, http://www.uniprot.org/uniprot/Q8WXF3) (also known as INSL7), insulin‐like peptide 3 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1995 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6086, http://www.uniprot.org/uniprot/P51460)) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2000 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6088, http://www.uniprot.org/uniprot/Q9Y5Q6). Species homologues of relaxin have distinct pharmacology and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1989 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10027, http://www.uniprot.org/uniprot/P04090) interacts with RXFP1, RXFP2 and RXFP3, whereas mouse and rat relaxin selectively bind to and activate RXFP1 [http://www.ncbi.nlm.nih.gov/pubmed/15956680?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1990 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:17135, http://www.uniprot.org/uniprot/Q8WXF3) is the ligand for RXFP3 but it also binds to RXFP1 and RXFP4 and has differential affinity for RXFP2 between species [http://www.ncbi.nlm.nih.gov/pubmed/15956681?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2000 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6088, http://www.uniprot.org/uniprot/Q9Y5Q6) is the ligand for RXFP4 but is a weak antagonist of RXFP3. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1989 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10027, http://www.uniprot.org/uniprot/P04090) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1995 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6086, http://www.uniprot.org/uniprot/P51460) have multiple complex binding interactions with RXFP1 [http://www.ncbi.nlm.nih.gov/pubmed/27088579?dopt=AbstractPlus] and RXFP2 [http://www.ncbi.nlm.nih.gov/pubmed/30594862?dopt=AbstractPlus] which direct the N‐terminal LDLa modules of the receptors together with a linker domain to act as a tethered ligand to direct receptor signaling [http://www.ncbi.nlm.nih.gov/pubmed/16963451?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2000 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6088, http://www.uniprot.org/uniprot/Q9Y5Q6) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1990 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:17135, http://www.uniprot.org/uniprot/Q8WXF3) interact with their receptors using distinct residues in their B‐chains for binding, and activation, respectively [http://www.ncbi.nlm.nih.gov/pubmed/28274616?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30131340?dopt=AbstractPlus].

Comments

543http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1989 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10027, http://www.uniprot.org/uniprot/P04090) is the cognate peptide ligand for RXFP1 and is in extended Phase III clinical trials for the treatment of acute heart failure [http://www.ncbi.nlm.nih.gov/pubmed/23273292?dopt=AbstractPlus]. Relaxin has vasodilatory, anti‐fibrotic, angiogenic, anti‐apoptotic and anti‐inflammatory effects. A small molecule allosteric agonists http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=8322 has been developed [http://www.ncbi.nlm.nih.gov/pubmed/18854305?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23764525?dopt=AbstractPlus], and a relaxin B‐chain mimetic peptide B7‐33 has been developed which that has cell specific signaling properties [http://www.ncbi.nlm.nih.gov/pubmed/30155023?dopt=AbstractPlus]. The antifibrotic actions of relaxin are dependent on the angiotensin receptor AT2 [http://www.ncbi.nlm.nih.gov/pubmed/24429402?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1995 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6086, http://www.uniprot.org/uniprot/P51460) is the cognate peptide for RXFP2 and is a circulating hormone that in males is essential for testicular descent in utero [http://www.ncbi.nlm.nih.gov/pubmed/10391220?dopt=AbstractPlus] and in females has important roles in ovarian follicle function [http://www.ncbi.nlm.nih.gov/pubmed/30204868?dopt=AbstractPlus]. In adults, INSL3 has potential roles in testicular function [http://www.ncbi.nlm.nih.gov/pubmed/20952422?dopt=AbstractPlus] and the musculoskeletal system [http://www.ncbi.nlm.nih.gov/pubmed/30625346?dopt=AbstractPlus]. RXFP2 is also present in brain, associated with cortico‐thalamic motor circuits [http://www.ncbi.nlm.nih.gov/pubmed/18706979?dopt=AbstractPlus]. cAMP elevation is the major signalling pathway for both RXFP1 and RXFP2 [http://www.ncbi.nlm.nih.gov/pubmed/10935549?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/11809971?dopt=AbstractPlus], but RXFP1 also activates MAP kinases, nitric oxide signalling, and tyrosine kinase phosphorylation; and relaxin can interact with glucocorticoid receptors [http://www.ncbi.nlm.nih.gov/pubmed/17293890?dopt=AbstractPlus]. Receptor expression profiles suggest that RXFP3 is a brain neuropeptide receptor and RXFP4 a gut hormone receptor. The brain relaxin‐3/RXFP3 system modulates feeding [http://www.ncbi.nlm.nih.gov/pubmed/23135160?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22854307?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21384867?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22257012?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/21899720?dopt=AbstractPlus] via effects in hypothalamus [http://www.ncbi.nlm.nih.gov/pubmed/28864207?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/23135160?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/28098344?dopt=AbstractPlus], anxiety [http://www.ncbi.nlm.nih.gov/pubmed/24297931?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/26057358?dopt=AbstractPlus], reward and motivated, goal‐directed behaviours [http://www.ncbi.nlm.nih.gov/pubmed/25257104?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/24297931?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25849482?dopt=AbstractPlus], and spatial and social memory [http://www.ncbi.nlm.nih.gov/pubmed/30368554?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/28100033?dopt=AbstractPlus]. Of the other relaxin peptides, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1990 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:17135, http://www.uniprot.org/uniprot/Q8WXF3)is anagonist atRXFP3 and RXFP4 whereashttp://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2000 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6088, http://www.uniprot.org/uniprot/Q9Y5Q6) is an agonist at RXFP4 and a weak antagonist at RXFP3. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2000 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:6088, http://www.uniprot.org/uniprot/Q9Y5Q6) is secreted from enteroendocrine L cells and the INSL5/RXFP4 system affects food intake [http://www.ncbi.nlm.nih.gov/pubmed/25028498?dopt=AbstractPlus] and glucose homeostasis [http://www.ncbi.nlm.nih.gov/pubmed/25514935?dopt=AbstractPlus]. RXFP3 and RXFP4 couple to Gi/o and inhibit adenylyl cyclase [http://www.ncbi.nlm.nih.gov/pubmed/14522968?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20159943?dopt=AbstractPlus], and also cause Erk1/2 phosphorylation [http://www.ncbi.nlm.nih.gov/pubmed/20159943?dopt=AbstractPlus]. RXFP4 also causes phosphorylation of p38MAPK, Akt and S6RP [http://www.ncbi.nlm.nih.gov/pubmed/27243554?dopt=AbstractPlus] and GLP‐1 secretion in vitro [http://www.ncbi.nlm.nih.gov/pubmed/29535183?dopt=AbstractPlus]. There is evidence that at RXFP3, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1989 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:10027, http://www.uniprot.org/uniprot/P04090) is a biased ligand compared to the cognate ligand http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1990 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:17135, http://www.uniprot.org/uniprot/Q8WXF3) [http://www.ncbi.nlm.nih.gov/pubmed/20159943?dopt=AbstractPlus].

Overview

548Somatostatin (somatotropin release inhibiting factor) is an abundant neuropeptide, which acts on five subtypes of somatostatin receptor (SST1‐SST5; nomenclature as agreed by the NC‐IUPHAR Subcommittee on Somatostatin Receptors [http://www.ncbi.nlm.nih.gov/pubmed/30232095?dopt=AbstractPlus]). Activation of these receptors produces a wide range of physiological effects throughout the body including the inhibition of secretion of many hormones. Endogenous ligands for these receptors are somatostatin‐14 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2019 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:11329, http://www.uniprot.org/uniprot/P61278)) and somatostatin‐28 (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2020 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:11329, http://www.uniprot.org/uniprot/P61278)). http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2007 {Mouse, Rat} has also been suggested to be an endogenous ligand for somatostatin receptors [http://www.ncbi.nlm.nih.gov/pubmed/8622767?dopt=AbstractPlus].

Comments

549[http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2060, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2023, [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2022 and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2024 may be used to label somatostatin receptors nonselectively. A number of nonpeptide subtype‐selective agonists have been synthesised [http://www.ncbi.nlm.nih.gov/pubmed/9784130?dopt=AbstractPlus]. Octreotide and lanreotide are being used in the treatment of SST2‐expressing neuroendocrine tumors and pasireotide for SST5‐expressing neuroendocrine tumors. A novel peptide somatostatin analogue, veldoreotide (COR‐005), has affinity for SST2, SST4 and SST5 receptors and is a potent inhibitor of GH secretion [http://www.ncbi.nlm.nih.gov/pubmed/22065857?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/15636423?dopt=AbstractPlus].

Overview

555Nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus]. The Succinate receptor has been identified as being activated by physiological levels of the Kreb's cycle intermediate succinate and other dicarboxylic acids such as maleate in 2004. Since its pairing with its endogenous ligand, the receptor has been the focus of intensive research and its role has been evidenced in various (patho)physiological processes such as regulation of renin production, retinal angiogenesis, inflammation or immune response.

Comments

556In humans, there is the possibility of two open‐reading frames (ORFs) for SUCNR1, one giving a protein of 330 amino acids (AA) and the other one 334‐AA. Wittenberger et al. [http://www.ncbi.nlm.nih.gov/pubmed/11273702?dopt=AbstractPlus] noted that the 330‐AA protein was more likely to be expressed given the Kozak sequence surrounding the second ATG. Some databases report SUCNR1 as being 334‐AA long.

Overview

561Tachykinin receptors (provisional nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by the endogenous peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2098 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:11517, http://www.uniprot.org/uniprot/P20366) (SP), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2089) (NKA; previously known as substance K, neurokinin α, neuromedin L), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2090 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:11521, http://www.uniprot.org/uniprot/Q9UHF0) (NKB; previously known as neurokinin β, neuromedin K), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2091 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:11517, http://www.uniprot.org/uniprot/P20366) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3667 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:11517) (N‐terminally extended forms of neurokinin A). The neurokinins (A and B) are mammalian members of the tachykinin family, which includes peptides of mammalian and nonmammalian origin containing the consensus sequence: Phe‐x‐Gly‐LeuMet. Marked species differences in in vitro pharmacology exist for all three receptors, in the context of nonpeptide ligands. Antagonists such as http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3490 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=7623 were approved by FDA and EMA, in combination with other antiemetic agents, for the prevention of nausea and vomiting associated with emetogenic cancer chemotherapy.

Comments

562The NK1 receptor has also been described to couple to G proteins other than Gq/11 [http://www.ncbi.nlm.nih.gov/pubmed/9654151?dopt=AbstractPlus]. The crystal structure of the human NK1 receptor in complex with antagonists has been determined [http://www.ncbi.nlm.nih.gov/pubmed/30604743?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/30538204?dopt=AbstractPlus]. The hexapeptide agonist septide appears to bind to an overlapping but non‐identical site to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2098 (https://www.genenames.org/data/gene‐symbol‐report/%23!/hgnc_id/HGNC:11517, http://www.uniprot.org/uniprot/P20366) on the NK1 receptor. There are additional subtypes of tachykinin receptor;an orphan receptor (Swis‐sProt http://www.ncbi.nlm.nih.gov/protein/266702/) with structural similarities to the NK3 receptor was found to respond to NKB when expressed in Xenopus oocytes or Chinese hamster ovary cells [http://www.ncbi.nlm.nih.gov/pubmed/8947459?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/8990205?dopt=AbstractPlus].

Overview

568Thyrotropin‐releasing hormone (TRH) receptors (provisional nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by the endogenous tripeptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2139 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12298, http://www.uniprot.org/uniprot/P20396) (pGlu‐His‐ProNH2). http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2139 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12298, http://www.uniprot.org/uniprot/P20396) and TRH analogues fail to distinguish TRH1 and TRH2 receptors [http://www.ncbi.nlm.nih.gov/pubmed/12683933?dopt=AbstractPlus]. [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3836) is able to label both TRH1 and TRH2 receptors with Kd values of 13 and 9 nM respectively. Synthesis and biology of ring‐modified L‐Histidine containing TRH analogues has been reported [http://www.ncbi.nlm.nih.gov/pubmed/26854379?dopt=AbstractPlus].

Overview

572Trace amine‐associated receptors were discovered from a search for novel 5‐HT receptors [http://www.ncbi.nlm.nih.gov/pubmed/11459929?dopt=AbstractPlus], where 15 mammalian orthologues were identified and divided into two families. The TA1 receptor (nomenclature as agreed by the NC‐IUPHAR Subcommittee for the Trace amine receptor [http://www.ncbi.nlm.nih.gov/pubmed/19325074?dopt=AbstractPlus]) has affinity for the endogenous trace amines http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2150, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2144 and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2149 in addition to the classical amine http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=940 [http://www.ncbi.nlm.nih.gov/pubmed/11459929?dopt=AbstractPlus]. Emerging evidence suggests that TA1 is a modulator of monoaminergic activity in the brain [http://www.ncbi.nlm.nih.gov/pubmed/19482011?dopt=AbstractPlus] with TA1 and dopamine D2 receptors shown to form constitutive heterodimers when co‐expressed [http://www.ncbi.nlm.nih.gov/pubmed/21670104?dopt=AbstractPlus]. In addition to trace amines, receptors can be activated by amphetamine‐like psychostimulants, and endogenous thyronamines.

Comments

573In addition to TA1, in man there are up to 5 functional TAAR genes (TAAR2,5,6,8,9). See [http://www.ncbi.nlm.nih.gov/pubmed/11459929?dopt=AbstractPlus] for detailed discussion. The product of the gene TAAR2 (also known as GPR58) appears to respond to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2144 > http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2150 and to couple through Gs [http://www.ncbi.nlm.nih.gov/pubmed/11459929?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=115#show_object_168, in some individuals, and http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=115#show_object_169 are pseudogenes in man, although functional in rodents. The signalling characteristics and pharmacology of http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=115#show_object_170 (PNR, Putative Neurotransmitter Receptor: https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30236, http://www.uniprot.org/uniprot/O14804), http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=115#show_object_171 http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=115#show_object_171 (Trace amine receptor 4, TaR‐4: https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:20978, http://www.uniprot.org/uniprot/96RI8), http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=115#show_object_172 (Trace amine receptor 5, GPR102: https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:14964, http://www.uniprot.org/uniprot/Q969N4) and http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=115#show_object_173 http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=115#show_object_173 (trace amine associated receptor 9: https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:20977, http://www.uniprot.org/uniprot/96RI9) are lacking. The thyronamines, endogenous derivatives of thyroid hormone, have affinity for rodent cloned trace amine receptors, including TA1 [http://www.ncbi.nlm.nih.gov/pubmed/15146179?dopt=AbstractPlus]. An antagonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=5457 has recently been described with a pKi of 9.1 at the mouse TA1 but >5.3 for human TA1 [http://www.ncbi.nlm.nih.gov/pubmed/21237643?dopt=AbstractPlus].

Overview

576The urotensin‐II (U‐II) receptor (UT, nomenclature as agreed by the NC‐IUPHAR Subcommittee on the Urotensin receptor [516, http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/25535277?dopt=AbstractPlus]) is activated by the endogenous dodecapeptide http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2153 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12636, http://www.uniprot.org/uniprot/O95399), originally isolated from the urophysis, the endocrine organ of the caudal neurosecretory system of teleost fish [http://www.ncbi.nlm.nih.gov/pubmed/2864726?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/20633133?dopt=AbstractPlus]. Several structural forms of U‐II exist in fish and amphibians. The goby orthologue was used to identify U‐II as the cognate ligand for the predicted receptor encoded by the rat gene gpr14 [http://www.ncbi.nlm.nih.gov/pubmed/9861051?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10581185?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10548501?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/10559967?dopt=AbstractPlus]. Human http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2153), an 11‐amino‐acid peptide [http://www.ncbi.nlm.nih.gov/pubmed/9861051?dopt=AbstractPlus], retains the cyclohexapeptide sequence of goby U‐II that is thought to beimportant in ligand binding [http://www.ncbi.nlm.nih.gov/pubmed/12807997?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/12203418?dopt=AbstractPlus]. This sequence is also conserved in the deduced amino‐acid sequence of rat http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2155 {Rat} (14 amino‐acids) and mouse http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2154 {Mouse} (14 amino‐acids), although the N‐terminal is more divergent from the human sequence [http://www.ncbi.nlm.nih.gov/pubmed/10486557?dopt=AbstractPlus]. A second endogenous ligand for the UT has been discovered in rat [http://www.ncbi.nlm.nih.gov/pubmed/17628210?dopt=AbstractPlus]. This is the http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2156 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:30894, http://www.uniprot.org/uniprot/Q765I0), an octapeptide that is derived from a different gene, but shares the C‐terminal sequence (CFWKYCV) common to U‐II from other species. Identical sequences to rat http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2156) are predicted for the mature mouse and human peptides [http://www.ncbi.nlm.nih.gov/pubmed/18710417?dopt=AbstractPlus]. UT exhibits relatively high sequence identity with somatostatin, opioid and galanin receptors [http://www.ncbi.nlm.nih.gov/pubmed/25535277?dopt=AbstractPlus].

Comments

577In the human vasculature, human http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2153 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12636, http://www.uniprot.org/uniprot/O95399) elicits both vasoconstrictor (pD 2 9.3‐10.1, [http://www.ncbi.nlm.nih.gov/pubmed/11015293?dopt=AbstractPlus]) and vasodilator (pIC50 10.3‐10.4, [http://www.ncbi.nlm.nih.gov/pubmed/11158995?dopt=AbstractPlus]) responses.

Overview

583Vasopressin (AVP) and oxytocin (OT) receptors (nomenclature as recommended by NC‐IUPHAR [http://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus]) are activated by the endogenous cyclic nonapeptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2168 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:894, http://www.uniprot.org/uniprot/P01185) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2174 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:8528, http://www.uniprot.org/uniprot/P01178). These peptides are derived from precursors which also produce neurophysins (neurophysin I for oxytocin; neurophysin II for vasopressin). Vasopressin and oxytocin differ at only 2 amino acids (positions 3 and 8). There are metabolites of these neuropeptides that may be biologically active [http://www.ncbi.nlm.nih.gov/pubmed/8258377?dopt=AbstractPlus].

Comments

584Vasopressin and oxytocin receptors have a characteristic and sometimes overlapping distribution in a number of tissues including brain. There are phylogenetic, ontogenetic and sex‐specific differences in the levels and distribution of these receptors, particularly in the brain. The V2 receptor exhibits marked species differences, such that many ligands (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2236 and [http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3817) exhibit low affinity at human V2 receptors [http://www.ncbi.nlm.nih.gov/pubmed/9773787?dopt=AbstractPlus]. Similarly, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2170 is more V2 selective in the rat than in the human [http://www.ncbi.nlm.nih.gov/pubmed/9264324?dopt=AbstractPlus]. The gene encoding the V2 receptor is polymorphic in man, underlying nephrogenic diabetes insipidus [http://www.ncbi.nlm.nih.gov/pubmed/9756088?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2187 is selective only for the human and bovine V1B receptors [http://www.ncbi.nlm.nih.gov/pubmed/12446593?dopt=AbstractPlus], while http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2191 has high affinity for the rat V1B receptor [http://www.ncbi.nlm.nih.gov/pubmed/17300166?dopt=AbstractPlus]. Knockouts of vasopressin and oxytocin receptors have systemspecific defects (e.g., impaired ability toconcentrate urine in V2 receptor knockouts) which include behavioural deficits (principally in V1A, V 1B and OT receptor knockouts).

Overview

590Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase‐activating peptide (PACAP) receptors (nomenclature as agreed by the NC‐IUPHAR Subcommittee on Vasoactive Intestinal Peptide Receptors [http://www.ncbi.nlm.nih.gov/pubmed/9647867?dopt=AbstractPlus, http://www.ncbi.nlm.nih.gov/pubmed/22289055?dopt=AbstractPlus]) are activated by the endogenous peptides http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1152 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12693, http://www.uniprot.org/uniprot/P01282), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2258 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:241, http://www.uniprot.org/uniprot/P18509), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2257), peptide histidine isoleucineamide (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=4397 {Mouse, Rat}), peptide histidine methionineamide (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2274)) and peptide histidine valine (http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3706)). VPAC1 and VPAC2 receptors display comparable affinity for the PACAP peptides, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2257) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2258), and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1152 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:12693, http://www.uniprot.org/uniprot/P01282), whereas http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2257 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:241, http://www.uniprot.org/uniprot/P18509) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2258) are >100 fold more potent than http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1152) as agonists of most isoforms of the PAC1 receptor. However, one splice variant of the human PAC1 receptor has been reported to respond to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2258), http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2257) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1152) with comparable affinity [http://www.ncbi.nlm.nih.gov/pubmed/10583729?dopt=AbstractPlus]. http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2272 [http://www.ncbi.nlm.nih.gov/pubmed/11068102?dopt=AbstractPlus] has been used as a selective VPAC2 receptor antagonist in a number of physiological studies, but has been reported to have significant activity at VPAC1 and PAC1 receptors [http://www.ncbi.nlm.nih.gov/pubmed/16930633?dopt=AbstractPlus]. The selective PAC1 receptor agonist http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2264, was extracted from the salivary glands of sand flies (Lutzomyia longipalpis) and has no sequence homology to http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1152) or the PACAP peptides [http://www.ncbi.nlm.nih.gov/pubmed/8995389?dopt=AbstractPlus]. Two deletion variants of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2264, http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=3305 [http://www.ncbi.nlm.nih.gov/pubmed/9928019?dopt=AbstractPlus] and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2265 [http://www.ncbi.nlm.nih.gov/pubmed/10438479?dopt=AbstractPlus] have been reported to be PAC1 receptor antagonists, but these peptides have not been extensively characterised.

Comments

591Subtypes of PAC1 receptors have been proposed based on tissue differences in the potencies of http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2257 (https://www.genenames.org/data/gene‐symbol‐report/#!/hgnc_id/HGNC:241, http://www.uniprot.org/uniprot/P18509) and http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=2258); these might result from differences in G protein coupling and second messenger mechanisms [http://www.ncbi.nlm.nih.gov/pubmed/8967982?dopt=AbstractPlus], or from alternative splicing of PAC1 receptor mRNA [http://www.ncbi.nlm.nih.gov/pubmed/8396727?dopt=AbstractPlus].

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Not in our library
83.
Ayme-Dietrich E et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28806488?dopt=AbstractPlus
Not in our library
84.
Ayoub MA et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15266022?dopt=AbstractPlus
Not in our library
85.
Azran S et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23751098?dopt=AbstractPlus
Not in our library
86.
Baba M et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9169459?dopt=AbstractPlus
Not in our library
87.
Baba M et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10318947?dopt=AbstractPlus
Not in our library
88.
Bach P et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24215345?dopt=AbstractPlus
Not in our library
89.
Bach T et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11218067?dopt=AbstractPlus
Not in our library
90.
Bachelerie F et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24218476?dopt=AbstractPlus
Not in our library
91.
Bachelerie F et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25958743?dopt=AbstractPlus
Not in our library
92.
Bae YS et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15210823?dopt=AbstractPlus
Not in our library
93.
Bahouth SW et al (1985 ) https://www.ncbi.nlm.nih.gov/pubmed/2410593?dopt=AbstractPlus
Not in our library
94.
Baker JG. (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20590599?dopt=AbstractPlus
Not in our library
95.
Baker JG. (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/21152092?dopt=AbstractPlus
Not in our library
96.
Baker JG. (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15655528?dopt=AbstractPlus
Not in our library
97.
Baker JG et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12770928?dopt=AbstractPlus
Not in our library
98.
Baker JG et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14645666?dopt=AbstractPlus
Not in our library
99.
Baker JG et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12920204?dopt=AbstractPlus
Not in our library
100.
Bakker RA et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16415177?dopt=AbstractPlus
Not in our library
101.
Balan G et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19442519?dopt=AbstractPlus
Not in our library
102.
Balogh J et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15893764?dopt=AbstractPlus
Not in our library
103.
Bamberg CE et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20044484?dopt=AbstractPlus
Not in our library
104.
Bandholtz S et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27791374?dopt=AbstractPlus
Not in our library
105.
Bang-Andersen B et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21486038?dopt=AbstractPlus
Not in our library
106.
Bard JA et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7592911?dopt=AbstractPlus
Not in our library
107.
Bard JA et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8226867?dopt=AbstractPlus
Not in our library
108.
Barda DA et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15149652?dopt=AbstractPlus
Not in our library
109.
Barnea G et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18165312?dopt=AbstractPlus
Not in our library
110.
Barrett MO et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23592514?dopt=AbstractPlus
Not in our library
111.
Barroso R et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22913878?dopt=AbstractPlus
Not in our library
112.
Barry GD et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20873792?dopt=AbstractPlus
Not in our library
113.
Barshop K et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25341626?dopt=AbstractPlus
Not in our library
114.
Bartfai T et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1720557?dopt=AbstractPlus
Not in our library
115.
Bartfai T et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/7504301?dopt=AbstractPlus
Not in our library
116.
Bartoi T et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20406808?dopt=AbstractPlus
Not in our library
117.
Bassi MT et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7647783?dopt=AbstractPlus
Not in our library
118.
Bastian S et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9313952?dopt=AbstractPlus
Not in our library
119.
Bastien L et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8163486?dopt=AbstractPlus
Not in our library
120.
Bathgate RA et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16507880?dopt=AbstractPlus
Not in our library
121.
Bayewitch M et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8626625?dopt=AbstractPlus
Not in our library
122.
Bayin NS et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27775701?dopt=AbstractPlus
Not in our library
123.
Beattie D et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22932315?dopt=AbstractPlus
Not in our library
124.
Beattie DT et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15466450?dopt=AbstractPlus
Not in our library
125.
Beaujouan JC et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9042606?dopt=AbstractPlus
Not in our library
126.
Bechtold DA et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22197240?dopt=AbstractPlus
Not in our library
127.
Beckers T et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11726197?dopt=AbstractPlus
Not in our library
128.
Beckers T et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7649152?dopt=AbstractPlus
Not in our library
129.
Beckers T et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9300077?dopt=AbstractPlus
Not in our library
130.
Bedendi I et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12969753?dopt=AbstractPlus
Not in our library
131.
Bednarek MA et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11087562?dopt=AbstractPlus
Not in our library
132.
Bednarek MA et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11606131?dopt=AbstractPlus
Not in our library
133.
Behrens M et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15178431?dopt=AbstractPlus
Not in our library
134.
Bekker P et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27768695?dopt=AbstractPlus
Not in our library
135.
Belgi A et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21866895?dopt=AbstractPlus
Not in our library
136.
Bell IM et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9622556?dopt=AbstractPlus
Not in our library
137.
Belley M et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10658574?dopt=AbstractPlus
Not in our library
138.
Bellier B et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14698161?dopt=AbstractPlus
Not in our library
139.
Bellucci F et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11786503?dopt=AbstractPlus
Not in our library
140.
Ben-Baruch A et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7545673?dopt=AbstractPlus
Not in our library
141.
Bender E et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10646498?dopt=AbstractPlus
Not in our library
142.
Bennacef I et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15265501?dopt=AbstractPlus
Not in our library
143.
Benned-Jensen T et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20148890?dopt=AbstractPlus
Not in our library
144.
Benya RV et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7838118?dopt=AbstractPlus
Not in our library
145.
Benyahia C et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23850788?dopt=AbstractPlus
Not in our library
146.
Beresford IJ et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9618428?dopt=AbstractPlus
Not in our library
147.
Beresford IJ et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7713168?dopt=AbstractPlus
Not in our library
148.
Bergman JM et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18207395?dopt=AbstractPlus
Not in our library
149.
Berizzi AE et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27461343?dopt=AbstractPlus
Not in our library
150.
Bern HA et al (1985 ) https://www.ncbi.nlm.nih.gov/pubmed/2864726?dopt=AbstractPlus
Not in our library
151.
Bernotas RC et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19523834?dopt=AbstractPlus
Not in our library
152.
Berque-Bestel I et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12801225?dopt=AbstractPlus
Not in our library
153.
Berrie CP et al (1984 ) https://www.ncbi.nlm.nih.gov/pubmed/6478115?dopt=AbstractPlus
Not in our library
154.
Berry CB et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25221667?dopt=AbstractPlus
Not in our library
155.
Bersani M et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1710578?dopt=AbstractPlus
Not in our library
156.
Bersani M et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1718731?dopt=AbstractPlus
Not in our library
157.
Bertini R et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15282370?dopt=AbstractPlus
Not in our library
158.
Besada P et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16942026?dopt=AbstractPlus
Not in our library
159.
Bettler B et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15269338?dopt=AbstractPlus
Not in our library
160.
Beukers MW et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11093773?dopt=AbstractPlus
Not in our library
161.
Beukers MW et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9384502?dopt=AbstractPlus
Not in our library
162.
Beukers MW et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12672250?dopt=AbstractPlus
Not in our library
163.
Bi Y et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25754495?dopt=AbstractPlus
Not in our library
164.
Bichet DG et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9756088?dopt=AbstractPlus
Not in our library
165.
Bigoni R et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12070757?dopt=AbstractPlus
Not in our library
166.
Binet V et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15126507?dopt=AbstractPlus
Not in our library
167.
Birdsall NJ et al (1979 ) https://www.ncbi.nlm.nih.gov/pubmed/497538?dopt=AbstractPlus
Not in our library
168.
Birke FW et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11259574?dopt=AbstractPlus
Not in our library
169.
Birrell MA et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/22747912?dopt=AbstractPlus
Not in our library
170.
Bjursell M et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16887097?dopt=AbstractPlus
Not in our library
171.
Blackhart BD et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8663335?dopt=AbstractPlus
Not in our library
172.
Blaho VA et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30343728?dopt=AbstractPlus
Not in our library
173.
Blaho VA et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26053123?dopt=AbstractPlus
Not in our library
174.
Blair JB et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11101361?dopt=AbstractPlus
Not in our library
175.
Blanpain C et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10477718?dopt=AbstractPlus
Not in our library
176.
Bley KR et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16331286?dopt=AbstractPlus
Not in our library
177.
Blin N et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/7903415?dopt=AbstractPlus
Not in our library
178.
Blondel O et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9603189?dopt=AbstractPlus
Not in our library
179.
Blue DR et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14678390?dopt=AbstractPlus
Not in our library
180.
Boatman PD et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22435740?dopt=AbstractPlus
Not in our library
181.
Bockaert J et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16896947?dopt=AbstractPlus
Not in our library
182.
Boden P et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8648606?dopt=AbstractPlus
Not in our library
183.
Boess FG et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9284367?dopt=AbstractPlus
Not in our library
184.
Boess FG et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9730917?dopt=AbstractPlus
Not in our library
185.
Bogdanov YD et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9647463?dopt=AbstractPlus
Not in our library
186.
Bohnekamp J et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/22025619?dopt=AbstractPlus
Not in our library
187.
Boie Y et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7512962?dopt=AbstractPlus
Not in our library
188.
Boie Y et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7642548?dopt=AbstractPlus
Not in our library
189.
Boie Y et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10513580?dopt=AbstractPlus
Not in our library
190.
Bolden C et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1346637?dopt=AbstractPlus
Not in our library
191.
Bolli MH et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20446681?dopt=AbstractPlus
Not in our library
192.
Bolli MH et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22862294?dopt=AbstractPlus
Not in our library
193.
Bolli MH et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15139756?dopt=AbstractPlus
Not in our library
194.
Bolliger MF et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21262840?dopt=AbstractPlus
Not in our library
195.
Bologa CG et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16520733?dopt=AbstractPlus
Not in our library
196.
Bolognini D et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27385588?dopt=AbstractPlus
Not in our library
197.
Bonaventure P et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22570363?dopt=AbstractPlus
Not in our library
198.
Bonaventure P et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14617685?dopt=AbstractPlus
Not in our library
199.
Bonhaus DW et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9225293?dopt=AbstractPlus
Not in our library
200.
Bonhaus DW et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10455251?dopt=AbstractPlus
Not in our library
201.
Bonhaus DW et al (1977 ) https://www.ncbi.nlm.nih.gov/pubmed/9225287?dopt=AbstractPlus
Not in our library
202.
Bonnefous C et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15686941?dopt=AbstractPlus
Not in our library
203.
Bonnefous C et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16046122?dopt=AbstractPlus
Not in our library
204.
Booth RG et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12065734?dopt=AbstractPlus
Not in our library
205.
Borowsky B et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11459929?dopt=AbstractPlus
Not in our library
206.
Borowsky B et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12118247?dopt=AbstractPlus
Not in our library
207.
Borowsky B et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9880084?dopt=AbstractPlus
Not in our library
208.
Borrmann T et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19569717?dopt=AbstractPlus
Not in our library
209.
Bosch MP et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15267242?dopt=AbstractPlus
Not in our library
210.
Bosnyak S et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21542804?dopt=AbstractPlus
Not in our library
211.
Botto JM et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9001400?dopt=AbstractPlus
Not in our library
212.
Boulanger L et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11814616?dopt=AbstractPlus
Not in our library
213.
Boulenguez P et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1738002?dopt=AbstractPlus
Not in our library
214.
Bourguignon-Bellefroid C et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1546952?dopt=AbstractPlus
Not in our library
215.
Bowery NG et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12037141?dopt=AbstractPlus
Not in our library
216.
Bowery NG et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10604925?dopt=AbstractPlus
Not in our library
217.
Bowles NP et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25535367?dopt=AbstractPlus
Not in our library
218.
Boyce M et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22607579?dopt=AbstractPlus
Not in our library
219.
Boyden SE et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26841242?dopt=AbstractPlus
Not in our library
220.
Boyer JL et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8913364?dopt=AbstractPlus
Not in our library
221.
Brabet I et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8532171?dopt=AbstractPlus
Not in our library
222.
Bradaia A et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19892733?dopt=AbstractPlus
Not in our library
223.
Bradshaw CG et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8027981?dopt=AbstractPlus
Not in our library
224.
Brady AE et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18772318?dopt=AbstractPlus
Not in our library
225.
Brambilla R et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10731034?dopt=AbstractPlus
Not in our library
226.
Brame AL et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25712721?dopt=AbstractPlus
Not in our library
227.
Branchek T et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2233697?dopt=AbstractPlus
Not in our library
228.
Breivogel CS et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9316881?dopt=AbstractPlus
Not in our library
229.
Brenchat A et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19118950?dopt=AbstractPlus
Not in our library
230.
Brennan et al (2007 ) Patent number: US2007/0074299.
Not in our library
231.
Breton C et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11337500?dopt=AbstractPlus
Not in our library
232.
Breu V et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8612786?dopt=AbstractPlus
Not in our library
233.
Brezillon S et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12401809?dopt=AbstractPlus
Not in our library
234.
Briddon SJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15070776?dopt=AbstractPlus
Not in our library
235.
Brighton PJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15331768?dopt=AbstractPlus
Not in our library
236.
Brink C et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15001665?dopt=AbstractPlus
Not in our library
237.
Brinkmann V et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11967257?dopt=AbstractPlus
Not in our library
238.
Briscoe CP et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16702987?dopt=AbstractPlus
Not in our library
239.
Briscoe CP et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12496284?dopt=AbstractPlus
Not in our library
240.
Brkovic A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12807997?dopt=AbstractPlus
Not in our library
241.
Broad J et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23190027?dopt=AbstractPlus
Not in our library
242.
Broad LM et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/30276808?dopt=AbstractPlus
Not in our library
243.
Broadhead GK et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21187282?dopt=AbstractPlus
Not in our library
244.
Brodbeck RM et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18753409?dopt=AbstractPlus
Not in our library
245.
Brodfuehrer J et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24190631?dopt=AbstractPlus
Not in our library
246.
Brodkin J et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12473093?dopt=AbstractPlus
Not in our library
247.
Bromidge SM et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9925723?dopt=AbstractPlus
Not in our library
248.
Bromidge SM et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11140733?dopt=AbstractPlus
Not in our library
249.
Brown AJ et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12496283?dopt=AbstractPlus
Not in our library
250.
Brown AM et al (1998 ) Br J Pharmacol 123: 233
Not in our library
251.
Brown AM et al (1993 ) Br J Pharmacol 110: 10
Not in our library
252.
Brown EM et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8255296?dopt=AbstractPlus
Not in our library
253.
Brown K et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28570277?dopt=AbstractPlus
Not in our library
254.
Browning C et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10696085?dopt=AbstractPlus
Not in our library
255.
Bruchas MR et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17702750?dopt=AbstractPlus
Not in our library
256.
Bruinvels AT et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8361548?dopt=AbstractPlus
Not in our library
257.
Bruns C et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8769372?dopt=AbstractPlus
Not in our library
258.
Bruns RF et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2174510?dopt=AbstractPlus
Not in our library
259.
Brunschweiger A et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16475938?dopt=AbstractPlus
Not in our library
260.
Bruzzone F et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17534937?dopt=AbstractPlus
Not in our library
261.
Bryant HU et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8845011?dopt=AbstractPlus
Not in our library
262.
Bryja V et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17426148?dopt=AbstractPlus
Not in our library
263.
Bryja V et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18953287?dopt=AbstractPlus
Not in our library
264.
Bräuner-Osborne H et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8759641?dopt=AbstractPlus
Not in our library
265.
Buckley NJ et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2704370?dopt=AbstractPlus
Not in our library
266.
Bunzow JR et al (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/2974511?dopt=AbstractPlus
Not in our library
267.
Burford NT et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23754417?dopt=AbstractPlus
Not in our library
268.
Burford NT et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25901762?dopt=AbstractPlus
Not in our library
269.
Burgaud JL et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9434758?dopt=AbstractPlus
Not in our library
270.
Burmakina S et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24778228?dopt=AbstractPlus
Not in our library
271.
Burnstock G et al (2012 ) Purinergic signalling and the nervous system. Springer: 1-715
Not in our library
272.
Burris KD et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7576010?dopt=AbstractPlus
Not in our library
273.
Burstein ES et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16135699?dopt=AbstractPlus
Not in our library
274.
Buvinic S et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12110609?dopt=AbstractPlus
Not in our library
275.
Buzard DJ et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25516790?dopt=AbstractPlus
Not in our library
276.
Bylund DB et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1353247?dopt=AbstractPlus
Not in our library
277.
Bylund DB et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7938162?dopt=AbstractPlus
Not in our library
278.
Byrne EFX et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27437577?dopt=AbstractPlus
Not in our library
279.
Bäck M et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21771892?dopt=AbstractPlus
Not in our library
280.
Bäck M et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24588652?dopt=AbstractPlus
Not in our library
281.
Béguin C. (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15869877?dopt=AbstractPlus
Not in our library
282.
Bélanger S et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19111586?dopt=AbstractPlus
Not in our library
283.
Béraud-Dufour S et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19891061?dopt=AbstractPlus
Not in our library
284.
Búzás B et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1313131?dopt=AbstractPlus
Not in our library
285.
Büllesbach EE et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15708846?dopt=AbstractPlus
Not in our library
286.
Büscher R et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16495779?dopt=AbstractPlus
Not in our library
287.
Cabrele C et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12069595?dopt=AbstractPlus
Not in our library
288.
Cahalan SM et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21445057?dopt=AbstractPlus
Not in our library
289.
Cai R et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24373935?dopt=AbstractPlus
Not in our library
290.
Cai TQ et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18952058?dopt=AbstractPlus
Not in our library
291.
Cain SA et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11773063?dopt=AbstractPlus
Not in our library
292.
Calderon SN et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8035418?dopt=AbstractPlus
Not in our library
293.
Callander GE et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24376396?dopt=AbstractPlus
Not in our library
294.
Calo G et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12010780?dopt=AbstractPlus
Not in our library
295.
Campion KL et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25556167?dopt=AbstractPlus
Not in our library
296.
Canals M et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22086918?dopt=AbstractPlus
Not in our library
297.
Candelore MR et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10411574?dopt=AbstractPlus
Not in our library
298.
Capodanno D et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23809135?dopt=AbstractPlus
Not in our library
299.
Cappelli A et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23466604?dopt=AbstractPlus
Not in our library
300.
Cappelli A et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15115399?dopt=AbstractPlus
Not in our library
301.
Capra V et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9504401?dopt=AbstractPlus
Not in our library
302.
Capra V et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25839425?dopt=AbstractPlus
Not in our library
303.
Capra V et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9547367?dopt=AbstractPlus
Not in our library
304.
Carmeci C et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9367686?dopt=AbstractPlus
Not in our library
305.
Carmon KS et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21693646?dopt=AbstractPlus
Not in our library
306.
Carnini C et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21753081?dopt=AbstractPlus
Not in our library
307.
Carpenter B et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27462812?dopt=AbstractPlus
Not in our library
308.
Carr JC et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/23158174?dopt=AbstractPlus
Not in our library
309.
Carroll FY et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11306677?dopt=AbstractPlus
Not in our library
310.
Carroll WA et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11354357?dopt=AbstractPlus
Not in our library
311.
Carter RL et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19759354?dopt=AbstractPlus
Not in our library
312.
Cascieri MA et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10085108?dopt=AbstractPlus
Not in our library
313.
Castro SW et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8646408?dopt=AbstractPlus
Not in our library
314.
Catalioto RM et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9484857?dopt=AbstractPlus
Not in our library
315.
Catalán V et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17371481?dopt=AbstractPlus
Not in our library
316.
Cattaneo M et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15476670?dopt=AbstractPlus
Not in our library
317.
Cattaneo M et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12578987?dopt=AbstractPlus
Not in our library
318.
Caulfield MP et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9647869?dopt=AbstractPlus
Not in our library
319.
Caunt CJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15059960?dopt=AbstractPlus
Not in our library
320.
Caunt CJ et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22808094?dopt=AbstractPlus
Not in our library
321.
Cavallari U et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17803810?dopt=AbstractPlus
Not in our library
322.
Cavanaugh DJ et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19451647?dopt=AbstractPlus
Not in our library
323.
Cayabyab M et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11090199?dopt=AbstractPlus
Not in our library
324.
Cembala TM et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9846649?dopt=AbstractPlus
Not in our library
325.
Cencetti F et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23913862?dopt=AbstractPlus
Not in our library
326.
Cescato R et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18543899?dopt=AbstractPlus
Not in our library
327.
Chackalamannil S et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18447380?dopt=AbstractPlus
Not in our library
328.
Chagnon YC et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9392003?dopt=AbstractPlus
Not in our library
329.
Chaki S et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15677346?dopt=AbstractPlus
Not in our library
330.
Chaki S et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10357258?dopt=AbstractPlus
Not in our library
331.
Chambers JK et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10753868?dopt=AbstractPlus
Not in our library
332.
Chan SD et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1334084?dopt=AbstractPlus
Not in our library
333.
Chan WY et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18678919?dopt=AbstractPlus
Not in our library
334.
Chandrashekar J et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10761935?dopt=AbstractPlus
Not in our library
335.
Chang DJ et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9490024?dopt=AbstractPlus
Not in our library
336.
Chang KJ et al (1983 ) https://www.ncbi.nlm.nih.gov/pubmed/6313901?dopt=AbstractPlus
Not in our library
337.
Chang RS et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2314387?dopt=AbstractPlus
Not in our library
338.
Chang RS et al (1986 ) https://www.ncbi.nlm.nih.gov/pubmed/3018478?dopt=AbstractPlus
Not in our library
339.
Chang W et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18765830?dopt=AbstractPlus
Not in our library
340.
Chang W et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17591780?dopt=AbstractPlus
Not in our library
341.
Chansel D et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8282008?dopt=AbstractPlus
Not in our library
342.
Chao TH et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10092660?dopt=AbstractPlus
Not in our library
343.
Chartrel N et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14657341?dopt=AbstractPlus
Not in our library
344.
Chatenet D et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17125276?dopt=AbstractPlus
Not in our library
345.
Chavkin C et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14718611?dopt=AbstractPlus
Not in our library
346.
Chen C et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8893829?dopt=AbstractPlus
Not in our library
347.
Chen H et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15163697?dopt=AbstractPlus
Not in our library
348.
Chen J et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15772293?dopt=AbstractPlus
Not in our library
349.
Chen J et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12706455?dopt=AbstractPlus
Not in our library
350.
Chen JK et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12391318?dopt=AbstractPlus
Not in our library
351.
Chen LH et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25050158?dopt=AbstractPlus
Not in our library
352.
Chen Q et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22697179?dopt=AbstractPlus
Not in our library
353.
Chen R et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/7692441?dopt=AbstractPlus
Not in our library
354.
Chen W et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12958365?dopt=AbstractPlus
Not in our library
355.
Chen YL et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18288792?dopt=AbstractPlus
Not in our library
356.
Chen Z et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15454210?dopt=AbstractPlus
Not in our library
357.
Cheng CK et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15561800?dopt=AbstractPlus
Not in our library
358.
Cheng K et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12235229?dopt=AbstractPlus
Not in our library
359.
Cheng LL et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15084136?dopt=AbstractPlus
Not in our library
360.
Cheng RKY et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28445455?dopt=AbstractPlus
Not in our library
361.
Cheng RKY et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28712806?dopt=AbstractPlus
Not in our library
362.
Cheng Z et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17615148?dopt=AbstractPlus
Not in our library
363.
Cherezov V et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17962520?dopt=AbstractPlus
Not in our library
364.
Chhatriwala M et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15345752?dopt=AbstractPlus
Not in our library
365.
Chiang N et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10748237?dopt=AbstractPlus
Not in our library
366.
Chiang N et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22538616?dopt=AbstractPlus
Not in our library
367.
Chin FT et al (2006 ) J Label Comp Radiopharm 17-31
Not in our library
368.
Chini B et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12942128?dopt=AbstractPlus
Not in our library
369.
Chini B et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7774575?dopt=AbstractPlus
Not in our library
370.
Chini B et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8955347?dopt=AbstractPlus
Not in our library
371.
Chiu AT et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2590220?dopt=AbstractPlus
Not in our library
372.
Chng SC et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24316148?dopt=AbstractPlus
Not in our library
373.
Chobanian HR et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/24900461?dopt=AbstractPlus
Not in our library
374.
Chopra M et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19389924?dopt=AbstractPlus
Not in our library
375.
Chou CC et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12381680?dopt=AbstractPlus
Not in our library
376.
Chow BK. (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7612008?dopt=AbstractPlus
Not in our library
377.
Chow BS et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24429402?dopt=AbstractPlus
Not in our library
378.
Chrencik JE et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26091040?dopt=AbstractPlus
Not in our library
379.
Christiansen E et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22724451?dopt=AbstractPlus
Not in our library
380.
Christiansen E et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23687558?dopt=AbstractPlus
Not in our library
381.
Christiansen E et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27074625?dopt=AbstractPlus
Not in our library
382.
Christiansen E et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25916176?dopt=AbstractPlus
Not in our library
383.
Christopher JA et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/29455526?dopt=AbstractPlus
Not in our library
384.
Christopoulos A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12446722?dopt=AbstractPlus
Not in our library
385.
Christopoulos A et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9614217?dopt=AbstractPlus
Not in our library
386.
Christopoulos A et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9890565?dopt=AbstractPlus
Not in our library
387.
Christopoulos A et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11578621?dopt=AbstractPlus
Not in our library
388.
Christopoulos G et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10385705?dopt=AbstractPlus
Not in our library
389.
Chu ZL et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19901198?dopt=AbstractPlus
Not in our library
390.
Chun J et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/30625282?dopt=AbstractPlus
Not in our library
391.
Chung AW et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11877318?dopt=AbstractPlus
Not in our library
392.
Chung DS et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9353394?dopt=AbstractPlus
Not in our library
393.
Chung FZ et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7476898?dopt=AbstractPlus
Not in our library
394.
Cialdai C et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16979621?dopt=AbstractPlus
Not in our library
395.
Ciana P et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16990797?dopt=AbstractPlus
Not in our library
396.
Cirillo R et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12660315?dopt=AbstractPlus
Not in our library
397.
Cirillo R et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17618756?dopt=AbstractPlus
Not in our library
398.
Claeysen S et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9351641?dopt=AbstractPlus
Not in our library
399.
Clark AL et al (1976 ) https://www.ncbi.nlm.nih.gov/pubmed/990587?dopt=AbstractPlus
Not in our library
400.
Clark BP et al (1997 ) Bioorg Med Chem Lett 7: 2777-2780
Not in our library
401.
Clish CB et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10393980?dopt=AbstractPlus
Not in our library
402.
Clozel M et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15146030?dopt=AbstractPlus
Not in our library
403.
Clozel M et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8035319?dopt=AbstractPlus
Not in our library
404.
Cogé F et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11284713?dopt=AbstractPlus
Not in our library
405.
Cohen JA et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21520239?dopt=AbstractPlus
Not in our library
406.
Combadiere C et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8530354?dopt=AbstractPlus
Not in our library
407.
Commery TA. (2010 ) Alzheimer's & Dementia 6: S548-S549
Not in our library
408.
Communi D et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10578132?dopt=AbstractPlus
Not in our library
409.
Comps-Agrar L et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21552208?dopt=AbstractPlus
Not in our library
410.
Congreve M et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22220592?dopt=AbstractPlus
Not in our library
411.
Conigrave AD et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10781086?dopt=AbstractPlus
Not in our library
412.
Conn PM et al (1982 ) https://www.ncbi.nlm.nih.gov/pubmed/6282571?dopt=AbstractPlus
Not in our library
413.
Conroy JL et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25660762?dopt=AbstractPlus
Not in our library
414.
Cook AE et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25220431?dopt=AbstractPlus
Not in our library
415.
Cooray SN et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24108355?dopt=AbstractPlus
Not in our library
416.
Corbett DF et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16002289?dopt=AbstractPlus
Not in our library
417.
Costantino G et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11249114?dopt=AbstractPlus
Not in our library
418.
Costes N et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16330560?dopt=AbstractPlus
Not in our library
419.
Cotte N et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10866830?dopt=AbstractPlus
Not in our library
420.
Cotte N et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9792651?dopt=AbstractPlus
Not in our library
421.
Cottingham C et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21859713?dopt=AbstractPlus
Not in our library
422.
Coulie B et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11461914?dopt=AbstractPlus
Not in our library
423.
Coulin F et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9346309?dopt=AbstractPlus
Not in our library
424.
Coulouarn Y et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10486557?dopt=AbstractPlus
Not in our library
425.
Coulouarn Y et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9861051?dopt=AbstractPlus
Not in our library
426.
Coulthard LG et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30449309?dopt=AbstractPlus
Not in our library
427.
Covic L et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12357249?dopt=AbstractPlus
Not in our library
428.
Cox BM et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/24528283?dopt=AbstractPlus
Not in our library
429.
Cox CD et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20565075?dopt=AbstractPlus
Not in our library
430.
Cox HM et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8590988?dopt=AbstractPlus
Not in our library
431.
Coy DH et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8993400?dopt=AbstractPlus
Not in our library
432.
Criscione L et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8242249?dopt=AbstractPlus
Not in our library
433.
Croker DE et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24060963?dopt=AbstractPlus
Not in our library
434.
Croker DE et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27108698?dopt=AbstractPlus
Not in our library
435.
Crombie AL et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20471258?dopt=AbstractPlus
Not in our library
436.
Croston GE et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12408704?dopt=AbstractPlus
Not in our library
437.
Croy CH et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24807965?dopt=AbstractPlus
Not in our library
438.
Cunha RA et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8692280?dopt=AbstractPlus
Not in our library
439.
Curtis AE et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19934405?dopt=AbstractPlus
Not in our library
440.
D’Amato M et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17854592?dopt=AbstractPlus
Not in our library
441.
Dairaghi DJ et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10419462?dopt=AbstractPlus
Not in our library
442.
Dalpiaz A et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9827575?dopt=AbstractPlus
Not in our library
443.
Daniels DV et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10334511?dopt=AbstractPlus
Not in our library
444.
Dardonville C et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15224384?dopt=AbstractPlus
Not in our library
445.
Darker JG et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11266181?dopt=AbstractPlus
Not in our library
446.
Das A et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19902968?dopt=AbstractPlus
Not in our library
447.
Das S et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21245295?dopt=AbstractPlus
Not in our library
448.
Dass NB et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14504130?dopt=AbstractPlus
Not in our library
449.
Daugherty BL et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8642344?dopt=AbstractPlus
Not in our library
450.
Dautzenberg FM et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9326293?dopt=AbstractPlus
Not in our library
451.
Dautzenberg FM et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15450949?dopt=AbstractPlus
Not in our library
452.
Dautzenberg FM et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10583729?dopt=AbstractPlus
Not in our library
453.
Dautzenberg FM et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11123370?dopt=AbstractPlus
Not in our library
454.
Davenport AP. (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12037137?dopt=AbstractPlus
Not in our library
455.
Davenport AP et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23686350?dopt=AbstractPlus
Not in our library
456.
Davenport AP et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16382107?dopt=AbstractPlus
Not in our library
457.
Davenport AP et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9489609?dopt=AbstractPlus
Not in our library
458.
Davenport AP et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8012722?dopt=AbstractPlus
Not in our library
459.
Davey AE et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22210744?dopt=AbstractPlus
Not in our library
460.
Davis MD et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15590668?dopt=AbstractPlus
Not in our library
461.
Davis TL et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10952683?dopt=AbstractPlus
Not in our library
462.
Davoren JE et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27275946?dopt=AbstractPlus
Not in our library
463.
Dawson LA et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19499624?dopt=AbstractPlus
Not in our library
464.
De Backer MD et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9794809?dopt=AbstractPlus
Not in our library
465.
de Gasparo M et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10977869?dopt=AbstractPlus
Not in our library
466.
de Gasparo M et al (1994 ) In Medicinal Chemistry of the Renin-Angiotensin System. Edited by Timmermanns PBMWM, Wexler RR: Elsevier: 269-294 [ISBN: 0444820531]
Not in our library
467.
de Lau W et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21727895?dopt=AbstractPlus
Not in our library
468.
De Lecea L et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8622767?dopt=AbstractPlus
Not in our library
469.
de Ligt RA et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15740718?dopt=AbstractPlus
Not in our library
470.
de Paulis T et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16722652?dopt=AbstractPlus
Not in our library
471.
De Ponti F et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8730727?dopt=AbstractPlus
Not in our library
472.
De Toni L et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/30625346?dopt=AbstractPlus
Not in our library
473.
De Vry J et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9495870?dopt=AbstractPlus
Not in our library
474.
de Wied D et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8258377?dopt=AbstractPlus
Not in our library
475.
de Ávila C et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/28864207?dopt=AbstractPlus
Not in our library
476.
Deal MJ et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1331460?dopt=AbstractPlus
Not in our library
477.
DeAlmeida VI et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17545618?dopt=AbstractPlus
Not in our library
478.
Dearry A et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2144334?dopt=AbstractPlus
Not in our library
479.
Del Borgo MP et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16547350?dopt=AbstractPlus
Not in our library
480.
Delahaye R et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9484907?dopt=AbstractPlus
Not in our library
481.
Demberg LM et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26188515?dopt=AbstractPlus
Not in our library10.1016/j.bbrc.2015.07.020
482.
Demberg LM et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28154189?dopt=AbstractPlus
Not in our library
483.
Deng C et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25995451?dopt=AbstractPlus
Not in our library
484.
Dennis MK et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19430488?dopt=AbstractPlus
Not in our library
485.
Dennis MK et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21782022?dopt=AbstractPlus
Not in our library
486.
Derick S et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12446593?dopt=AbstractPlus
Not in our library
487.
Devedjian JC et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7908642?dopt=AbstractPlus
Not in our library
488.
Dhawan BN et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8981566?dopt=AbstractPlus
Not in our library
489.
Di Marzo V et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11181068?dopt=AbstractPlus
Not in our library
490.
Di Pardo A et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29688337?dopt=AbstractPlus
Not in our library
491.
Di Salvo J et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11104827?dopt=AbstractPlus
Not in our library
492.
Diallo M et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18082287?dopt=AbstractPlus
Not in our library
493.
Dickson L et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16930633?dopt=AbstractPlus
Not in our library
494.
Dietis N et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22194444?dopt=AbstractPlus
Not in our library
495.
Dietis N et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29524334?dopt=AbstractPlus
Not in our library
496.
Dijksterhuis JP et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24032637?dopt=AbstractPlus
Not in our library
497.
Dijkstra D et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12086487?dopt=AbstractPlus
Not in our library
498.
Dillon JS et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8404634?dopt=AbstractPlus
Not in our library
499.
Dinter J et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25706283?dopt=AbstractPlus
Not in our library
500.
Dionisotti S et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9179373?dopt=AbstractPlus
Not in our library
501.
Disse B et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8441333?dopt=AbstractPlus
Not in our library
502.
Divorty N et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25805994?dopt=AbstractPlus
Not in our library
503.
Doan ND et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22044114?dopt=AbstractPlus
Not in our library
504.
Dodé C et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23596439?dopt=AbstractPlus
Not in our library
505.
Dolan JA et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7912272?dopt=AbstractPlus
Not in our library
506.
Domenech T et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9303569?dopt=AbstractPlus
Not in our library
507.
Domschke K et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/20603625?dopt=AbstractPlus
Not in our library
508.
Donaldson CJ et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8612563?dopt=AbstractPlus
Not in our library
509.
Donaldson LF et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8947459?dopt=AbstractPlus
Not in our library
510.
Donner J et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20705147?dopt=AbstractPlus
Not in our library
511.
Doods H et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10611450?dopt=AbstractPlus
Not in our library
512.
Doods H et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10711339?dopt=AbstractPlus
Not in our library
513.
Doods HN et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7562541?dopt=AbstractPlus
Not in our library
514.
Dooley CT et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9353393?dopt=AbstractPlus
Not in our library
515.
Doré AS et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25042998?dopt=AbstractPlus
Not in our library
516.
Douglas SA Ohlstein EH. (2000 ) Urotensinreceptors In The IUPHAR Receptor Compendium of Receptor Characterization and Classification. Edited by Girdlestone D: IUPHAR Media Ltd: 365-372
Not in our library
517.
Douglas SA et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15852036?dopt=AbstractPlus
Not in our library
518.
Doumazane E et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/20826542?dopt=AbstractPlus
Not in our library
519.
Dowling MR et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16847442?dopt=AbstractPlus
Not in our library
520.
Drake MT et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18086673?dopt=AbstractPlus
Not in our library
521.
Draper-Joyce CJ et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29925945?dopt=AbstractPlus
Not in our library
522.
Drummond AH et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2566295?dopt=AbstractPlus
Not in our library
523.
Dubessy C et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18710417?dopt=AbstractPlus
Not in our library
524.
Dubocovich ML. (1985 ) https://www.ncbi.nlm.nih.gov/pubmed/2991499?dopt=AbstractPlus
Not in our library
525.
Dubocovich ML et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20605968?dopt=AbstractPlus
Not in our library
526.
Dubocovich ML et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9089668?dopt=AbstractPlus
Not in our library
527.
Dubocovich ML et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9737724?dopt=AbstractPlus
Not in our library
528.
Dudley DT et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2402226?dopt=AbstractPlus
Not in our library
529.
Dudley DT et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8469774?dopt=AbstractPlus
Not in our library
530.
Dufourny L et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18400093?dopt=AbstractPlus
Not in our library
531.
Duggal P et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12761559?dopt=AbstractPlus
Not in our library
532.
Dumont Y et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15337369?dopt=AbstractPlus
Not in our library
533.
Dunlop J et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15705738?dopt=AbstractPlus
Not in our library
534.
Dupuis DS et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16966477?dopt=AbstractPlus
Not in our library
535.
Dwyer MP et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17181143?dopt=AbstractPlus
Not in our library
536.
Díaz-González F et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17170051?dopt=AbstractPlus
Not in our library
537.
Dörje F et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1994002?dopt=AbstractPlus
Not in our library
538.
Eason MG et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7559592?dopt=AbstractPlus
Not in our library
539.
Eckle T et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17353435?dopt=AbstractPlus
Not in our library
540.
Edgar AJ. (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17454009?dopt=AbstractPlus
Not in our library
541.
Edinger AL et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9405683?dopt=AbstractPlus
Not in our library
542.
Edson MA et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19887567?dopt=AbstractPlus
Not in our library
543.
Edwards RM et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1309870?dopt=AbstractPlus
Not in our library
544.
Egan C et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10611640?dopt=AbstractPlus
Not in our library
545.
Eggerickx D et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7639700?dopt=AbstractPlus
Not in our library
546.
Eison AS et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8246675?dopt=AbstractPlus
Not in our library
547.
El Messari S et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15341513?dopt=AbstractPlus
Not in our library
548.
El-Tayeb A et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16213725?dopt=AbstractPlus
Not in our library
549.
El-Tayeb A et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17125260?dopt=AbstractPlus
Not in our library
550.
El-Tayeb A et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21417463?dopt=AbstractPlus
Not in our library
551.
Elands J et al (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/2827511?dopt=AbstractPlus
Not in our library
552.
Ellacott KL et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15752583?dopt=AbstractPlus
Not in our library
553.
Elliott JD et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8201588?dopt=AbstractPlus
Not in our library
554.
Elshourbagy NA et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11976263?dopt=AbstractPlus
Not in our library
555.
Emonds-Alt X et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7830490?dopt=AbstractPlus
Not in our library
556.
Emonds-Alt X et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/7682062?dopt=AbstractPlus
Not in our library
557.
Emson PC. (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17499108?dopt=AbstractPlus
Not in our library
558.
Engel KM et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/22216272?dopt=AbstractPlus
Not in our library
559.
Engers DW et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19469556?dopt=AbstractPlus
Not in our library
560.
Engers JL et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26335039?dopt=AbstractPlus
Not in our library
561.
Engstrom M et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12606605?dopt=AbstractPlus
Not in our library
562.
Engstrom M et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15333679?dopt=AbstractPlus
Not in our library
563.
Enna SJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15451397?dopt=AbstractPlus
Not in our library
564.
Ennis MD et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9632349?dopt=AbstractPlus
Not in our library
565.
Erchegyi J et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15658864?dopt=AbstractPlus
Not in our library
566.
Eriksson H et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9802391?dopt=AbstractPlus
Not in our library
567.
Erlinge D. (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21586366?dopt=AbstractPlus
Not in our library
568.
Erspamer V et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2544892?dopt=AbstractPlus
Not in our library
569.
Esbenshade TA et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15294456?dopt=AbstractPlus
Not in our library
570.
Esbenshade TA et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12606603?dopt=AbstractPlus
Not in our library
571.
Escribano A et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9871538?dopt=AbstractPlus
Not in our library
572.
Espinoza S et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21670104?dopt=AbstractPlus
Not in our library
573.
Eubelen M et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30026314?dopt=AbstractPlus
Not in our library
574.
Evangelou E et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21068099?dopt=AbstractPlus
Not in our library
575.
Evans BA et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/20978120?dopt=AbstractPlus
Not in our library
576.
Evans BA et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10455305?dopt=AbstractPlus
Not in our library
577.
Evans BA et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20132209?dopt=AbstractPlus
Not in our library
578.
Evans BN et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10903324?dopt=AbstractPlus
Not in our library
579.
Evans HF et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1714839?dopt=AbstractPlus
Not in our library
580.
Eveleigh P et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2704371?dopt=AbstractPlus
Not in our library
581.
Faedo S et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22796453?dopt=AbstractPlus
Not in our library
582.
Failli AA et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16297621?dopt=AbstractPlus
Not in our library
583.
Fan H et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25176008?dopt=AbstractPlus
Not in our library
584.
Fan X et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12939143?dopt=AbstractPlus
Not in our library
585.
Farb TB et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28938487?dopt=AbstractPlus
Not in our library
586.
Farooqi IS et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18779842?dopt=AbstractPlus
Not in our library
587.
Faust R et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10737738?dopt=AbstractPlus
Not in our library
588.
Feighner SD et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10381885?dopt=AbstractPlus
Not in our library
589.
Felder CC et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9435190?dopt=AbstractPlus
Not in our library
590.
Felder CC et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7565624?dopt=AbstractPlus
Not in our library
591.
Feng YH et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7759541?dopt=AbstractPlus
Not in our library
592.
Feoktistov I et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11705449?dopt=AbstractPlus
Not in our library
593.
Fernández J et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15771415?dopt=AbstractPlus
Not in our library
594.
Fierens F et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10079018?dopt=AbstractPlus
Not in our library
595.
Filardo EJ. (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/28595943?dopt=AbstractPlus
Not in our library
596.
Filardo EJ et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11043579?dopt=AbstractPlus
Not in our library
597.
Finch AR et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20009083?dopt=AbstractPlus
Not in our library
598.
Finch AR et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19888967?dopt=AbstractPlus
Not in our library
599.
Finnerup NB et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24507378?dopt=AbstractPlus
Not in our library
600.
Fiore S et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8006586?dopt=AbstractPlus
Not in our library
601.
Fiore S et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1322894?dopt=AbstractPlus
Not in our library
602.
Fiore S et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8527441?dopt=AbstractPlus
Not in our library
603.
Fiorino F et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28943244?dopt=AbstractPlus
Not in our library
604.
Fischer DJ et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11562440?dopt=AbstractPlus
Not in our library
605.
Fischetti C et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19445927?dopt=AbstractPlus
Not in our library
606.
Fister S et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19638591?dopt=AbstractPlus
Not in our library
607.
Fitzgerald LW et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10217294?dopt=AbstractPlus
Not in our library
608.
Fitzgerald LW et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9808667?dopt=AbstractPlus
Not in our library
609.
Flacco N et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23373597?dopt=AbstractPlus
Not in our library
610.
Fong TM et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1281470?dopt=AbstractPlus
Not in our library
611.
Foord APDW et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8632751?dopt=AbstractPlus
Not in our library
612.
Foord SM et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15914470?dopt=AbstractPlus
Not in our library
613.
Forbes IT et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12392747?dopt=AbstractPlus
Not in our library
614.
Ford APDW et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9249248?dopt=AbstractPlus
Not in our library
615.
Forrest M et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14747617?dopt=AbstractPlus
Not in our library
616.
Foss FW et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17113298?dopt=AbstractPlus
Not in our library
617.
Foudi N et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21323896?dopt=AbstractPlus
Not in our library
618.
Foudi N et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18516068?dopt=AbstractPlus
Not in our library
619.
Fox JC et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25497737?dopt=AbstractPlus
Not in our library
620.
Franchetti P et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19317449?dopt=AbstractPlus
Not in our library
621.
Francis BE et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8287060?dopt=AbstractPlus
Not in our library
622.
Fraser GL. (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18719021?dopt=AbstractPlus
Not in our library
623.
Fraser NJ et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10347248?dopt=AbstractPlus
Not in our library
624.
Fredholm BB et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11734617?dopt=AbstractPlus
Not in our library
625.
Fredman G et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20702811?dopt=AbstractPlus
Not in our library
626.
Fredriksson R et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12761335?dopt=AbstractPlus
Not in our library
627.
Free RB et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24755247?dopt=AbstractPlus
Not in our library
628.
Freedman SB et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8301582?dopt=AbstractPlus
Not in our library
629.
Freer RJ et al (1982 ) https://www.ncbi.nlm.nih.gov/pubmed/6280748?dopt=AbstractPlus
Not in our library
630.
Freer RJ et al (1980 ) https://www.ncbi.nlm.nih.gov/pubmed/7387981?dopt=AbstractPlus
Not in our library
631.
Fricker AC et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19285517?dopt=AbstractPlus
Not in our library
632.
Fricks IP et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18252808?dopt=AbstractPlus
Not in our library
633.
Frielle T et al (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/2849109?dopt=AbstractPlus
Not in our library
634.
Froestl W. (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21428811?dopt=AbstractPlus
Not in our library
635.
Froestl W et al (1997 ) In The GABA Receptors Edited by Enna SJ, Bowery NG: Humana Press: 271-296 [ISBN: 0896034585]
Not in our library
636.
Fruchart-Gaillard C et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16439611?dopt=AbstractPlus
Not in our library
637.
Fuchs AR et al (1982 ) https://www.ncbi.nlm.nih.gov/pubmed/6278592?dopt=AbstractPlus
Not in our library
638.
Fujii R et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12118011?dopt=AbstractPlus
Not in our library
639.
Fukukawa C et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18271942?dopt=AbstractPlus
Not in our library
640.
Fukunaga K et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11560941?dopt=AbstractPlus
Not in our library
641.
Fukusumi S et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12960173?dopt=AbstractPlus
Not in our library
642.
Furman CA et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25583363?dopt=AbstractPlus
Not in our library
643.
Gado F et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/29990428?dopt=AbstractPlus
Not in our library
644.
Galandrin S et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16901982?dopt=AbstractPlus
Not in our library
645.
Galandrin S et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18403719?dopt=AbstractPlus
Not in our library
646.
Galemmo RA Jr et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2170649?dopt=AbstractPlus
Not in our library
647.
Gallo-Rodriguez C et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8126704?dopt=AbstractPlus
Not in our library
648.
Gallwitz B et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8795084?dopt=AbstractPlus
Not in our library
649.
Galvani S et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26268607?dopt=AbstractPlus
Not in our library
650.
Galvez T et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10692480?dopt=AbstractPlus
Not in our library
651.
Gama L et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11489900?dopt=AbstractPlus
Not in our library
652.
Ganella DE et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23135160?dopt=AbstractPlus
Not in our library
653.
Ganella DE et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22854307?dopt=AbstractPlus
Not in our library
654.
Ganesh T et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23914286?dopt=AbstractPlus
Not in our library
655.
Gao H et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15784721?dopt=AbstractPlus
Not in our library
656.
Gao ZG et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10927024?dopt=AbstractPlus
Not in our library
657.
Gao ZG et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15193995?dopt=AbstractPlus
Not in our library
658.
Gao ZG et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15476669?dopt=AbstractPlus
Not in our library
659.
Gardell LR et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17519387?dopt=AbstractPlus
Not in our library
660.
Gardella TJ et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8702701?dopt=AbstractPlus
Not in our library
661.
Gardella TJ et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7896796?dopt=AbstractPlus
Not in our library
662.
Gardella TJ et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25713287?dopt=AbstractPlus
Not in our library
663.
Gareau Y et al (1996 ) Bioorg Med Chem Lett 6: 189-194
Not in our library
664.
Garin A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14607932?dopt=AbstractPlus
Not in our library
665.
Gasparini F et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11814808?dopt=AbstractPlus
Not in our library
666.
Gasparini F et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10336568?dopt=AbstractPlus
Not in our library
667.
Gasparini F et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10530811?dopt=AbstractPlus
Not in our library
668.
Gasser A. (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25831128?dopt=AbstractPlus
Not in our library
669.
Gassmann M et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15240800?dopt=AbstractPlus
Not in our library
670.
Gaster LM et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9548813?dopt=AbstractPlus
Not in our library
671.
Gates E. (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9735753?dopt=AbstractPlus
Not in our library
672.
Gault VA et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12627321?dopt=AbstractPlus
Not in our library
673.
Gavrilyuk V et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15715664?dopt=AbstractPlus
Not in our library
674.
Gbahou F et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16432504?dopt=AbstractPlus
Not in our library
675.
Ge X et al (2018 ) Cell Metabolism https://www.ncbi.nlm.nih.gov/pubmed/29233536?dopt=AbstractPlus
Not in our library
676.
Gee CE et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24596089?dopt=AbstractPlus
Not in our library
677.
Gehlert DR et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8632753?dopt=AbstractPlus
Not in our library
678.
Gembardt F et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18636314?dopt=AbstractPlus
Not in our library
679.
Generoso SF et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25751279?dopt=AbstractPlus
Not in our library
680.
Genet C et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19911773?dopt=AbstractPlus
Not in our library
681.
Geng Y et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24305054?dopt=AbstractPlus
Not in our library
682.
Geng Y et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27434672?dopt=AbstractPlus
Not in our library
683.
Geng Y et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22660477?dopt=AbstractPlus
Not in our library
684.
Gentry PR et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24692176?dopt=AbstractPlus
Not in our library
685.
Gentry PR et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24164599?dopt=AbstractPlus
Not in our library
686.
Gentry PR et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25147929?dopt=AbstractPlus
Not in our library
687.
Georgsson J et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24937104?dopt=AbstractPlus
Not in our library
688.
Georgsson J et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25875054?dopt=AbstractPlus
Not in our library
689.
Gera L et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16368899?dopt=AbstractPlus
Not in our library
690.
Gerald C et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7796807?dopt=AbstractPlus
Not in our library
691.
Gerald C et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8700207?dopt=AbstractPlus
Not in our library
692.
Gerald C et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7592910?dopt=AbstractPlus
Not in our library
693.
Gerbino A et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16247029?dopt=AbstractPlus
Not in our library
694.
Gergely P et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22646698?dopt=AbstractPlus
Not in our library
695.
Gershon MD. (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10429737?dopt=AbstractPlus
Not in our library
696.
Geubelle P et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28160606?dopt=AbstractPlus
Not in our library
697.
Ghoneim OM et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16782354?dopt=AbstractPlus
Not in our library
698.
Giagulli C et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22262769?dopt=AbstractPlus
Not in our library
699.
Giannotti D et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11063600?dopt=AbstractPlus
Not in our library
700.
Giardina GA et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8691422?dopt=AbstractPlus
Not in our library
701.
Giles H et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2924081?dopt=AbstractPlus
Not in our library
702.
Gilet M et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25316608?dopt=AbstractPlus
Not in our library
703.
Gilissen J et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26386312?dopt=AbstractPlus
Not in our library
704.
Gillberg PG et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9671109?dopt=AbstractPlus
Not in our library
705.
Gingell JJ et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24169554?dopt=AbstractPlus
Not in our library
706.
Ginsburg-Shmuel T et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22901672?dopt=AbstractPlus
Not in our library
707.
Gironacci MM et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21670420?dopt=AbstractPlus
Not in our library
708.
Gladue RP et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12909630?dopt=AbstractPlus
Not in our library
709.
Glaenzel U et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29735753?dopt=AbstractPlus
Not in our library
710.
Glennon RA. (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12825922?dopt=AbstractPlus
Not in our library
711.
Glennon RA et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10715164?dopt=AbstractPlus
Not in our library
712.
Glukhova A et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28235198?dopt=AbstractPlus
Not in our library
713.
Gobeil F et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8901831?dopt=AbstractPlus
Not in our library
714.
Gobeil F et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8735629?dopt=AbstractPlus
Not in our library
715.
Gobeil Jr F et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24361511?dopt=AbstractPlus
Not in our library
716.
Goldring WP et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15922596?dopt=AbstractPlus
Not in our library
717.
Goldstein A et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2549383?dopt=AbstractPlus
Not in our library
718.
Gomes I et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24043826?dopt=AbstractPlus
Not in our library
719.
Gomes I et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27117253?dopt=AbstractPlus
Not in our library
720.
Gong X et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9115216?dopt=AbstractPlus
Not in our library
721.
Gonzalez-Cabrera PJ et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18708635?dopt=AbstractPlus
Not in our library
722.
González N et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19463875?dopt=AbstractPlus
Not in our library
723.
González N et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26066663?dopt=AbstractPlus
Not in our library
724.
Goodfellow NM et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22539842?dopt=AbstractPlus
Not in our library
725.
Goold CP et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11602681?dopt=AbstractPlus
Not in our library
726.
Gorojankina T et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23448715?dopt=AbstractPlus
Not in our library
727.
Gottlieb DJ et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17903308?dopt=AbstractPlus
Not in our library
728.
Gouardères C et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17011599?dopt=AbstractPlus
Not in our library
729.
Gouardères C et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12421602?dopt=AbstractPlus
Not in our library
730.
Gouardères C et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17337079?dopt=AbstractPlus
Not in our library
731.
Goudet C et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22223752?dopt=AbstractPlus
Not in our library
732.
Gougat J et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14747609?dopt=AbstractPlus
Not in our library
733.
Gouldson P et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10988332?dopt=AbstractPlus
Not in our library
734.
Gourlet P et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9437716?dopt=AbstractPlus
Not in our library
735.
Gourlet P et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9145428?dopt=AbstractPlus
Not in our library
736.
Graaf Cd et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27630114?dopt=AbstractPlus
Not in our library
737.
Grailhe R et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11343685?dopt=AbstractPlus
Not in our library
738.
Granas C et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10513577?dopt=AbstractPlus
Not in our library
739.
Grant GE et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19450703?dopt=AbstractPlus
Not in our library
740.
Grant MK et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16002459?dopt=AbstractPlus
Not in our library
741.
Gravel S et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20956518?dopt=AbstractPlus
Not in our library
742.
Greaves DR et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9294138?dopt=AbstractPlus
Not in our library
743.
Gregor P et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8641440?dopt=AbstractPlus
Not in our library
744.
Gregori-Puigjané E et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22711801?dopt=AbstractPlus
Not in our library
745.
Grieco P et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11150170?dopt=AbstractPlus
Not in our library
746.
Grieco P et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17482720?dopt=AbstractPlus
Not in our library
747.
Grieco P et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12238917?dopt=AbstractPlus
Not in our library
748.
Griffante C et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16158071?dopt=AbstractPlus
Not in our library
749.
Grisshammer R et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7719707?dopt=AbstractPlus
Not in our library
750.
Gronert K et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11141472?dopt=AbstractPlus
Not in our library
751.
Grosse J et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25028498?dopt=AbstractPlus
Not in our library
752.
Grosse R et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10734055?dopt=AbstractPlus
Not in our library
753.
Groves A et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23518370?dopt=AbstractPlus
Not in our library
754.
Groves A et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30255127?dopt=AbstractPlus
Not in our library
755.
Grundt P et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17095222?dopt=AbstractPlus
Not in our library
756.
Grundt P et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17672446?dopt=AbstractPlus
Not in our library
757.
Gründker C et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12237622?dopt=AbstractPlus
Not in our library
758.
Gu ZF et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7529309?dopt=AbstractPlus
Not in our library
759.
Guan XM et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20096642?dopt=AbstractPlus
Not in our library
760.
Guard S et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/1694464?dopt=AbstractPlus
Not in our library
761.
Guerrero M et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21570287?dopt=AbstractPlus
Not in our library
762.
Guerrero M et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/23762933?dopt=AbstractPlus
Not in our library
763.
Guerrero M et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/22834040?dopt=AbstractPlus
Not in our library
764.
Guerrini R et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9191955?dopt=AbstractPlus
Not in our library
765.
Guilford WJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15056011?dopt=AbstractPlus
Not in our library
766.
Gully D et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11907190?dopt=AbstractPlus
Not in our library
767.
Gully D et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9023294?dopt=AbstractPlus
Not in our library
768.
Guo D et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22324512?dopt=AbstractPlus
Not in our library
769.
Guo Y et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21712392?dopt=AbstractPlus
Not in our library
770.
Gupte J et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22575658?dopt=AbstractPlus
Not in our library
771.
Gurney A et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22753465?dopt=AbstractPlus
Not in our library
772.
Göblyös A et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16722654?dopt=AbstractPlus
Not in our library
773.
Günther T et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30232095?dopt=AbstractPlus
Not in our library
774.
Haas M et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24970757?dopt=AbstractPlus
Not in our library
775.
Habasque C et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11994538?dopt=AbstractPlus
Not in our library
776.
Haffar BM et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1702423?dopt=AbstractPlus
Not in our library
777.
Haga K et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22278061?dopt=AbstractPlus
Not in our library
778.
Hagan RM et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8210508?dopt=AbstractPlus
Not in our library
779.
Hague C et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14718583?dopt=AbstractPlus
Not in our library
780.
Haidar M et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28100033?dopt=AbstractPlus
Not in our library
781.
Hale JJ et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10737756?dopt=AbstractPlus
Not in our library
782.
Hale JJ et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9804700?dopt=AbstractPlus
Not in our library
783.
Hall DA et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10188995?dopt=AbstractPlus
Not in our library
784.
Hall H et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11044889?dopt=AbstractPlus
Not in our library
785.
Halls ML et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25761609?dopt=AbstractPlus
Not in our library
786.
Halls ML et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15649866?dopt=AbstractPlus
Not in our library
787.
Halls ML et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17293890?dopt=AbstractPlus
Not in our library
788.
Hamann J et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25713288?dopt=AbstractPlus
Not in our library
789.
Hamann J et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/9064337?dopt=AbstractPlus
Not in our library
790.
Hamblin MW et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1652050?dopt=AbstractPlus
Not in our library
791.
Hameg A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12527336?dopt=AbstractPlus
Not in our library
792.
Han G et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10187777?dopt=AbstractPlus
Not in our library
793.
Han S et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26048791?dopt=AbstractPlus
Not in our library
794.
Hancock AA et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15033391?dopt=AbstractPlus
Not in our library
795.
Hancock AA et al (1998 ) Drug Dev Res 44: 140-162
Not in our library
796.
Handa BK et al (1981 ) https://www.ncbi.nlm.nih.gov/pubmed/6263640?dopt=AbstractPlus
Not in our library
797.
Hanessian S et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12502358?dopt=AbstractPlus
Not in our library
798.
Hannan FM et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27647839?dopt=AbstractPlus
Not in our library
799.
Hannedouche S et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21796212?dopt=AbstractPlus
Not in our library
800.
Hannon J et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18571247?dopt=AbstractPlus
Not in our library
801.
Hansen AH et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30247908?dopt=AbstractPlus
Not in our library
802.
Hansen C et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19651774?dopt=AbstractPlus
Not in our library
803.
Hansen W et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20200545?dopt=AbstractPlus
Not in our library
804.
Hanson J et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23643932?dopt=AbstractPlus
Not in our library
805.
Hanson MA et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22344443?dopt=AbstractPlus
Not in our library
806.
Hanus L et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10588688?dopt=AbstractPlus
Not in our library
807.
Harada K et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17074317?dopt=AbstractPlus
Not in our library
808.
Haramura M et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11806718?dopt=AbstractPlus
Not in our library
809.
Harford-Wright E et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/29053791?dopt=AbstractPlus
Not in our library
810.
Harland SP et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8587429?dopt=AbstractPlus
Not in our library
811.
Harmar AJ. (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11790261?dopt=AbstractPlus
Not in our library
812.
Harmar AJ et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9647867?dopt=AbstractPlus
Not in our library
813.
Harmar AJ et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22289055?dopt=AbstractPlus
Not in our library
814.
Harrison GS et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15613448?dopt=AbstractPlus
Not in our library
815.
Harrison T et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11708932?dopt=AbstractPlus
Not in our library
816.
Hartig PR. (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8936345?dopt=AbstractPlus
Not in our library
817.
Hase M et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18347022?dopt=AbstractPlus
Not in our library
818.
Hasegawa Y et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12554733?dopt=AbstractPlus
Not in our library
819.
Haskell CA et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16221874?dopt=AbstractPlus
Not in our library
820.
Hastrup H et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8985159?dopt=AbstractPlus
Not in our library
821.
Hata AN et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12721327?dopt=AbstractPlus
Not in our library
822.
Hatae N et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17312275?dopt=AbstractPlus
Not in our library
823.
Haugaard-Kedström LM et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21384867?dopt=AbstractPlus
Not in our library
824.
Hauger RL et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12615952?dopt=AbstractPlus
Not in our library
825.
Hawkins KN et al (1987 ) https://www.ncbi.nlm.nih.gov/pubmed/3030778?dopt=AbstractPlus
Not in our library
826.
Hay DL. (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29797087?dopt=AbstractPlus
Not in our library
827.
Hay DL et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15692146?dopt=AbstractPlus
Not in our library
828.
Hay DL et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16959943?dopt=AbstractPlus
Not in our library
829.
Hay DL et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12970090?dopt=AbstractPlus
Not in our library
830.
Hay DL et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18552275?dopt=AbstractPlus
Not in our library
831.
Hay DL et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21051558?dopt=AbstractPlus
Not in our library
832.
Hayallah AM et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11906291?dopt=AbstractPlus
Not in our library
833.
He HQ et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23160941?dopt=AbstractPlus
Not in our library
834.
He J et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19696113?dopt=AbstractPlus
Not in our library
835.
He L et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10669572?dopt=AbstractPlus
Not in our library
836.
He S et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20167483?dopt=AbstractPlus
Not in our library
837.
He S et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/24900499?dopt=AbstractPlus
Not in our library
838.
He W et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15141213?dopt=AbstractPlus
Not in our library
839.
Heasley BH et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15125924?dopt=AbstractPlus
Not in our library
840.
Hecht JH et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8922387?dopt=AbstractPlus
Not in our library
841.
Hegde SS et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9113359?dopt=AbstractPlus
Not in our library
842.
Hegde SS et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8903510?dopt=AbstractPlus
Not in our library
843.
Heier RF et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9057850?dopt=AbstractPlus
Not in our library
844.
Heise CE et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10851239?dopt=AbstractPlus
Not in our library
845.
Heise CE et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15761110?dopt=AbstractPlus
Not in our library
846.
Heise CE et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11723223?dopt=AbstractPlus
Not in our library
847.
Heitman LH et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19161279?dopt=AbstractPlus
Not in our library
848.
Heitman LH et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16444290?dopt=AbstractPlus
Not in our library
849.
Hellyer SD et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29514854?dopt=AbstractPlus
Not in our library
850.
Hemstapat K et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17416742?dopt=AbstractPlus
Not in our library
851.
Henke BR et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9276016?dopt=AbstractPlus
Not in our library
852.
Henstridge CM et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20136841?dopt=AbstractPlus
Not in our library
853.
Herbert JM et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8395255?dopt=AbstractPlus
Not in our library
854.
Herbert JM et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/15199474?dopt=AbstractPlus
Not in our library
855.
Hermans E et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9283723?dopt=AbstractPlus
Not in our library
856.
Hern JA et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20133736?dopt=AbstractPlus
Not in our library
857.
Herr KJ et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21878565?dopt=AbstractPlus
Not in our library
858.
Herrick-Davis K et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10991983?dopt=AbstractPlus
Not in our library
859.
Herron DK et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1316967?dopt=AbstractPlus
Not in our library
860.
Hertzog DL et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16870432?dopt=AbstractPlus
Not in our library
861.
Hesselgesser J et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9551924?dopt=AbstractPlus
Not in our library
862.
Hesselgesser J et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9624164?dopt=AbstractPlus
Not in our library
863.
Hetherington SL et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15514209?dopt=AbstractPlus
Not in our library
864.
Heusler P. (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20799027?dopt=AbstractPlus
Not in our library
865.
Heynen-Genel S et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/22091481?dopt=AbstractPlus
Not in our library
866.
Hidaka K et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7777184?dopt=AbstractPlus
Not in our library
867.
Hieble JP. (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10812954?dopt=AbstractPlus
Not in our library
868.
Hieble JP et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7658428?dopt=AbstractPlus
Not in our library
869.
Hieble JP et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7568329?dopt=AbstractPlus
Not in our library
870.
Hilditch A et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7853190?dopt=AbstractPlus
Not in our library
871.
Hill SJ et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9311023?dopt=AbstractPlus
Not in our library
872.
Hillard CJ et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10336536?dopt=AbstractPlus
Not in our library
873.
Hillmann P et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19419204?dopt=AbstractPlus
Not in our library
874.
Hilton JM et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10856900?dopt=AbstractPlus
Not in our library
875.
Hinuma S et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11025660?dopt=AbstractPlus
Not in our library
876.
Hirasawa A et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15619630?dopt=AbstractPlus
Not in our library
877.
Hirata T et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21819041?dopt=AbstractPlus
Not in our library
878.
Hirose H et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11303071?dopt=AbstractPlus
Not in our library
879.
Hirose M et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14643355?dopt=AbstractPlus
Not in our library
880.
Hirst RA et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8981483?dopt=AbstractPlus
Not in our library
881.
Hirst WD et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12663046?dopt=AbstractPlus
Not in our library
882.
Hirst WD et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17069795?dopt=AbstractPlus
Not in our library
883.
Hisatsune C et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17925404?dopt=AbstractPlus
Not in our library
884.
Hla T et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2160972?dopt=AbstractPlus
Not in our library
885.
Ho C et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7493018?dopt=AbstractPlus
Not in our library
886.
Hoare BL et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/30594862?dopt=AbstractPlus
Not in our library
887.
Hoare SR et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10854439?dopt=AbstractPlus
Not in our library
888.
Hoare SR et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10882389?dopt=AbstractPlus
Not in our library
889.
Hobson AD et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26509640?dopt=AbstractPlus
Not in our library
890.
Hoch L et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25636740?dopt=AbstractPlus
Not in our library
891.
Hoffmann C et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14730417?dopt=AbstractPlus
Not in our library
892.
Hoffmann SH et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10894158?dopt=AbstractPlus
Not in our library
893.
Holenz J et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15771424?dopt=AbstractPlus
Not in our library
894.
Hollenberg MD et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12037136?dopt=AbstractPlus
Not in our library
895.
Hollenberg MD et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18477767?dopt=AbstractPlus
Not in our library
896.
Holloway AC et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11901215?dopt=AbstractPlus
Not in our library
897.
Holst B et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12907757?dopt=AbstractPlus
Not in our library
898.
Holst B et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/16959833?dopt=AbstractPlus
Not in our library
899.
Holst B et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/18923064?dopt=AbstractPlus
Not in our library
900.
Holst B et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15383539?dopt=AbstractPlus
Not in our library
901.
Homey B et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10725697?dopt=AbstractPlus
Not in our library
902.
Honczarenko M et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15990859?dopt=AbstractPlus
Not in our library
903.
Hong Y et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/21658025?dopt=AbstractPlus
Not in our library
904.
Horie K et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8564227?dopt=AbstractPlus
Not in our library
905.
Horwell DC et al (1995 ) Bioorg Med Chem Lett 5: 2501-2506
Not in our library
906.
Hosken IT et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25257104?dopt=AbstractPlus
Not in our library
907.
Hosoda H et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10801861?dopt=AbstractPlus
Not in our library
908.
Hosoi T et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12065583?dopt=AbstractPlus
Not in our library
909.
Hosoya M et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10777510?dopt=AbstractPlus
Not in our library
910.
Hosoya M et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10887190?dopt=AbstractPlus
Not in our library
911.
Hossain MA et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/30155023?dopt=AbstractPlus
Not in our library
912.
Hossain MA et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18434306?dopt=AbstractPlus
Not in our library
913.
Hossain MA et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20043231?dopt=AbstractPlus
Not in our library
914.
Hoyer D et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7938165?dopt=AbstractPlus
Not in our library
915.
Hoyer D et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11888546?dopt=AbstractPlus
Not in our library
916.
Hoyer D et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15135911?dopt=AbstractPlus
Not in our library
917.
Hoyer D et al (2004 ) Soc Neuroscience Abs -
Not in our library
918.
Hsu SH et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17652154?dopt=AbstractPlus
Not in our library
919.
Hsu SY et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10935549?dopt=AbstractPlus
Not in our library
920.
Hsu SY et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11809971?dopt=AbstractPlus
Not in our library
921.
Hu MJ et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28274616?dopt=AbstractPlus
Not in our library
922.
Huang C et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/12954603?dopt=AbstractPlus
Not in our library
923.
Huang F et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/12049493?dopt=AbstractPlus
Not in our library
924.
Huang P et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29804838?dopt=AbstractPlus
Not in our library
925.
Huang XP et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26550826?dopt=AbstractPlus
Not in our library
926.
Hudson BD et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24870406?dopt=AbstractPlus
Not in our library
927.
Hudson BD et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/23066016?dopt=AbstractPlus
Not in our library
928.
Huete-Toral F et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25344385?dopt=AbstractPlus
Not in our library
929.
Huey R et al (1985 ) https://www.ncbi.nlm.nih.gov/pubmed/4020139?dopt=AbstractPlus
Not in our library
930.
Huffman JW et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10658595?dopt=AbstractPlus
Not in our library
931.
Hughes J et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/1975695?dopt=AbstractPlus
Not in our library
932.
Humphries RG et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7582510?dopt=AbstractPlus
Not in our library
933.
Humphries RG et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7858849?dopt=AbstractPlus
Not in our library
934.
Hunter JC et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2178014?dopt=AbstractPlus
Not in our library
935.
Hunter JC et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8474432?dopt=AbstractPlus
Not in our library
936.
Hutchinson DS et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11959793?dopt=AbstractPlus
Not in our library
937.
Hwang SB et al (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/2841449?dopt=AbstractPlus
Not in our library
938.
Ichimura A et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22343897?dopt=AbstractPlus
Not in our library
939.
Ignatov A et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15111018?dopt=AbstractPlus
Not in our library
940.
Ignatov A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12574419?dopt=AbstractPlus
Not in our library
941.
Ignatov A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14592418?dopt=AbstractPlus
Not in our library
942.
Ignatov A et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17001303?dopt=AbstractPlus
Not in our library
943.
Ignatowska-Jankowska BM et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26052038?dopt=AbstractPlus
Not in our library
944.
Ihara M et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7768260?dopt=AbstractPlus
Not in our library
945.
Ikubo M et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25970039?dopt=AbstractPlus
Not in our library
946.
Im DS et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10799507?dopt=AbstractPlus
Not in our library
947.
Imai T et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9430724?dopt=AbstractPlus
Not in our library
948.
Inngjerdingen M et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11154210?dopt=AbstractPlus
Not in our library
949.
Inoue A et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22983457?dopt=AbstractPlus
Not in our library
950.
Iredale PA et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8032613?dopt=AbstractPlus
Not in our library
951.
Irukayama-Tomobe Y et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28507129?dopt=AbstractPlus
Not in our library
952.
Irwin DM. (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11179772?dopt=AbstractPlus
Not in our library
953.
Isberg V et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24826842?dopt=AbstractPlus
Not in our library
954.
Ishibashi T et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20404009?dopt=AbstractPlus
Not in our library
955.
Ishiwata K et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15093820?dopt=AbstractPlus
Not in our library
956.
Isogaya M et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10531390?dopt=AbstractPlus
Not in our library
957.
Ito M et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8349705?dopt=AbstractPlus
Not in our library
958.
Itoh Y et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12629551?dopt=AbstractPlus
Not in our library
959.
Ivanov AA et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17088057?dopt=AbstractPlus
Not in our library
960.
Ivanov AA et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17302398?dopt=AbstractPlus
Not in our library
961.
Ivell R et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30204868?dopt=AbstractPlus
Not in our library
962.
Ivell R et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/20952422?dopt=AbstractPlus
Not in our library
963.
Iwamoto Y et al (1987 ) https://www.ncbi.nlm.nih.gov/pubmed/2437574?dopt=AbstractPlus
Not in our library
964.
Jaakola VP et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18832607?dopt=AbstractPlus
Not in our library
965.
Jackson RH et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1320692?dopt=AbstractPlus
Not in our library
966.
Jacobson KA. (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23597047?dopt=AbstractPlus
Not in our library
967.
Jacobson KA et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21484092?dopt=AbstractPlus
Not in our library
968.
Jacobson KA et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16518376?dopt=AbstractPlus
Not in our library
969.
Jacobson KA et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/18600475?dopt=AbstractPlus
Not in our library
970.
Jacobson KA et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12213051?dopt=AbstractPlus
Not in our library
971.
Jacobson KA et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9364471?dopt=AbstractPlus
Not in our library
972.
Jacobson MA et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7558011?dopt=AbstractPlus
Not in our library
973.
Jacobson SG et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18463160?dopt=AbstractPlus
Not in our library
974.
Jagerschmidt A et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8720482?dopt=AbstractPlus
Not in our library
975.
Jagoda EM et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12668051?dopt=AbstractPlus
Not in our library
976.
Jakubik J et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9224827?dopt=AbstractPlus
Not in our library
977.
Jakubik J et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16675658?dopt=AbstractPlus
Not in our library
978.
Jalan-Sakrikar N et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25225882?dopt=AbstractPlus
Not in our library
979.
Jane DE et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/9121605?dopt=AbstractPlus
Not in our library
980.
Jansen FP et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7834183?dopt=AbstractPlus
Not in our library
981.
Janssens R et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10401562?dopt=AbstractPlus
Not in our library
982.
January B et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9295336?dopt=AbstractPlus
Not in our library
983.
Jarvis MF et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2600819?dopt=AbstractPlus
Not in our library
984.
Jasper JR et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7475979?dopt=AbstractPlus
Not in our library
985.
Jasper JR et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9605427?dopt=AbstractPlus
Not in our library
986.
Jayasekara PS et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24712832?dopt=AbstractPlus
Not in our library
987.
Jenck F et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10758169?dopt=AbstractPlus
Not in our library
988.
Jenei V et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19901340?dopt=AbstractPlus
Not in our library
989.
Jenh CH et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10201891?dopt=AbstractPlus
Not in our library
990.
Jensen RT et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18055507?dopt=AbstractPlus
Not in our library
991.
Jensen RT et al (2013 ) In Handbook of Biologically Active Peptides. 2nd Revised edition Edited by Kastin AJ: Elsevier: 1188-1196 [ISBN: 9780123850959]
Not in our library
992.
Jensen RT et al (2013 ) In Handbook of Biologically Active Peptides. 2nd Revised edition Edited by Kastin AJ: Elsevier: 506-511 [ISBN: 9780123850959]
Not in our library
993.
Jensen T et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25442311?dopt=AbstractPlus
Not in our library
994.
Jerning E et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9851589?dopt=AbstractPlus
Not in our library
995.
Ji X et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11266650?dopt=AbstractPlus
Not in our library
996.
Ji XD et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10624567?dopt=AbstractPlus
Not in our library
997.
Jia XC et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1922095?dopt=AbstractPlus
Not in our library
998.
Jiang JL et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8917655?dopt=AbstractPlus
Not in our library
999.
Jiang Y et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12714592?dopt=AbstractPlus
Not in our library
1000.
Jiang Y et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29263243?dopt=AbstractPlus
Not in our library
1001.
Jimenez-Vargas NN et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30012612?dopt=AbstractPlus
Not in our library
1002.
Jin C et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18487371?dopt=AbstractPlus
Not in our library
1003.
Jinsmaa Y et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11179594?dopt=AbstractPlus
Not in our library
1004.
Jo E et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22971058?dopt=AbstractPlus
Not in our library
1005.
Jockers R. (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7798201?dopt=AbstractPlus
Not in our library
1006.
Johansson B et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7566470?dopt=AbstractPlus
Not in our library
1007.
Johansson L et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9336327?dopt=AbstractPlus
Not in our library
1008.
Johnson BG et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10530814?dopt=AbstractPlus
Not in our library
1009.
Johnson MP et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12852748?dopt=AbstractPlus
Not in our library
1010.
Johnson MP et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15717213?dopt=AbstractPlus
Not in our library
1011.
Jolkkonen M et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7925952?dopt=AbstractPlus
Not in our library
1012.
Jones C et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10422787?dopt=AbstractPlus
Not in our library
1013.
Jones CE et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12606753?dopt=AbstractPlus
Not in our library
1014.
Jones CK et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18842902?dopt=AbstractPlus
Not in our library
1015.
Jones KA et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9872315?dopt=AbstractPlus
Not in our library
1016.
Jones PG et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17363172?dopt=AbstractPlus
Not in our library
1017.
Jones RM et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10822054?dopt=AbstractPlus
Not in our library
1018.
Jonsson KB et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11159842?dopt=AbstractPlus
Not in our library
1019.
Jordan BA et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10385123?dopt=AbstractPlus
Not in our library
1020.
Jorgensen R et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15528268?dopt=AbstractPlus
Not in our library
1021.
Joseph SS et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15060759?dopt=AbstractPlus
Not in our library
1022.
Joshi P et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24405707?dopt=AbstractPlus
Not in our library
1023.
Juarranz MG et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10570056?dopt=AbstractPlus
Not in our library
1024.
Jugus MJ et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19486006?dopt=AbstractPlus
Not in our library
1025.
Jung M et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/8978752?dopt=AbstractPlus
Not in our library
1026.
Juteau H et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11504634?dopt=AbstractPlus
Not in our library
1027.
Kabarowski JH et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11474113?dopt=AbstractPlus
Not in our library
1028.
Kaku K et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25787200?dopt=AbstractPlus
Not in our library
1029.
Kalant D et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12540846?dopt=AbstractPlus
Not in our library
1030.
Kalant D et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15833747?dopt=AbstractPlus
Not in our library
1031.
Kalinichev M et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23257312?dopt=AbstractPlus
Not in our library
1032.
Kalipatnapu S et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15628665?dopt=AbstractPlus
Not in our library
1033.
Kalk P et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17558436?dopt=AbstractPlus
Not in our library
1034.
Kamali F. (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11757797?dopt=AbstractPlus
Not in our library
1035.
Kamohara M et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15823563?dopt=AbstractPlus
Not in our library
1036.
Kanaoka Y et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23504326?dopt=AbstractPlus
Not in our library
1037.
Kanatani A et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10872822?dopt=AbstractPlus
Not in our library
1038.
Kanesaka M et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17486669?dopt=AbstractPlus
Not in our library
1039.
Kania A et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28098344?dopt=AbstractPlus
Not in our library
1040.
Kanke T et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15765104?dopt=AbstractPlus
Not in our library
1041.
Kapas S et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7592696?dopt=AbstractPlus
Not in our library
1042.
Kapur A et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19723626?dopt=AbstractPlus
Not in our library
1043.
Karamitri A et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/30531911?dopt=AbstractPlus
Not in our library10.1038/s41574-018-0130-1
1044.
Kargl J et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23639801?dopt=AbstractPlus
Not in our library
1045.
Karnik SS et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26315714?dopt=AbstractPlus
Not in our library
1046.
Karteris E et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15687100?dopt=AbstractPlus
Not in our library
1047.
Katafuchi T et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12556539?dopt=AbstractPlus
Not in our library
1048.
Kathmann M et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16489449?dopt=AbstractPlus
Not in our library
1049.
Kato K et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15695169?dopt=AbstractPlus
Not in our library
1050.
Katugampola SD et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11250876?dopt=AbstractPlus
Not in our library
1051.
Katugampola SD et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11522606?dopt=AbstractPlus
Not in our library
1052.
Kaupmann K et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9069281?dopt=AbstractPlus
Not in our library
1053.
Kawabata A et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9862790?dopt=AbstractPlus
Not in our library
1054.
Kawai M. (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1732540?dopt=AbstractPlus
Not in our library
1055.
Kawamata Y et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12524422?dopt=AbstractPlus
Not in our library
1056.
Kawamata Y et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11336787?dopt=AbstractPlus
Not in our library
1057.
Kawamoto H et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10602690?dopt=AbstractPlus
Not in our library
1058.
Kawamoto Y et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29208511?dopt=AbstractPlus
Not in our library
1059.
Kazda CM et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26681715?dopt=AbstractPlus
Not in our library
1060.
Keir MJ et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10521582?dopt=AbstractPlus
Not in our library
1061.
Kelly E et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/24973897?dopt=AbstractPlus
Not in our library
1062.
Kelly LM et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21844396?dopt=AbstractPlus
Not in our library
1063.
Kelly RP et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25656305?dopt=AbstractPlus
Not in our library
1064.
Kemp PA et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15231488?dopt=AbstractPlus
Not in our library
1065.
Kennedy AJ et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29279348?dopt=AbstractPlus
Not in our library
1066.
Kennedy AJ et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27742615?dopt=AbstractPlus
Not in our library
1067.
Kennedy C et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10779375?dopt=AbstractPlus
Not in our library
1068.
Kennedy K et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7654246?dopt=AbstractPlus
Not in our library
1069.
Kennedy PC et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21632869?dopt=AbstractPlus
Not in our library
1070.
Kennedy SP et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9535752?dopt=AbstractPlus
Not in our library
1071.
Kennett GA et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9225286?dopt=AbstractPlus
Not in our library
1072.
Kerkhof HJ et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20112360?dopt=AbstractPlus
Not in our library
1073.
Khanolkar AD et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8893848?dopt=AbstractPlus
Not in our library
1074.
Khattar SK et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16369696?dopt=AbstractPlus
Not in our library
1075.
Khawaja X et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9048968?dopt=AbstractPlus
Not in our library
1076.
Khroyan TV et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21177476?dopt=AbstractPlus
Not in our library
1077.
Khusal KG et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25324134?dopt=AbstractPlus
Not in our library
1078.
Kiefer L et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21406038?dopt=AbstractPlus
Not in our library
1079.
Kiesel LA et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12072036?dopt=AbstractPlus
Not in our library10.1046/j.1365-2265.2002.01291.x
1080.
Kihara Y et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24602016?dopt=AbstractPlus
Not in our library
1081.
Kikuchi A et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19208479?dopt=AbstractPlus
Not in our library
1082.
Kikuchi C et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10052959?dopt=AbstractPlus
Not in our library
1083.
Kilander MB et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24873871?dopt=AbstractPlus
Not in our library
1084.
Kim GH et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17476309?dopt=AbstractPlus
Not in our library
1085.
Kim HO et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7932588?dopt=AbstractPlus
Not in our library
1086.
Kim HS et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14584948?dopt=AbstractPlus
Not in our library
1087.
Kim HS et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11754592?dopt=AbstractPlus
Not in our library
1088.
Kim J et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7775460?dopt=AbstractPlus
Not in our library
1089.
Kim SV et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23661644?dopt=AbstractPlus
Not in our library
1090.
Kim TH et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23721409?dopt=AbstractPlus
Not in our library
1091.
Kim Y et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23541835?dopt=AbstractPlus
Not in our library
1092.
Kim YC et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10737749?dopt=AbstractPlus
Not in our library
1093.
Kim YC et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8863790?dopt=AbstractPlus
Not in our library
1094.
Kim YC et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15913566?dopt=AbstractPlus
Not in our library
1095.
Kimura I et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21518883?dopt=AbstractPlus
Not in our library
1096.
Kimura T et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7921228?dopt=AbstractPlus
Not in our library
1097.
Kimura Y et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14709324?dopt=AbstractPlus
Not in our library
1098.
Kinghorn AD et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21650152?dopt=AbstractPlus
Not in our library
1099.
Kingston AE et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9680254?dopt=AbstractPlus
Not in our library
1100.
Kinney GG et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15608073?dopt=AbstractPlus
Not in our library
1101.
Kinney WA et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12203418?dopt=AbstractPlus
Not in our library
1102.
Kirby HR et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/21079036?dopt=AbstractPlus
Not in our library
1103.
Kirihara T et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29332128?dopt=AbstractPlus
Not in our library
1104.
Kiselev E et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26303895?dopt=AbstractPlus
Not in our library
1105.
Kiselev E et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25299434?dopt=AbstractPlus
Not in our library
1106.
Kiss GN et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22968304?dopt=AbstractPlus
Not in our library
1107.
Kitamura H et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22343749?dopt=AbstractPlus
Not in our library
1108.
Kitaura M et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10488147?dopt=AbstractPlus
Not in our library
1109.
Kitbunnadaj R et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15771452?dopt=AbstractPlus
Not in our library
1110.
Kitbunnadaj R et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15115383?dopt=AbstractPlus
Not in our library
1111.
Kittaka H et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28176353?dopt=AbstractPlus
Not in our library
1112.
Klein J et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9175608?dopt=AbstractPlus
Not in our library
1113.
Klein MT et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21422162?dopt=AbstractPlus
Not in our library
1114.
Klos A et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23383423?dopt=AbstractPlus
Not in our library
1115.
Klotz K‐N et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9459566?dopt=AbstractPlus
Not in our library
1116.
Knepper SM et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7616455?dopt=AbstractPlus
Not in our library
1117.
Knight AR et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15322733?dopt=AbstractPlus
Not in our library
1118.
Knoflach F et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11606768?dopt=AbstractPlus
Not in our library
1119.
Knudsen LB et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10794683?dopt=AbstractPlus
Not in our library
1120.
Kobayashi T et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20580563?dopt=AbstractPlus
Not in our library
1121.
Kobilka B. (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23650120?dopt=AbstractPlus
Not in our library
1122.
Koe BK et al (1992 ) Drug Dev Res 26: 241250
Not in our library
1123.
Koga H et al (1994 ) Bioorg Med Chem Lett 4: 1347-1352
Not in our library
1124.
Kogushi M et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21300059?dopt=AbstractPlus
Not in our library
1125.
Kohara A et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15976016?dopt=AbstractPlus
Not in our library
1126.
Kohno M et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16844083?dopt=AbstractPlus
Not in our library
1127.
Koike H et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11451212?dopt=AbstractPlus
Not in our library
1128.
Kojima M et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10604470?dopt=AbstractPlus
Not in our library
1129.
Kolakowski Jr LF. (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8081729?dopt=AbstractPlus
Not in our library
1130.
Kolczewski S et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10465539?dopt=AbstractPlus
Not in our library
1131.
Kongsamut S et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12176106?dopt=AbstractPlus
Not in our library
1132.
Konkel MJ et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16789730?dopt=AbstractPlus
Not in our library
1133.
Konkel MJ et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16730981?dopt=AbstractPlus
Not in our library
1134.
Kono M et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/29079828?dopt=AbstractPlus
Not in our library
1135.
Kono M et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24667638?dopt=AbstractPlus
Not in our library
1136.
Konteatis ZD et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7930622?dopt=AbstractPlus
Not in our library
1137.
Koo C et al (1982 ) https://www.ncbi.nlm.nih.gov/pubmed/6285921?dopt=AbstractPlus
Not in our library
1138.
Kopanchuk S et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15840392?dopt=AbstractPlus
Not in our library
1139.
Kopin AS et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1373504?dopt=AbstractPlus
Not in our library
1140.
Korstanje R et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18796533?dopt=AbstractPlus
Not in our library
1141.
Kortagere S et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15448188?dopt=AbstractPlus
Not in our library
1142.
Kotani M et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11457843?dopt=AbstractPlus
Not in our library
1143.
Kotani M et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7476918?dopt=AbstractPlus
Not in our library
1144.
Kotarsky K et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12565875?dopt=AbstractPlus
Not in our library
1145.
Kottyan LC et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19641187?dopt=AbstractPlus
Not in our library
1146.
Kovacs A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/15107597?dopt=AbstractPlus
Not in our library
1147.
Kovacs I et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9454790?dopt=AbstractPlus
Not in our library
1148.
Kozian DH et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22801643?dopt=AbstractPlus
Not in our library
1149.
Kraus A et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19072936?dopt=AbstractPlus
Not in our library
1150.
Krause JE et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/8990205?dopt=AbstractPlus
Not in our library
1151.
Krauss AH et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8882612?dopt=AbstractPlus
Not in our library
1152.
Krishnamoorthy S et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22449948?dopt=AbstractPlus
Not in our library
1153.
Krishnamoorthy S et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20080636?dopt=AbstractPlus
Not in our library
1154.
Kritikou E et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27883026?dopt=AbstractPlus
Not in our library
1155.
Kroeger KM et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11278883?dopt=AbstractPlus
Not in our library
1156.
Kroeze WK et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12629531?dopt=AbstractPlus
Not in our library
1157.
Krsmanovic LZ et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12591945?dopt=AbstractPlus
Not in our library
1158.
Kruse AC et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24256733?dopt=AbstractPlus
Not in our library
1159.
Krushinski Jr JH et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17804228?dopt=AbstractPlus
Not in our library
1160.
Ku GM et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22253604?dopt=AbstractPlus
Not in our library
1161.
Kubo Y et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15922585?dopt=AbstractPlus
Not in our library
1162.
Kuc D et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18235993?dopt=AbstractPlus
Not in our library
1163.
Kuc RE et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8587419?dopt=AbstractPlus
Not in our library
1164.
Kuc RE et al (2006 ) Proceedings ofthe British Pharmacological Society 4: abst186
Not in our library
1165.
Kuei C et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17606621?dopt=AbstractPlus
Not in our library
1166.
Kukkonen JP. (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23034387?dopt=AbstractPlus
Not in our library
1167.
Kukkonen JP. (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27237973?dopt=AbstractPlus
Not in our library
1168.
Kukkonen JP. (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26582739?dopt=AbstractPlus
Not in our library
1169.
Kukkonen JP. (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/27909990?dopt=AbstractPlus
Not in our library
1170.
Kukkonen JP et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/23902572?dopt=AbstractPlus
Not in our library
1171.
Kulagowski JJ et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8642550?dopt=AbstractPlus
Not in our library
1172.
Kulkarni PM et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26529344?dopt=AbstractPlus
Not in our library
1173.
Kull B et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9920286?dopt=AbstractPlus
Not in our library
1174.
Kumagai J et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12114498?dopt=AbstractPlus
Not in our library
1175.
Kumar S et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12604693?dopt=AbstractPlus
Not in our library
1176.
Kumar S et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19786130?dopt=AbstractPlus
Not in our library
1177.
Kunishima N et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11069170?dopt=AbstractPlus
Not in our library
1178.
Kuphal D et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8013367?dopt=AbstractPlus
Not in our library
1179.
Kursar JD et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8078486?dopt=AbstractPlus
Not in our library
1180.
Kuszak AJ et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19542234?dopt=AbstractPlus
Not in our library
1181.
Kuwano K et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17545310?dopt=AbstractPlus
Not in our library
1182.
Kuwasako K et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14722252?dopt=AbstractPlus
Not in our library
1183.
Kuwasako K et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12565884?dopt=AbstractPlus
Not in our library
1184.
Köhler C et al (1985 ) https://www.ncbi.nlm.nih.gov/pubmed/4015674?dopt=AbstractPlus
Not in our library
1185.
Kühn B et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8961278?dopt=AbstractPlus
Not in our library
1186.
Laas K et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/23325374?dopt=AbstractPlus
Not in our library
1187.
Labarrere P et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12943190?dopt=AbstractPlus
Not in our library
1188.
Labbé-Jullié C et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7746272?dopt=AbstractPlus
Not in our library
1189.
Laeremans H et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21931076?dopt=AbstractPlus
Not in our library
1190.
Lagerström MC et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15885496?dopt=AbstractPlus
Not in our library
1191.
Lahti RA et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8102973?dopt=AbstractPlus
Not in our library
1192.
Lahti RA et al (1985 ) https://www.ncbi.nlm.nih.gov/pubmed/2986999?dopt=AbstractPlus
Not in our library
1193.
Laitinen T et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15073379?dopt=AbstractPlus
Not in our library
1194.
Lameh J et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20354177?dopt=AbstractPlus
Not in our library
1195.
Lan R et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/11741201?dopt=AbstractPlus
Not in our library
1196.
Lan R et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10052983?dopt=AbstractPlus
Not in our library
1197.
Lang R et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15944009?dopt=AbstractPlus
Not in our library
1198.
Langmead CJ et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18454168?dopt=AbstractPlus
Not in our library
1199.
Langmead CJ et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16207821?dopt=AbstractPlus
Not in our library
1200.
Langmead CJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14691055?dopt=AbstractPlus
Not in our library
1201.
Langmead CJ et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11030716?dopt=AbstractPlus
Not in our library
1202.
Lansu K. (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28288109?dopt=AbstractPlus
Not in our library
1203.
Lappano R et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/28249728?dopt=AbstractPlus
Not in our library
1204.
Laprairie RB et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26218440?dopt=AbstractPlus
Not in our library
1205.
Laprairie RB et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28103441?dopt=AbstractPlus
Not in our library
1206.
Lau J et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26308095?dopt=AbstractPlus
Not in our library
1207.
Lau OC et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24511227?dopt=AbstractPlus
Not in our library
1208.
Lautner RQ et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23446738?dopt=AbstractPlus
Not in our library
1209.
Lavreysen H et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12695537?dopt=AbstractPlus
Not in our library
1210.
Lavreysen H et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15555631?dopt=AbstractPlus
Not in our library
1211.
Lawrence AJ et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12110614?dopt=AbstractPlus
Not in our library
1212.
Lazareno S et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7651370?dopt=AbstractPlus
Not in our library
1213.
Lazareno S et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14722259?dopt=AbstractPlus
Not in our library
1214.
Lazareno S et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9495826?dopt=AbstractPlus
Not in our library
1215.
Lazareno S et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10860942?dopt=AbstractPlus
Not in our library
1216.
Lazareno S et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12435818?dopt=AbstractPlus
Not in our library
1217.
Lazarowski ER et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8564228?dopt=AbstractPlus
Not in our library
1218.
Lazarowski ER et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8825364?dopt=AbstractPlus
Not in our library
1219.
Le Bourdonnec B et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18313920?dopt=AbstractPlus
Not in our library
1220.
Le Bourdonnec B et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18788723?dopt=AbstractPlus
Not in our library
1221.
Le Bourdonnec B et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19694468?dopt=AbstractPlus
Not in our library
1222.
Le MT et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12006574?dopt=AbstractPlus
Not in our library
1223.
Le Poul E et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12711604?dopt=AbstractPlus
Not in our library
1224.
Le Y et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12401407?dopt=AbstractPlus
Not in our library
1225.
Leach K et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21300722?dopt=AbstractPlus
Not in our library
1226.
Leach K et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27002221?dopt=AbstractPlus
Not in our library
1227.
Leach K et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19940843?dopt=AbstractPlus
Not in our library
1228.
Leach K et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24111791?dopt=AbstractPlus
Not in our library
1229.
Leach K et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23372019?dopt=AbstractPlus
Not in our library
1230.
Leaños-Miranda A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12843188?dopt=AbstractPlus
Not in our library
1231.
Leban JJ et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8446610?dopt=AbstractPlus
Not in our library
1232.
Lebon G et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25762024?dopt=AbstractPlus
Not in our library
1233.
Lebon G et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21593763?dopt=AbstractPlus
Not in our library
1234.
Ledent C et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15956199?dopt=AbstractPlus
Not in our library
1235.
Leduc M et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19584306?dopt=AbstractPlus
Not in our library
1236.
Lee C et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/21124972?dopt=AbstractPlus
Not in our library
1237.
Lee DK et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11574155?dopt=AbstractPlus
Not in our library
1238.
Lee DK et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15486224?dopt=AbstractPlus
Not in our library
1239.
Lee J et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1379593?dopt=AbstractPlus
Not in our library
1240.
Lee JW et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27759003?dopt=AbstractPlus
Not in our library
1241.
Lee MC et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18179608?dopt=AbstractPlus
Not in our library
1242.
Lee YM et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/7681836?dopt=AbstractPlus
Not in our library
1243.
Leeb-Lundberg LM et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15734727?dopt=AbstractPlus
Not in our library
1244.
Lefkowitz RJ. (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23650015?dopt=AbstractPlus
Not in our library
1245.
Legros C et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23698757?dopt=AbstractPlus
Not in our library
1246.
Lehmann F et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19481466?dopt=AbstractPlus
Not in our library
1247.
Lehmann F et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15781415?dopt=AbstractPlus
Not in our library
1248.
Lehmann F et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17112638?dopt=AbstractPlus
Not in our library
1249.
Leibowitz SF et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1283559?dopt=AbstractPlus
Not in our library
1250.
Leja J et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/18953328?dopt=AbstractPlus
Not in our library
1251.
Lejeune F et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9067310?dopt=AbstractPlus
Not in our library
1252.
Lelianova VG et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9261169?dopt=AbstractPlus
Not in our library
1253.
Lembo PM et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11850634?dopt=AbstractPlus
Not in our library
1254.
Lennertz L et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22078257?dopt=AbstractPlus
Not in our library
1255.
Leonard CS et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/23848055?dopt=AbstractPlus
Not in our library
1256.
Leonardi A et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9190863?dopt=AbstractPlus
Not in our library
1257.
Leopoldo M et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17649988?dopt=AbstractPlus
Not in our library
1258.
Leopoldo M et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18800769?dopt=AbstractPlus
Not in our library
1259.
Leprince J et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28613414?dopt=AbstractPlus
Not in our library
1260.
Lesage AS et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9605573?dopt=AbstractPlus
Not in our library
1261.
Leung T et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18755178?dopt=AbstractPlus
Not in our library
1262.
Leurs R et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7921611?dopt=AbstractPlus
Not in our library
1263.
Leuthauser K et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11023820?dopt=AbstractPlus
Not in our library
1264.
Lever JR et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9696425?dopt=AbstractPlus
Not in our library
1265.
Levoye A et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16778767?dopt=AbstractPlus
Not in our library
1266.
Lewis TA et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15482930?dopt=AbstractPlus
Not in our library
1267.
Leysen JE et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8967979?dopt=AbstractPlus
Not in our library
1268.
Li AH et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9703464?dopt=AbstractPlus
Not in our library
1269.
Li JJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15027861?dopt=AbstractPlus
Not in our library
1270.
Li L et al (2002 ) Neuropharmacology 43: 295
Not in our library
1271.
Li R et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23239822?dopt=AbstractPlus
Not in our library
1272.
Li X et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12013525?dopt=AbstractPlus
Not in our library
1273.
Liang BT Urso R Sambraski E et al (2010 ) In Adenosine Receptors from Cell Biology to Pharmacology Edited by Borea P: Springer: 257-280 [ISBN: 9789048131440]
Not in our library
1274.
Liang M et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10748002?dopt=AbstractPlus
Not in our library
1275.
Liang TS et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11714831?dopt=AbstractPlus
Not in our library
1276.
Liaw CW et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19630535?dopt=AbstractPlus
Not in our library
1277.
Liebscher I et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21097509?dopt=AbstractPlus
Not in our library
1278.
Liebscher I et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25533341?dopt=AbstractPlus
Not in our library
1279.
Liggett SB. (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/15090197?dopt=AbstractPlus
Not in our library
1280.
Ligneau X et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11090094?dopt=AbstractPlus
Not in our library
1281.
Liljebris C et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7830272?dopt=AbstractPlus
Not in our library
1282.
Lim HD et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17154494?dopt=AbstractPlus
Not in our library
1283.
Lim HD et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15947036?dopt=AbstractPlus
Not in our library
1284.
Limonta P et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14726258?dopt=AbstractPlus
Not in our library
1285.
Lin DC et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11886876?dopt=AbstractPlus
Not in our library
1286.
Lin DC et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22859723?dopt=AbstractPlus
Not in our library
1287.
Lin L et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10458611?dopt=AbstractPlus
Not in our library
1288.
Lin Q et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9890897?dopt=AbstractPlus
Not in our library
1289.
Linden J et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10496952?dopt=AbstractPlus
Not in our library
1290.
Lindsley CW et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15537338?dopt=AbstractPlus
Not in our library
1291.
Lindström E et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10385255?dopt=AbstractPlus
Not in our library
1292.
Linz K et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24713140?dopt=AbstractPlus
Not in our library
1293.
Litschig S et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10051528?dopt=AbstractPlus
Not in our library
1294.
Liu C et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15465925?dopt=AbstractPlus
Not in our library
1295.
Liu C et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14522967?dopt=AbstractPlus
Not in our library
1296.
Liu C et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14522968?dopt=AbstractPlus
Not in our library
1297.
Liu C et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22434674?dopt=AbstractPlus
Not in our library
1298.
Liu C et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11179434?dopt=AbstractPlus
Not in our library
1299.
Liu C et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11561071?dopt=AbstractPlus
Not in our library
1300.
Liu C et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19047060?dopt=AbstractPlus
Not in our library
1301.
Liu C et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21796211?dopt=AbstractPlus
Not in our library
1302.
Liu JJ et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22267580?dopt=AbstractPlus
Not in our library
1303.
Liu JJ et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19369576?dopt=AbstractPlus
Not in our library
1304.
Liu Q et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10581185?dopt=AbstractPlus
Not in our library
1305.
Liu Q et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/20004959?dopt=AbstractPlus
Not in our library
1306.
Liu S et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9822540?dopt=AbstractPlus
Not in our library
1307.
Liu W et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22798613?dopt=AbstractPlus
Not in our library
1308.
Llinares M et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10231715?dopt=AbstractPlus
Not in our library
1309.
Lobo MK et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17934457?dopt=AbstractPlus
Not in our library
1310.
Loetscher M et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8276799?dopt=AbstractPlus
Not in our library
1311.
Loetscher P et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9712844?dopt=AbstractPlus
Not in our library
1312.
Logue SF et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19796684?dopt=AbstractPlus
Not in our library
1313.
Londregan AT et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23337601?dopt=AbstractPlus
Not in our library
1314.
Long DD et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22959244?dopt=AbstractPlus
Not in our library
1315.
Longrois D et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22342278?dopt=AbstractPlus
Not in our library
1316.
Lopez VM et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18828673?dopt=AbstractPlus
Not in our library
1317.
Lopez-Gimenez JF et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11562430?dopt=AbstractPlus
Not in our library
1318.
Lorenzen A et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8937447?dopt=AbstractPlus
Not in our library
1319.
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Not in our library
1320.
Lovenberg TW et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10869375?dopt=AbstractPlus
Not in our library
1321.
Lu X et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15944007?dopt=AbstractPlus
Not in our library
1322.
Lu X et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20660766?dopt=AbstractPlus
Not in our library
1323.
Lu ZL et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17452338?dopt=AbstractPlus
Not in our library
1324.
Lucchelli A et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9283717?dopt=AbstractPlus
Not in our library
1325.
Luchetti G et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27705744?dopt=AbstractPlus
Not in our library
1326.
Lumley P et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2527074?dopt=AbstractPlus
Not in our library
1327.
Lundell I et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7493937?dopt=AbstractPlus
Not in our library
1328.
Lundkvist J et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8874139?dopt=AbstractPlus
Not in our library
1329.
Luo J et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19605502?dopt=AbstractPlus
Not in our library
1330.
Luo R et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21768377?dopt=AbstractPlus
Not in our library
1331.
Luo X et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25514935?dopt=AbstractPlus
Not in our library
1332.
Luttrell LM et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20427692?dopt=AbstractPlus
Not in our library
1333.
Lynch KR et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10391245?dopt=AbstractPlus
Not in our library
1334.
Lüttichau HR. (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20044480?dopt=AbstractPlus
Not in our library
1335.
Lüttichau HR et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12554737?dopt=AbstractPlus
Not in our library
1336.
Ma L et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19717450?dopt=AbstractPlus
Not in our library
1337.
Ma L et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26808470?dopt=AbstractPlus
Not in our library
1338.
Macaluso NJ et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21560248?dopt=AbstractPlus
Not in our library
1339.
MacDonald E et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9227000?dopt=AbstractPlus
Not in our library
1340.
Machwate M et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11408598?dopt=AbstractPlus
Not in our library
1341.
MacKenzie RG et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7907989?dopt=AbstractPlus
Not in our library
1342.
MacLennan SJ et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9283709?dopt=AbstractPlus
Not in our library
1343.
Maddox JF et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8551217?dopt=AbstractPlus
Not in our library
1344.
Madsen K et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21831646?dopt=AbstractPlus
Not in our library
1345.
Madsen P et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9857085?dopt=AbstractPlus
Not in our library
1346.
Madsen U et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15996690?dopt=AbstractPlus
Not in our library
1347.
Maeda DY et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25254640?dopt=AbstractPlus
Not in our library
1348.
Maeda K et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16476734?dopt=AbstractPlus
Not in our library
1349.
Maeda K et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11454872?dopt=AbstractPlus
Not in our library
1350.
Maekawa A et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19561298?dopt=AbstractPlus
Not in our library
1351.
Maggio R et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7805774?dopt=AbstractPlus
Not in our library
1352.
Maggiolini M et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15090535?dopt=AbstractPlus
Not in our library
1353.
Maguire JJ et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7647976?dopt=AbstractPlus
Not in our library
1354.
Maguire JJ et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11015293?dopt=AbstractPlus
Not in our library
1355.
Maguire JJ et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19325074?dopt=AbstractPlus
Not in our library
1356.
Maier DL et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19401496?dopt=AbstractPlus
Not in our library
1357.
Maiti K et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14651258?dopt=AbstractPlus
Not in our library
1358.
Maj M et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14573382?dopt=AbstractPlus
Not in our library
1359.
Majumdar ID et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21042212?dopt=AbstractPlus
Not in our library
1360.
Majumdar ID et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22157398?dopt=AbstractPlus
Not in our library
1361.
Majumdar S et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21621410?dopt=AbstractPlus
Not in our library
1362.
Malgouris C et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8472747?dopt=AbstractPlus
Not in our library
1363.
Malherbe P et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19751316?dopt=AbstractPlus
Not in our library
1364.
Malherbe P et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19542319?dopt=AbstractPlus
Not in our library
1365.
Malherbe P et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10216218?dopt=AbstractPlus
Not in our library
1366.
Malherbe P et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18536733?dopt=AbstractPlus
Not in our library
1367.
Malherbe P et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20404073?dopt=AbstractPlus
Not in our library
1368.
Mallee JJ et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11847213?dopt=AbstractPlus
Not in our library
1369.
Mamedova LK et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15081875?dopt=AbstractPlus
Not in our library
1370.
Mamillapalli R et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20032198?dopt=AbstractPlus
Not in our library
1371.
Mandala S et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11923495?dopt=AbstractPlus
Not in our library
1372.
Manglik A et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25981665?dopt=AbstractPlus
Not in our library
1373.
Mannaioni G et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10428410?dopt=AbstractPlus
Not in our library
1374.
Manning DR et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26179037?dopt=AbstractPlus
Not in our library
1375.
Mantey S et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/7684815?dopt=AbstractPlus
Not in our library
1376.
Mantey SA et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15102928?dopt=AbstractPlus
Not in our library
1377.
Mantey SA et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9325344?dopt=AbstractPlus
Not in our library
1378.
Marathe GK et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10497200?dopt=AbstractPlus
Not in our library
1379.
Maravillas-Montero JL et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25411203?dopt=AbstractPlus
Not in our library
1380.
Marazziti D et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19398891?dopt=AbstractPlus
Not in our library
1381.
Marazziti D et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21372109?dopt=AbstractPlus
Not in our library
1382.
Marazziti D et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17519329?dopt=AbstractPlus
Not in our library
1383.
Marchingo AJ et al (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/2964362?dopt=AbstractPlus
Not in our library10.1210/endo-122-4-1328
1384.
Marin P et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/21777185?dopt=AbstractPlus
Not in our library
1385.
Marlo JE et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19047481?dopt=AbstractPlus
Not in our library
1386.
Marteau F et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12815166?dopt=AbstractPlus
Not in our library
1387.
Martin PL et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8632314?dopt=AbstractPlus
Not in our library
1388.
Martin S et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12360476?dopt=AbstractPlus
Not in our library
1389.
Maruoka H et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20446735?dopt=AbstractPlus
Not in our library
1390.
Maruoka H et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21528910?dopt=AbstractPlus
Not in our library
1391.
Maruyama T et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11454473?dopt=AbstractPlus
Not in our library
1392.
Maruyama T et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12419312?dopt=AbstractPlus
Not in our library
1393.
Masuda Y et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12054613?dopt=AbstractPlus
Not in our library
1394.
Mathiesen JM et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16418339?dopt=AbstractPlus
Not in our library
1395.
Mathiesen JM et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12684257?dopt=AbstractPlus
Not in our library
1396.
Mathieu MC et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16154494?dopt=AbstractPlus
Not in our library
1397.
Matsufuji T et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25497965?dopt=AbstractPlus
Not in our library
1398.
Matsufuji T et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24412111?dopt=AbstractPlus
Not in our library
1399.
Matsumoto M et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11549267?dopt=AbstractPlus
Not in our library
1400.
Matsuura B et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15677347?dopt=AbstractPlus
Not in our library
1401.
Matsuura B et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11781320?dopt=AbstractPlus
Not in our library
1402.
Matsuura B et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16531413?dopt=AbstractPlus
Not in our library
1403.
Matteson PG et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18250320?dopt=AbstractPlus
Not in our library
1404.
Matthes H et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8450829?dopt=AbstractPlus
Not in our library
1405.
Mattsson C et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16055331?dopt=AbstractPlus
Not in our library
1406.
Matuszek MA et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9718274?dopt=AbstractPlus
Not in our library
1407.
Maudsley S et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15492280?dopt=AbstractPlus
Not in our library
1408.
May LT et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17525129?dopt=AbstractPlus
Not in our library
1409.
Mayeux PR et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1830308?dopt=AbstractPlus
Not in our library
1410.
Mayo KE et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12615957?dopt=AbstractPlus
Not in our library
1411.
Mazella J et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8795617?dopt=AbstractPlus
Not in our library
1412.
Maïga A et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23935897?dopt=AbstractPlus
Not in our library
1413.
McAllister G et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1608964?dopt=AbstractPlus
Not in our library
1414.
McAtee LC et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15261275?dopt=AbstractPlus
Not in our library
1415.
McCall RB et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15980060?dopt=AbstractPlus
Not in our library
1416.
McCall RB et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7965808?dopt=AbstractPlus
Not in our library
1417.
McClellan KJ et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9878991?dopt=AbstractPlus
Not in our library
1418.
McDonald J et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12967935?dopt=AbstractPlus
Not in our library
1419.
McGuire JJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14976230?dopt=AbstractPlus
Not in our library
1420.
McHugh D et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20346144?dopt=AbstractPlus
Not in our library
1421.
McHugh D et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16207832?dopt=AbstractPlus
Not in our library
1422.
McHugh D et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/21595653?dopt=AbstractPlus
Not in our library
1423.
McKeage K. (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25859983?dopt=AbstractPlus
Not in our library
1424.
McKee KK et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9441746?dopt=AbstractPlus
Not in our library
1425.
McKinnell RM et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23756062?dopt=AbstractPlus
Not in our library
1426.
McLatchie LM et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9620797?dopt=AbstractPlus
Not in our library
1427.
Mead EJ et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17023533?dopt=AbstractPlus
Not in our library
1428.
Medhurst AD et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12603839?dopt=AbstractPlus
Not in our library
1429.
Meena CL et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26854379?dopt=AbstractPlus
Not in our library
1430.
Meis S et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19815812?dopt=AbstractPlus
Not in our library
1431.
Mejean A et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8719421?dopt=AbstractPlus
Not in our library
1432.
Meng T et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18358099?dopt=AbstractPlus
Not in our library
1433.
Methven L et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19572943?dopt=AbstractPlus
Not in our library
1434.
Methven L et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19888965?dopt=AbstractPlus
Not in our library
1435.
Metra M et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23273292?dopt=AbstractPlus
Not in our library
1436.
Meyer MD et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9379432?dopt=AbstractPlus
Not in our library
1437.
Meyer MR et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/28343901?dopt=AbstractPlus
Not in our library
1438.
Meyer RC et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23690594?dopt=AbstractPlus
Not in our library
1439.
Meyerhof W. (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9600011?dopt=AbstractPlus
Not in our library
1440.
Mialet J et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10683202?dopt=AbstractPlus
Not in our library
1441.
Mialet J et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11030734?dopt=AbstractPlus
Not in our library
1442.
Mialet J et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10821780?dopt=AbstractPlus
Not in our library
1443.
Michel AD et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/1970500?dopt=AbstractPlus
Not in our library
1444.
Michel MC et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9549761?dopt=AbstractPlus
Not in our library
1445.
Middlemiss DN et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10443589?dopt=AbstractPlus
Not in our library
1446.
Mierau J et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7664822?dopt=AbstractPlus
Not in our library
1447.
Migeotte I et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15623572?dopt=AbstractPlus
Not in our library
1448.
Millan MJ et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7988633?dopt=AbstractPlus
Not in our library
1449.
Millan MJ et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9732398?dopt=AbstractPlus
Not in our library
1450.
Millan MJ et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10869410?dopt=AbstractPlus
Not in our library
1451.
Millan MJ et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12388666?dopt=AbstractPlus
Not in our library
1452.
Millan MJ et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10611634?dopt=AbstractPlus
Not in our library
1453.
Millan MJ et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7473180?dopt=AbstractPlus
Not in our library
1454.
Millar R et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11493674?dopt=AbstractPlus
Not in our library
1455.
Millar RP. (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16140177?dopt=AbstractPlus
Not in our library
1456.
Millar RP et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15082521?dopt=AbstractPlus
Not in our library
1457.
Miller BE et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26092545?dopt=AbstractPlus
Not in our library
1458.
Minamino N et al (1985 ) https://www.ncbi.nlm.nih.gov/pubmed/3839674?dopt=AbstractPlus
Not in our library
1459.
Minneman KP et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7969082?dopt=AbstractPlus
Not in our library
1460.
Miranda LP et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18412318?dopt=AbstractPlus
Not in our library
1461.
Mirzadegan T et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10770925?dopt=AbstractPlus
Not in our library
1462.
Mitselos A et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17074305?dopt=AbstractPlus
Not in our library
1463.
Mitsukawa K et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16339898?dopt=AbstractPlus
Not in our library
1464.
Miura S et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10066768?dopt=AbstractPlus
Not in our library
1465.
Mizuguchi T et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9113361?dopt=AbstractPlus
Not in our library
1466.
Mizuno H et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/30463988?dopt=AbstractPlus
Not in our library
1467.
Moeller I et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9166749?dopt=AbstractPlus
Not in our library
1468.
Mogha A et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24227709?dopt=AbstractPlus
Not in our library
1469.
Moguilevsky N et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7925364?dopt=AbstractPlus
Not in our library
1470.
Mohr M et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15163212?dopt=AbstractPlus
Not in our library
1471.
Molenaar P et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1472961?dopt=AbstractPlus
Not in our library
1472.
Molenaar P et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9117106?dopt=AbstractPlus
Not in our library
1473.
Molinari EJ et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8773460?dopt=AbstractPlus
Not in our library
1474.
Mollay C et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10422759?dopt=AbstractPlus
Not in our library
1475.
Mollereau C et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11325787?dopt=AbstractPlus
Not in our library
1476.
Mollereau C et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12242085?dopt=AbstractPlus
Not in our library
1477.
Mollereau C et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8849681?dopt=AbstractPlus
Not in our library
1478.
Mollereau C et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8137918?dopt=AbstractPlus
Not in our library
1479.
Mombaerts P. (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15034552?dopt=AbstractPlus
Not in our library
1480.
Monczor F et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12869657?dopt=AbstractPlus
Not in our library
1481.
Monk KR et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19745155?dopt=AbstractPlus
Not in our library
1482.
Monn JA et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25602126?dopt=AbstractPlus
Not in our library
1483.
Monn JA et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10090786?dopt=AbstractPlus
Not in our library
1484.
Monneret G et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12490611?dopt=AbstractPlus
Not in our library
1485.
Monnier C et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21063387?dopt=AbstractPlus
Not in our library
1486.
Montrose-Rafizadeh C et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9261127?dopt=AbstractPlus
Not in our library
1487.
Moody TW et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11931347?dopt=AbstractPlus
Not in our library
1488.
Moody TW et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25554218?dopt=AbstractPlus
Not in our library
1489.
Moody TW et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15134870?dopt=AbstractPlus
Not in our library
1490.
Moore K et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19723586?dopt=AbstractPlus
Not in our library
1491.
Moreland RB et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16153699?dopt=AbstractPlus
Not in our library
1492.
Moreno D et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11068102?dopt=AbstractPlus
Not in our library
1493.
Moreno Delgado D et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28661401?dopt=AbstractPlus
Not in our library
1494.
Moreno P et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23892571?dopt=AbstractPlus
Not in our library
1495.
Morfis M et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18599553?dopt=AbstractPlus
Not in our library
1496.
Morgan K et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12538601?dopt=AbstractPlus
Not in our library
1497.
Mori K et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15635449?dopt=AbstractPlus
Not in our library
1498.
Mori M et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10548501?dopt=AbstractPlus
Not in our library
1499.
Moriconi A et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25385614?dopt=AbstractPlus
Not in our library
1500.
Morinelli TA et al (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2530338?dopt=AbstractPlus
Not in our library
1501.
Morishima S et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17162094?dopt=AbstractPlus
Not in our library
1502.
Moriya Y et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/30044673?dopt=AbstractPlus
Not in our library
1503.
Moro O et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/8995389?dopt=AbstractPlus
Not in our library
1504.
Moro O et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10438479?dopt=AbstractPlus
Not in our library
1505.
Morokata T et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16339911?dopt=AbstractPlus
Not in our library
1506.
Moroni F et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12015200?dopt=AbstractPlus
Not in our library
1507.
Moroni F et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9152378?dopt=AbstractPlus
Not in our library
1508.
Morrow GB et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25015314?dopt=AbstractPlus
Not in our library
1509.
Morse KL et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11181941?dopt=AbstractPlus
Not in our library
1510.
Morton MF et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21493750?dopt=AbstractPlus
Not in our library
1511.
Mosberg HI et al (1983 ) https://www.ncbi.nlm.nih.gov/pubmed/6310598?dopt=AbstractPlus
Not in our library
1512.
Motoike T et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27140610?dopt=AbstractPlus
Not in our library
1513.
Mould R et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/23692283?dopt=AbstractPlus
Not in our library
1514.
Moulin A et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/22798076?dopt=AbstractPlus
Not in our library
1515.
Muccioli G et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11314756?dopt=AbstractPlus
Not in our library
1516.
Muda M et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16051677?dopt=AbstractPlus
Not in our library
1517.
Muff R et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10342886?dopt=AbstractPlus
Not in our library
1518.
Muley MM et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26140667?dopt=AbstractPlus
Not in our library
1519.
Munk SA et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8784451?dopt=AbstractPlus
Not in our library
1520.
Munro TA et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23976952?dopt=AbstractPlus
Not in our library
1521.
Murai N et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28859883?dopt=AbstractPlus
Not in our library
1522.
Murakami A et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20097776?dopt=AbstractPlus
Not in our library
1523.
Murakami M et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18466763?dopt=AbstractPlus
Not in our library
1524.
Murphy PM. (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12037138?dopt=AbstractPlus
Not in our library
1525.
Murphy PM et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10699158?dopt=AbstractPlus
Not in our library
1526.
Murphy PM et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1373134?dopt=AbstractPlus
Not in our library
1527.
Murugesan N et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12502366?dopt=AbstractPlus
Not in our library
1528.
Murza A et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26986036?dopt=AbstractPlus
Not in our library
1529.
Mutel V et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11080213?dopt=AbstractPlus
Not in our library
1530.
Muto T et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17360426?dopt=AbstractPlus
Not in our library
1531.
Müller A et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23335960?dopt=AbstractPlus
Not in our library
1532.
Müller A et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25516095?dopt=AbstractPlus
Not in our library
1533.
Müller A et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26505631?dopt=AbstractPlus
Not in our library
1534.
Müller T et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12727981?dopt=AbstractPlus
Not in our library
1535.
Nagahara T et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26267383?dopt=AbstractPlus
Not in our library
1536.
Nagase T et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18598020?dopt=AbstractPlus
Not in our library
1537.
Nagata-Kuroiwa R et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21390312?dopt=AbstractPlus
Not in our library
1538.
Naka M et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1386885?dopt=AbstractPlus
Not in our library
1539.
Nakamura M et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1657923?dopt=AbstractPlus
Not in our library
1540.
Nakamura M et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1333988?dopt=AbstractPlus
Not in our library
1541.
Nakamura S et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10780976?dopt=AbstractPlus
Not in our library
1542.
Nakamura T et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11118334?dopt=AbstractPlus
Not in our library
1543.
Nakane M et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15992586?dopt=AbstractPlus
Not in our library
1544.
Nambi P. (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8301559?dopt=AbstractPlus
Not in our library
1545.
Nambu H et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21971119?dopt=AbstractPlus
Not in our library
1546.
Namour F et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26852904?dopt=AbstractPlus
Not in our library
1547.
Napier C et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16298345?dopt=AbstractPlus
Not in our library
1548.
Napier C et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10193663?dopt=AbstractPlus
Not in our library
1549.
Navarro G et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25926444?dopt=AbstractPlus
Not in our library
1550.
Nawaratne V et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20406819?dopt=AbstractPlus
Not in our library
1551.
Nawaratne V et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18628403?dopt=AbstractPlus
Not in our library
1552.
Naya A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12614873?dopt=AbstractPlus
Not in our library
1553.
Neale JH. (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21740441?dopt=AbstractPlus
Not in our library
1554.
Nederpelt I et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26398856?dopt=AbstractPlus
Not in our library
1555.
Nederpelt I et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26774084?dopt=AbstractPlus
Not in our library
1556.
Nef S et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10391220?dopt=AbstractPlus
Not in our library
1557.
Negishi M et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7608175?dopt=AbstractPlus
Not in our library
1558.
Negoro N et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/24900210?dopt=AbstractPlus
Not in our library
1559.
Negri L et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16113687?dopt=AbstractPlus
Not in our library
1560.
Neill JD. (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11861490?dopt=AbstractPlus
Not in our library
1561.
Nelson CP et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16188951?dopt=AbstractPlus
Not in our library
1562.
Nelson DL et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9933142?dopt=AbstractPlus
Not in our library
1563.
Nelson DL et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20855361?dopt=AbstractPlus
Not in our library
1564.
Nelson G et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11509186?dopt=AbstractPlus
Not in our library
1565.
Nemeth EF. (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24050279?dopt=AbstractPlus
Not in our library
1566.
Nemeth EF et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11561095?dopt=AbstractPlus
Not in our library
1567.
Nemeth EF et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9520489?dopt=AbstractPlus
Not in our library
1568.
Nenasheva TA et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23357106?dopt=AbstractPlus
Not in our library
1569.
Nergårdh R et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16318870?dopt=AbstractPlus
Not in our library
1570.
Neschadim A et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24812057?dopt=AbstractPlus
Not in our library
1571.
Neumeyer JL et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14613319?dopt=AbstractPlus
Not in our library
1572.
Neveu C et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22800498?dopt=AbstractPlus
Not in our library
1573.
Newman-Tancredi A et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11040052?dopt=AbstractPlus
Not in our library
1574.
Newman-Tancredi A et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10431754?dopt=AbstractPlus
Not in our library
1575.
Newman-Tancredi A et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9760039?dopt=AbstractPlus
Not in our library
1576.
Newman-Tancredi A et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19154445?dopt=AbstractPlus
Not in our library
1577.
Newman-Tancredi A et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9550290?dopt=AbstractPlus
Not in our library
1578.
Newman-Tancredi A et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1386736?dopt=AbstractPlus
Not in our library
1579.
Nguyen T et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11179435?dopt=AbstractPlus
Not in our library
1580.
Ni YY et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24574718?dopt=AbstractPlus
Not in our library
1581.
Nickolls SA et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12604699?dopt=AbstractPlus
Not in our library
1582.
Nicole P et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10801840?dopt=AbstractPlus
Not in our library
1583.
Nie YY et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22410249?dopt=AbstractPlus
Not in our library
1584.
Niedernberg A et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12618218?dopt=AbstractPlus
Not in our library
1585.
Nielsen MS et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10085125?dopt=AbstractPlus
Not in our library
1586.
Nieto-Posadas A et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22101604?dopt=AbstractPlus
Not in our library
1587.
Nieuwenhuijs VB et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10092986?dopt=AbstractPlus
Not in our library
1588.
Nikaido Y et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25425658?dopt=AbstractPlus
Not in our library
1589.
Nile AH et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29632413?dopt=AbstractPlus
Not in our library
1590.
Nilsson I et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11738246?dopt=AbstractPlus
Not in our library
1591.
Nilsson NE et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12684041?dopt=AbstractPlus
Not in our library
1592.
Ning Y et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18724386?dopt=AbstractPlus
Not in our library
1593.
Nishizawa N et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27589480?dopt=AbstractPlus
Not in our library
1594.
Niswender CM et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20026717?dopt=AbstractPlus
Not in our library
1595.
Niswender CM et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18664603?dopt=AbstractPlus
Not in our library
1596.
No authors listed. (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/3071214?dopt=AbstractPlus
Not in our library
1597.
No authors listed. (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16498716?dopt=AbstractPlus
Not in our library
1598.
Noble F et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10581329?dopt=AbstractPlus
Not in our library
1599.
Noda M et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12558985?dopt=AbstractPlus
Not in our library
1600.
Nonaka Y et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16185654?dopt=AbstractPlus
Not in our library
1601.
Nosjean O et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10913150?dopt=AbstractPlus
Not in our library
1602.
Nosjean O et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11331072?dopt=AbstractPlus
Not in our library
1603.
Nothacker H‐P et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10559967?dopt=AbstractPlus
Not in our library
1604.
Nothacker HP et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11093801?dopt=AbstractPlus
Not in our library
1605.
Nygaard R et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23374348?dopt=AbstractPlus
Not in our library
1606.
Näsman J et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10799315?dopt=AbstractPlus
Not in our library
1607.
O’Flaherty JT et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9829988?dopt=AbstractPlus
Not in our library
1608.
O’Sullivan SE. (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17704824?dopt=AbstractPlus
Not in our library
1609.
Obiefuna PC et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16020631?dopt=AbstractPlus
Not in our library
1610.
Obika K et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8719417?dopt=AbstractPlus
Not in our library
1611.
Ochi T et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15686911?dopt=AbstractPlus
Not in our library
1612.
Oda T et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10973974?dopt=AbstractPlus
Not in our library
1613.
Oertel BG et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19116204?dopt=AbstractPlus
Not in our library
1614.
Offermanns S et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21454438?dopt=AbstractPlus
Not in our library
1615.
Ogita T et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9038918?dopt=AbstractPlus
Not in our library
1616.
Oh da Y et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24997608?dopt=AbstractPlus
Not in our library
1617.
Oh DY et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20813258?dopt=AbstractPlus
Not in our library
1618.
Ohashi T et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25959255?dopt=AbstractPlus
Not in our library
1619.
Ohki-Hamazaki H et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9367152?dopt=AbstractPlus
Not in our library
1620.
Ohlmann P et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/22892887?dopt=AbstractPlus
Not in our library
1621.
Ohsu T et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19892707?dopt=AbstractPlus
Not in our library10.1074/jbc.m109.029165
1622.
Ohta H et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14500756?dopt=AbstractPlus
Not in our library
1623.
Ohtaki T et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10601261?dopt=AbstractPlus
Not in our library
1624.
Ohtaki T et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11385580?dopt=AbstractPlus
Not in our library
1625.
Oka S et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17765871?dopt=AbstractPlus
Not in our library
1626.
Oka S et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20361937?dopt=AbstractPlus
Not in our library
1627.
Oka S et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/18845565?dopt=AbstractPlus
Not in our library
1628.
Okamoto H et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9765227?dopt=AbstractPlus
Not in our library
1629.
Okamura N et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17669576?dopt=AbstractPlus
Not in our library
1630.
Okawa H et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10369464?dopt=AbstractPlus
Not in our library
1631.
Okinaga S et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12899627?dopt=AbstractPlus
Not in our library
1632.
Okuda-Ashitaka E et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8940129?dopt=AbstractPlus
Not in our library
1633.
Okuno T et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18378794?dopt=AbstractPlus
Not in our library
1634.
Olender T et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/19129093?dopt=AbstractPlus
Not in our library
1635.
Olianas MC et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9862767?dopt=AbstractPlus
Not in our library
1636.
Ongini E et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9933143?dopt=AbstractPlus
Not in our library
1637.
Oo ML et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17237497?dopt=AbstractPlus
Not in our library
1638.
Osada M et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12445827?dopt=AbstractPlus
Not in our library
1639.
Osborn O et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22653059?dopt=AbstractPlus
Not in our library
1640.
Ott TR et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16904643?dopt=AbstractPlus
Not in our library
1641.
Oury-Donat F et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7616392?dopt=AbstractPlus
Not in our library
1642.
Overington JP et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17139284?dopt=AbstractPlus
Not in our library
1643.
Overton HA et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16517404?dopt=AbstractPlus
Not in our library
1644.
Padmanabhan S et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19059244?dopt=AbstractPlus
Not in our library
1645.
Palacios JM et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28265714?dopt=AbstractPlus
Not in our library
1646.
Palani A et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/24900372?dopt=AbstractPlus
Not in our library
1647.
Palani A et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11585437?dopt=AbstractPlus
Not in our library
1648.
Palchaudhuri MR et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9851694?dopt=AbstractPlus
Not in our library
1649.
Pan S et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24900670?dopt=AbstractPlus
Not in our library
1650.
Pan S et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/17114004?dopt=AbstractPlus
Not in our library
1651.
Pang L et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9832122?dopt=AbstractPlus
Not in our library
1652.
Pantel J et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16511605?dopt=AbstractPlus
Not in our library
1653.
Panula P et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26084539?dopt=AbstractPlus
Not in our library
1654.
Parent JL et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8798529?dopt=AbstractPlus
Not in our library
1655.
Park D et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17960134?dopt=AbstractPlus
Not in our library
1656.
Parker CA et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22223878?dopt=AbstractPlus
Not in our library
1657.
Parker EM et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8863519?dopt=AbstractPlus
Not in our library
1658.
Parody TR et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15207250?dopt=AbstractPlus
Not in our library
1659.
Paruchuri S et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19822647?dopt=AbstractPlus
Not in our library
1660.
Pasternak GW et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24076545?dopt=AbstractPlus
Not in our library
1661.
Patacchini R et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14645137?dopt=AbstractPlus
Not in our library
1662.
Patane MA et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9548811?dopt=AbstractPlus
Not in our library
1663.
Patat O et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27476656?dopt=AbstractPlus
Not in our library
1664.
Patel P et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18292294?dopt=AbstractPlus
Not in our library
1665.
Patel S et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8967990?dopt=AbstractPlus
Not in our library
1666.
Patel YC et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7988476?dopt=AbstractPlus
Not in our library
1667.
Patra MC et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24938207?dopt=AbstractPlus
Not in our library
1668.
Pauli A et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24407481?dopt=AbstractPlus
Not in our library
1669.
Pauwels PJ et al (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/2462161?dopt=AbstractPlus
Not in our library
1670.
Pauwels PJ et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12649300?dopt=AbstractPlus
Not in our library
1671.
Payza K. (2003 ) In The Delta Receptor Edited by Chang KJ: CRC Press: 261-275 [ISBN: 0824740319]
Not in our library
1672.
Pazos A et al (1984 ) https://www.ncbi.nlm.nih.gov/pubmed/6519175?dopt=AbstractPlus
Not in our library
1673.
Pearlstein R et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12747773?dopt=AbstractPlus
Not in our library
1674.
Peirce SM et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11406470?dopt=AbstractPlus
Not in our library
1675.
Pellegrini-Giampietro DE et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8799579?dopt=AbstractPlus
Not in our library
1676.
Pellicciari R et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/20014870?dopt=AbstractPlus
Not in our library
1677.
Pellicciari R et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8667369?dopt=AbstractPlus
Not in our library
1678.
Peltonen JM et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9760042?dopt=AbstractPlus
Not in our library10.1016/s0014-2999(98)00518-4
1679.
Pena A et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17300166?dopt=AbstractPlus
Not in our library
1680.
Pendergast W et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11206448?dopt=AbstractPlus
Not in our library
1681.
Peng Y et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29398112?dopt=AbstractPlus
Not in our library
1682.
Peng YM et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21724806?dopt=AbstractPlus
Not in our library
1683.
Peralta EG et al (1987 ) https://www.ncbi.nlm.nih.gov/pubmed/3443095?dopt=AbstractPlus
Not in our library
1684.
Perdonà E et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21034740?dopt=AbstractPlus
Not in our library
1685.
Pereira JP. (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19597478?dopt=AbstractPlus
Not in our library
1686.
Perkins AV et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7595134?dopt=AbstractPlus
Not in our library
1687.
Perlman S et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7829475?dopt=AbstractPlus
Not in our library
1688.
Perretti M et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12368905?dopt=AbstractPlus
Not in our library
1689.
Perron A et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15637074?dopt=AbstractPlus
Not in our library
1690.
Pertwee RG. (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/23108552?dopt=AbstractPlus
Not in our library
1691.
Pertwee RG. (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11060760?dopt=AbstractPlus
Not in our library
1692.
Pertwee RG et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/21079038?dopt=AbstractPlus
Not in our library
1693.
Peter MG et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/7881728?dopt=AbstractPlus
Not in our library
1694.
Petersen J et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28790300?dopt=AbstractPlus
Not in our library
1695.
Petersen KF et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11719833?dopt=AbstractPlus
Not in our library
1696.
Petersen PS et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21784784?dopt=AbstractPlus
Not in our library
1697.
Petersen SC et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25695270?dopt=AbstractPlus
Not in our library
1698.
Petitet F et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8733746?dopt=AbstractPlus
Not in our library
1699.
Petrel C et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/14506236?dopt=AbstractPlus
Not in our library
1700.
Petrie WK et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24379833?dopt=AbstractPlus
Not in our library
1701.
Petrucci V et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28842619?dopt=AbstractPlus
Not in our library
1702.
Phebus LA et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9395253?dopt=AbstractPlus
Not in our library
1703.
Piali L et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/29226621?dopt=AbstractPlus
Not in our library
1704.
Pihlavisto M et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9824686?dopt=AbstractPlus
Not in our library
1705.
Pin J‐P et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10443583?dopt=AbstractPlus
Not in our library
1706.
Pin JP et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12769621?dopt=AbstractPlus
Not in our library
1707.
Pin JP et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27905440?dopt=AbstractPlus
Not in our library
1708.
Pin JP et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19723778?dopt=AbstractPlus
Not in our library
1709.
Pin JP et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15451400?dopt=AbstractPlus
Not in our library
1710.
Pin JP et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17329545?dopt=AbstractPlus
Not in our library
1711.
Pinard A et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20655485?dopt=AbstractPlus
Not in our library
1712.
Pisegna JR et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11193823?dopt=AbstractPlus
Not in our library
1713.
Pitkin SL et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20605969?dopt=AbstractPlus
Not in our library
1714.
Pittolo S et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25173999?dopt=AbstractPlus
Not in our library
1715.
Pizzonero M et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25380412?dopt=AbstractPlus
Not in our library
1716.
Planagumà A et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23607720?dopt=AbstractPlus
Not in our library
1717.
Plöckinger U et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22065857?dopt=AbstractPlus
Not in our library
1718.
Pohl SL et al (1969 ) https://www.ncbi.nlm.nih.gov/pubmed/4305077?dopt=AbstractPlus
Not in our library
1719.
Popova JS et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7798906?dopt=AbstractPlus
Not in our library
1720.
Popp BD et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14744619?dopt=AbstractPlus
Not in our library
1721.
Porcher C et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15726424?dopt=AbstractPlus
Not in our library
1722.
Porter RA et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11459658?dopt=AbstractPlus
Not in our library
1723.
Porter RH et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16040814?dopt=AbstractPlus
Not in our library
1724.
Portoghese PS et al (1987 ) https://www.ncbi.nlm.nih.gov/pubmed/2444704?dopt=AbstractPlus
Not in our library
1725.
Portoghese PS et al (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/2832195?dopt=AbstractPlus
Not in our library
1726.
Posokhova E et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25558062?dopt=AbstractPlus
Not in our library
1727.
Poulain R et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11585443?dopt=AbstractPlus
Not in our library
1728.
Powell WS et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9920859?dopt=AbstractPlus
Not in our library
1729.
Powell WS et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1326548?dopt=AbstractPlus
Not in our library
1730.
Power CA et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9294137?dopt=AbstractPlus
Not in our library
1731.
Powers SP et al (1988 ) https://www.ncbi.nlm.nih.gov/pubmed/3410633?dopt=AbstractPlus
Not in our library
1732.
Poyner DR et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12037140?dopt=AbstractPlus
Not in our library
1733.
Prat M et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19653626?dopt=AbstractPlus
Not in our library
1734.
Price MJ. (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/27886821?dopt=AbstractPlus
Not in our library
1735.
Price MR. (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16113085?dopt=AbstractPlus
Not in our library
1736.
Primus RJ et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9262371?dopt=AbstractPlus
Not in our library
1737.
Procopiou PA et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20462258?dopt=AbstractPlus
Not in our library
1738.
Procopiou PA et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21381763?dopt=AbstractPlus
Not in our library
1739.
Proia RL et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25831442?dopt=AbstractPlus
Not in our library
1740.
Prossnitz ER et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26023144?dopt=AbstractPlus
Not in our library
1741.
Prossnitz ER et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/26189910?dopt=AbstractPlus
Not in our library
1742.
Pruneau D et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10596852?dopt=AbstractPlus
Not in our library
1743.
Prömel S et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23850273?dopt=AbstractPlus
Not in our library
1744.
Prömel S et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22837050?dopt=AbstractPlus
Not in our library
1745.
Pugsley TA et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/8531103?dopt=AbstractPlus
Not in our library
1746.
Putula J et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22079339?dopt=AbstractPlus
Not in our library
1747.
Putula J et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25132134?dopt=AbstractPlus
Not in our library
1748.
Putula J et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21362456?dopt=AbstractPlus
Not in our library
1749.
Pérez-Garci E et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16701210?dopt=AbstractPlus
Not in our library
1750.
Qi T et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/22946511?dopt=AbstractPlus
Not in our library
1751.
Quancard J et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22999882?dopt=AbstractPlus
Not in our library
1752.
Quinn SJ et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15201280?dopt=AbstractPlus
Not in our library
1753.
Quinn SJ et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9677383?dopt=AbstractPlus
Not in our library
1754.
Quinn SJ et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9357776?dopt=AbstractPlus
Not in our library
1755.
Quinton L et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20015090?dopt=AbstractPlus
Not in our library
1756.
Quitterer U et al (2019 ) https://www.ncbi.nlm.nih.gov/pubmed/30503206?dopt=AbstractPlus
Not in our library
1757.
Quock RM et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9178661?dopt=AbstractPlus
Not in our library
1758.
Raczka KA et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20628342?dopt=AbstractPlus
Not in our library
1759.
Rajaratnam SM et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19054552?dopt=AbstractPlus
Not in our library
1760.
Rakowski E et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16171813?dopt=AbstractPlus
Not in our library
1761.
Raleigh DR et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30340023?dopt=AbstractPlus
Not in our library
1762.
Ramachandran R et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21576245?dopt=AbstractPlus
Not in our library
1763.
Ramachandran R et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28126849?dopt=AbstractPlus
Not in our library
1764.
Ramachandran R et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22212680?dopt=AbstractPlus
Not in our library
1765.
Ramage AG et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/19086344?dopt=AbstractPlus
Not in our library
1766.
Ramos-Álvarez I et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25976083?dopt=AbstractPlus
Not in our library
1767.
Ramos-Álvarez I et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26524625?dopt=AbstractPlus
Not in our library
1768.
Ramsay D et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15266013?dopt=AbstractPlus
Not in our library
1769.
Randeva HS et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11600545?dopt=AbstractPlus
Not in our library
1770.
Rao A et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/28476646?dopt=AbstractPlus
Not in our library
1771.
Rashid M et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12738034?dopt=AbstractPlus
Not in our library
1772.
Rask-Andersen M et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24016212?dopt=AbstractPlus
Not in our library
1773.
Rasmussen SG et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21228869?dopt=AbstractPlus
Not in our library
1774.
Rasmussen SG et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21772288?dopt=AbstractPlus
Not in our library
1775.
Ratnala VR et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15206929?dopt=AbstractPlus
Not in our library
1776.
Raufman JP et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1704369?dopt=AbstractPlus
Not in our library
1777.
Ravasi S et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11996896?dopt=AbstractPlus
Not in our library
1778.
Rawashdeh O et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21182402?dopt=AbstractPlus
Not in our library
1779.
Raychowdhury MK et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8034687?dopt=AbstractPlus
Not in our library
1780.
Raynor K et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8114680?dopt=AbstractPlus
Not in our library
1781.
Read C et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/27475715?dopt=AbstractPlus
Not in our library
1782.
Reavill C et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10188965?dopt=AbstractPlus
Not in our library
1783.
Reavill C et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10945872?dopt=AbstractPlus
Not in our library
1784.
Regoli D et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9650825?dopt=AbstractPlus
Not in our library
1785.
Reid RC et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/25259874?dopt=AbstractPlus
Not in our library
1786.
Reid RC et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24257095?dopt=AbstractPlus
Not in our library
1787.
Reinscheid RK et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16144971?dopt=AbstractPlus
Not in our library
1788.
Resnati M et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11818541?dopt=AbstractPlus
Not in our library
1789.
Revankar CM et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15705806?dopt=AbstractPlus
Not in our library
1790.
Revel FG et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21525407?dopt=AbstractPlus
Not in our library
1791.
Rexen Ulven E et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29968758?dopt=AbstractPlus
Not in our library
1792.
Reynaud R et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22466334?dopt=AbstractPlus
Not in our library
1793.
Reynolds EE et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7733918?dopt=AbstractPlus
Not in our library
1794.
Reynolds GP et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7780656?dopt=AbstractPlus
Not in our library
1795.
Rezgaoui M et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16443751?dopt=AbstractPlus
Not in our library
1796.
Rhee MH et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9379442?dopt=AbstractPlus
Not in our library
1797.
Ricci A et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8051291?dopt=AbstractPlus
Not in our library
1798.
Ricci A et al (1995 ) https://www.ncbi.nlm.nih.gov/pubmed/7759603?dopt=AbstractPlus
Not in our library
1799.
Riccio G et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/29293331?dopt=AbstractPlus
Not in our library
1800.
Rice AS et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24507377?dopt=AbstractPlus
Not in our library
1801.
Richard F et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11723247?dopt=AbstractPlus
Not in our library
1802.
Richardson RM et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12626541?dopt=AbstractPlus
Not in our library
1803.
Riddy DM et al (2017 ) https://www.ncbi.nlm.nih.gov/pubmed/27864425?dopt=AbstractPlus
Not in our library
1804.
Rinaldi-Carmona M et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/8070571?dopt=AbstractPlus
Not in our library
1805.
Rinaldi-Carmona M et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9454810?dopt=AbstractPlus
Not in our library
1806.
Rinaldi-Carmona M et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8614277?dopt=AbstractPlus
Not in our library
1807.
Rinne MK et al (2018 ) https://www.ncbi.nlm.nih.gov/pubmed/30194937?dopt=AbstractPlus
Not in our library
1808.
Riobo NA et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16885213?dopt=AbstractPlus
Not in our library
1809.
Rivail L et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15351779?dopt=AbstractPlus
Not in our library
1810.
Rivier J et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12361401?dopt=AbstractPlus
Not in our library
1811.
Rivier J et al (1991 ) https://www.ncbi.nlm.nih.gov/pubmed/1850267?dopt=AbstractPlus
Not in our library
1812.
Rivier JE et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24269930?dopt=AbstractPlus
Not in our library
1813.
Rivkees SA et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/9920910?dopt=AbstractPlus
Not in our library
1814.
Rizzi A et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9095082?dopt=AbstractPlus
Not in our library
1815.
Robas N et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12915402?dopt=AbstractPlus
Not in our library
1816.
Roecker AJ et al (2016 ) https://www.ncbi.nlm.nih.gov/pubmed/26317591?dopt=AbstractPlus
Not in our library
1817.
Rohrer SP et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9784130?dopt=AbstractPlus
Not in our library
1818.
Romano M et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8757340?dopt=AbstractPlus
Not in our library
1819.
Roos RS et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9211859?dopt=AbstractPlus
Not in our library
1820.
Rosenbaum DM et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21228876?dopt=AbstractPlus
Not in our library
1821.
Rosengren AH et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/19965390?dopt=AbstractPlus
Not in our library
1822.
Roseweir AK et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19321788?dopt=AbstractPlus
Not in our library
1823.
Rosier A et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/9027929?dopt=AbstractPlus
Not in our library
1824.
Ross RA et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10188977?dopt=AbstractPlus
Not in our library
1825.
Roth BL et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/12192085?dopt=AbstractPlus
Not in our library
1826.
Roth BL et al (1994 ) https://www.ncbi.nlm.nih.gov/pubmed/7908055?dopt=AbstractPlus
Not in our library
1827.
Rothman RB et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/11104741?dopt=AbstractPlus
Not in our library
1828.
Roush ED et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9654151?dopt=AbstractPlus
Not in our library
1829.
Roussin A et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/16129413?dopt=AbstractPlus
Not in our library
1830.
Rovati GE et al (1992 ) https://www.ncbi.nlm.nih.gov/pubmed/1329767?dopt=AbstractPlus
Not in our library
1831.
Rowley M et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8642551?dopt=AbstractPlus
Not in our library
1832.
Royer JF et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17714552?dopt=AbstractPlus
Not in our library
1833.
Ruffing N et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9790730?dopt=AbstractPlus
Not in our library
1834.
Ruffner H et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22815884?dopt=AbstractPlus
Not in our library
1835.
Ruiu S et al (2003 ) https://www.ncbi.nlm.nih.gov/pubmed/12663689?dopt=AbstractPlus
Not in our library
1836.
Ruiz-Ferrer M et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21858136?dopt=AbstractPlus
Not in our library
1837.
Ruiz-Medina J et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21352831?dopt=AbstractPlus
Not in our library
1838.
Russell FD et al (1996 ) https://www.ncbi.nlm.nih.gov/pubmed/8904635?dopt=AbstractPlus
Not in our library
1839.
Russell JL et al (2012 ) https://www.ncbi.nlm.nih.gov/pubmed/22462679?dopt=AbstractPlus
Not in our library
1840.
Ruzza C et al (2015 ) https://www.ncbi.nlm.nih.gov/pubmed/25692025?dopt=AbstractPlus
Not in our library
1841.
Ruzza C et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20172007?dopt=AbstractPlus
Not in our library
1842.
Ryan PJ et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/24297931?dopt=AbstractPlus
Not in our library
1843.
Ryberg E et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17876302?dopt=AbstractPlus
Not in our library
1844.
Ryman-Rasmussen JP et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17067639?dopt=AbstractPlus
Not in our library
1845.
Römpler H et al (2005 ) https://www.ncbi.nlm.nih.gov/pubmed/15987686?dopt=AbstractPlus
Not in our library
1846.
Rühmann A et al (2002 ) https://www.ncbi.nlm.nih.gov/pubmed/11835994?dopt=AbstractPlus
Not in our library
1847.
Saar I et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23600864?dopt=AbstractPlus
Not in our library
1848.
Sabbatini FM et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20593439?dopt=AbstractPlus
Not in our library
1849.
Sabroe I et al (2000 ) https://www.ncbi.nlm.nih.gov/pubmed/10854442?dopt=AbstractPlus
Not in our library
1850.
Sairam MR. (1989 ) https://www.ncbi.nlm.nih.gov/pubmed/2542111?dopt=AbstractPlus
Not in our library
1851.
Saito M et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9264324?dopt=AbstractPlus
Not in our library
1852.
Sakurai T et al (1998 ) https://www.ncbi.nlm.nih.gov/pubmed/9491897?dopt=AbstractPlus
Not in our library
1853.
Sakurai T et al (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24486398?dopt=AbstractPlus
Not in our library
1854.
Sakurai T et al (1990 ) https://www.ncbi.nlm.nih.gov/pubmed/2175397?dopt=AbstractPlus
Not in our library
1855.
Sallinen J et al (2007 ) https://www.ncbi.nlm.nih.gov/pubmed/17220913?dopt=AbstractPlus
Not in our library
1856.
Salmon M et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23435542?dopt=AbstractPlus
Not in our library
1857.
Salvatore CA et al (2008 ) https://www.ncbi.nlm.nih.gov/pubmed/18039958?dopt=AbstractPlus
Not in our library
1858.
Salvatore CA et al (1993 ) https://www.ncbi.nlm.nih.gov/pubmed/8234299?dopt=AbstractPlus
Not in our library
1859.
Sams AG et al (2010 ) https://www.ncbi.nlm.nih.gov/pubmed/20684563?dopt=AbstractPlus
Not in our library
1860.
Sanger GJ. (2014 ) https://www.ncbi.nlm.nih.gov/pubmed/24438586?dopt=AbstractPlus
Not in our library
1861.
Sanger GJ et al (2011 ) https://www.ncbi.nlm.nih.gov/pubmed/21531468?dopt=AbstractPlus
Not in our library
1862.
Sanger GJ et al (2013 ) https://www.ncbi.nlm.nih.gov/pubmed/23189978?dopt=AbstractPlus
Not in our library
1863.
Sanger GJ et al (2009 ) https://www.ncbi.nlm.nih.gov/pubmed/19374732?dopt=AbstractPlus
Not in our library
1864.
Sanna MG et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/14732717?dopt=AbstractPlus
Not in our library
1865.
Sanna MG et al (2006 ) https://www.ncbi.nlm.nih.gov/pubmed/16829954?dopt=AbstractPlus
Not in our library
1866.
Sano H et al (2004 ) https://www.ncbi.nlm.nih.gov/pubmed/15203211?dopt=AbstractPlus
Not in our library
1867.
Sarau HM et al (1999 ) https://www.ncbi.nlm.nih.gov/pubmed/10462554?dopt=AbstractPlus
Not in our library
1868.
Sarau HM et al (2001 ) https://www.ncbi.nlm.nih.gov/pubmed/11226387?dopt=AbstractPlus
Not in our library
1869.
Sarau HM et al (1997 ) https://www.ncbi.nlm.nih.gov/pubmed/9190866?dopt=AbstractPlus
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1871.
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1872.
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The first 2000 of 2444 references. The rest are in the paper itself.

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THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: G protein‐coupled receptors

Abstract

Full text

Conflict of interest

Overview

GPCR families

Pseudogenes

Olfactory receptors

Further reading on G protein‐coupled receptors

Family structure

Overview

Table 1

Further reading on Class A Orphans

Overview

Further reading on Class C Orphans

Overview

Sweet/Umami

Comments

Further reading on Taste 1 receptors

http://www.guidetopharmacology.org/GRAC/FamilyDisplayForward?familyId=117

Overview

Further reading on Taste 2 receptors

Further reading on Orphan and other 7TM receptors

Overview

Comments

Further reading on 5‐Hydroxytryptamine receptors

Overview

Comments

Further reading on Acetylcholine receptors (muscarinic)

Overview

Comments

Further reading on Adenosine receptors

Overview

Further reading on Adhesion Class GPCRs

Overview

Adrenoceptors, α1

Comments

Adrenoceptors, α2

Comments

Adrenoceptors, β

Comments

Further reading on Adrenoceptors

Overview

Comments

Further reading on Angiotensin receptors

Overview

Comments

Further reading on Apelin receptor

Overview

Comments

Further reading on Bile acid receptor

Overview

Comments

Further reading on Bombesin receptors

Overview

Further reading on Bradykinin receptors

Overview

Comments

Further reading on Calcitonin receptors

Overview

Comments

Further reading on Calcium‐sensing receptor

Overview

Comments

Further reading on Cannabinoid receptors

Overview

Comments

Further reading on Chemerin receptors

Overview

Comments

Further reading on Chemokine receptors

Overview

Comments

Further reading on Cholecystokinin receptors

Overview

Comments

Ligands associated with FZD signalling

Further reading on Class Frizzled GPCRs

Overview

Comments