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DISC1-binding proteins in neural development, signalling and schizophrenia

Nicholas J. Bradshaw, David J. Porteous

Neuropharmacology · 2012 · Review

doi:10.1016/j.neuropharm.2010.12.027

Abstract

In the decade since Disrupted in Schizophrenia 1 (DISC1) was first identified it has become one of the most convincing risk genes for major mental illness. As a multi-functional scaffold protein, DISC1 has multiple identified protein interaction partners that highlight pathologically relevant molecular pathways with potential for pharmaceutical intervention. Amongst these are proteins involved in neuronal migration (e.g. APP, Dixdc1, LIS1, NDE1, NDEL1), neural progenitor proliferation (GSK3β), neurosignalling (Girdin, GSK3β, PDE4) and synaptic function (Kal7, TNIK). Furthermore, emerging evidence of genetic association (NDEL1, PCM1, PDE4B) and copy number variation (NDE1) implicate several DISC1-binding partners as risk factors for schizophrenia in their own right. Thus, a picture begins to emerge of DISC1 as a key hub for multiple critical developmental pathways within the brain, disruption of which can lead to a variety of psychiatric illness phenotypes.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 22, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

A key objective of genetics and genomics research into psychiatric illness is to identify perturbed biological pathways and, as a consequence, potential targets for pharmacological intervention. The genetic entrée point need not itself explain a large fraction of the liability to schizophrenia – it is sufficient that genetic abrogation can cause schizophrenia. DISC1 and the extended DISC1 pathway illustrate this contention par excellence. DISC1 was identified through a unique family in which a chromosomal translocation event co-segregates strongly with major mental illness. This translocation event directly disrupts both a protein coding gene, DISC1, and an antisense RNA only gene, DISC2. In the intervening period, the DISC locus has been repeatedly implicated in psychiatric illness by genetic linkage, association and mutation detection (reviewed in, see Table 1 for references and summaries of recent studies). Some studies have also pointed to epistatic interactions between the DISC locus and other candidate genes. Despite these many confirmatory studies, there are also negative studies ( and references in Table 1) and, as yet, no firm basis on which to estimate the proportion of genetic liability attributable to the DISC locus. The DISC locus has appeared as a gene-wide, but not a genome-wide finding in some but not other studies. The critical issue is what we can learn from the identification of DISC1 regarding the specifics and generalities of the biological underpinning of schizophrenia and other major mental illness.

The DISC1 protein has no known enzymatic activity; rather it exerts its effect on multiple proteins through interaction to modulate their functional states and biological activities in time and space. Many putative interacting proteins have been identified through extensive yeast-2-hybrid screening and, where these have been examined, a large proportion have been validated by downstream experimentation (reviewed in ). These multiple interactions, combined with the widespread subcellular distribution of DISC1 (reviewed in ), a complex pattern of protein isoforms and splice variants, have led to the suggestion that DISC1 acts as a protein scaffold within the cell, dynamically interacting with and affecting the function of different proteins at different locations and developmental times. DISC1-related psychiatric illness is therefore likely to arise through the simultaneous dysregulation of not just one, but more likely several, protein interactions, physiological states and activities, with a consequential complexity and pervasiveness of effect. Identifying the key DISC1 interactors is therefore of exceptional importance in coming to understand the nature of the devastating condition that is schizophrenia, and will facilitate the search for downstream elements which may be susceptible to pharmaceutical intervention.

In this review, we will focus on what is known about the biological functions of DISC1-interacting proteins, with particular attention to aspects of their biology which potentially relate to psychiatric illness, through effects on neurodevelopment, neurotransmission or neurosignalling, along with the emerging genetic evidence implicating many of these as schizophrenia-risk factors in their own right. Whereas a neurodevelopmental component to schizophrenia is well established, and pre-morbid features are recognised, it is typically not until adolescence or early adulthood that the debilitating symptoms emerge. That DISC1 and its pathway of interacting proteins affect both neurodevelopmental pathways and also signalling pathways in the adult brain, suggest that the study of DISC1 genetics and biology may help towards a more unified understanding of schizophrenia and with it the potential to develop rational interventions in the symptomatic adult and or even earlier.

DISC1-binding partners in cytoskeletal functions and neurite outgrowth

The complex and intricate task of co-ordinating the microtubule network of neurons, which is vital for maintaining correct development, morphology and migration, is performed in large part by the microtubule organising centre, or centrosome. Multiple lines of evidence demonstrate that DISC1 is part of a protein complex at the centrosome (Fig. 1 and references in the legend) and is involved in cytoskeletal processes involved in neuronal migration, including nucleokinesis and neurite outgrowth. LIS1, NDE1, and NDEL1 are a trio of such centrosomal DISC1 interactors which play pivotal roles in the progression of the cell cycle, dynein-related transport along microtubules and nucleokinesis (reviewed in ). The localisation of NDEL1 and LIS1 in axons is known to be dependent on expression of DISC1. Knock-down of either NDEL1 or LIS1 using RNAi in culture leads to reduced neurite outgrowth, while granule neurons from heterozygous NDEL1 or LIS1 knock-out mice show impaired migration in in vitro assays. NDEL1 is also known to play a role in axon regeneration after injury and has an additional DISC1-modulated function as a cysteine endopeptidase which appears to be important for regulation of neurite outgrowth. Although highly similar in amino-acid sequence to NDEL1, the role of NDE1 in many of these processes has yet to be determined.

DISC1 is also known to be involved in transport along microtubules to the distal parts of axons as part of a ternary complex with kinesin-1 and the adaptor protein Grb2. Cargo transported in this manner includes the DISC1 interactors LIS1, NDEL1 and 14-3-3ɛ. The interaction of DISC1 with Grb2 may also be required for neutrophin-3-related axon elongation. Of potential therapeutic relevance, expression of GRB2 mRNA is known to be upregulated following electroconvulsive seizure, an established anti-depression therapy. FEZ1, another DISC1-interacting protein, is known to be involved in the activation of the kinesin-1 motor protein, regulation of neurite outgrowth and the establishment of neuronal polarity. DISC1-FEZ1 interaction is enhanced during neurodifferentiation, and expression of the FEZ1-binding domain of DISC1 has a dominant negative effect on neurite outgrowth in a cellular model, implying co-operation of DISC1 and FEZ1 in this signalling pathway.

At the centrosome, DISC1 also interacts with the scaffold protein pericentrin (also known as kendrin, ), a molecule that is known to play important roles in microtubule nucleation and aster formation (reviewed in ) in a seemingly DISC1-dependent manner. Intriguingly, mutations in the PCNT gene, which encodes pericentrin, are heavily implicated in a form of dwarfism associated with reduced brain size, suggesting it to be important for neurodevelopment. Recruitment of pericentrin to the centrosome is essential for correct microtubule organisation and is facilitated by another large scaffold protein PCM1. PCM1 in turn is recruited co-operatively by interacting proteins DISC1 and BBS4. Centrosomal PCM1 is known to be required for correct axon morphology and embryonic neurogenesis. Intriguingly, the level of localisation of PCM1 to the centrosome in human glial cells is altered by two common DISC1 amino-acid substitutions, Ser704Cys and Leu607Phe, one possible mechanism by which these alleles lead to DISC1 dysfunction, as measured by brain imaging and elevated risk of psychiatric illness (Table 1 and references therein).

Other centrosomal interactors of DISC1 include the DISC1-Binding Zinc finger protein (DBZ, also known as Su48 or ZNF365). DBZ is a brain expressed protein which binds to DISC1, NDE1 and NDEL1. Co-expression of DISC1 and DBZ results in a reduction in the number of PC12 cells bearing neurites, while expression of the DISC1-binding domain of DBZ lead to reduced neurite outgrowth in mouse primary hippocampal neurons.

DISC1-binding proteins in neuronal migration and differentiation within the mouse brain

Results from cell-based models such as those described above beg the question as to how binding partners of DISC1 might be involved in regulating neurodevelopment. Important insights have come from various in vivo mouse studies. In the hippocampus, knock-down of DISC1 using shRNA methods have been shown to lead to aberrant positioning and dendritic structure of adult-born neurons. Intriguingly, the defects caused by one DISC1 shRNA of mild effect were greatly enhanced by co-expression of an shRNA to knock-down levels of NDEL1, strongly implying that these two proteins co-operate together, and consistent with the role of NDEL1 established in cultured cells. Deficiencies in the migration of neurons in the developing cortex can be seen following silencing of DISC1, PCM1 or BBS4 and in NDE1 and NDEL1 knock-out mice implying that the various DISC1-containing complexes involved in microtubule regulation are critical for cortical development.

Migration defects in cortical neurons can also be caused by silencing the DISC1-interacting protein Dixdc1 or by inhibiting DISC1-Dixdc1 interaction using an interfering peptide. Intriguingly, Dixdc1 is also an interactor of NDEL1, and a phosphorylation site key to this interaction is required to rescue migration defects caused by suppression of DIXDC1 expression. Thus, DISC1, Dixdc1 and NDEL1 appear to co-operate in regulating migration in the developing cortex. Another potential member of this pathway is the Alzheimer’s disease-related Amyloid Precursor Protein (APP, ). Knock-down of APP levels by RNAi in the developing cortex leads to migration defects reminiscent of DISC1 knock-down which can be largely reversed by DISC1 over-expression. There is also evidence to suggest that APP is involved in the localisation of DISC1 to the centrosome in the cortex.

Both Dixdc1 and DISC1 impact on the Wnt-signalling pathway. Silencing of DISC1 or Dixdc1 reduces lymphoid enhancer factor/T cell factor (LEF/TCF) mediated transcription and thus differentiation of neural progenitors. These effects caused by down-regulation of DISC1 expression can be rescued by expression of Dixdc1 and vice versa. The key linking molecules are Glycogen Synthase Kinase 3β (GSK3β) and β-catenin. The kinase activity of GSK3β is inhibited on binding to DISC1, preventing degradation of β-catenin and allowing it to translocate to the nucleus where it stimulates transcription of neurogenesis-related genes. These effects of DISC1/Dixdc1 silencing can be rescued by expression of β-catenin or by inhibiting GSK3β. Also, and of clinical relevance, GSK3β is a well-established target for lithium chloride, widely used in the management of bipolar disorder. GSK3β-specific inhibitors can also rescue hyperlocomotion in open field tests observed in mice expressing the DISC1-L100P mutant or in which DISC1 has been silenced in the hippocampus as well as pre-pulse and latent inhibition deficits in the L100P mouse. Intriguingly, GSK3 activity is also regulated by the APP-derived β-amyloid peptide (reviewed in ).

Girdin (also known as KIAA1212, APE, GIV and HkRP1) is another DISC1-interacting protein, over-expression of which leads to adult-born neurons of the dentate gyrus displaying enhanced dendritic growth, increased dendritic number and over-extended migration into the outer granule cell layer and molecular layer, mirroring the effects of DISC1 depletion. Incorrect neuronal localisation and impaired mossy fibre development are also seen in girdin knock-out mice. These effects of girdin appear to be mediated via its ability to bind to and increase the activity of the serine/threonine kinase Akt. DISC1 depletion increases Akt activity at least in part through binding to girdin and preventing its Akt-stimulating activity. In agreement with this, use of rapamycin to inhibit mTOR, which lies downstream of Akt signalling, can rescue the neuronal abnormalities caused by Girdin over-expression or DISC1 knock-down. Akt is also a negative modulator of GSK3β, although an inhibitor of GSK3β was not seen to rescue these girdin-related developmental defects.

DISC1-binding partners at the post-synaptic density

In addition to modulating the proliferation, migration and integration of neurons, it can also be postulated that proteins of the DISC1 complex might impact upon major mental illness by modulation of synaptic transmission. In support of this, DISC1 and several of its binding partners, including citron, PDE4B, LIS1, NDE1 and NDEL1, have been found to localise to the post-synaptic density (PSD, ). To date however, relatively little is understood of the synaptic functions of these proteins.

In contrast, more is known about the role of the PSD-localised DISC1 interactor TNIK, a kinase expressed in the mouse hippocampus whose activity is involved in regulation of the cytoskeleton. DISC1-binding inhibits the kinase activity of TNIK, leading to the degradation of several key PSD proteins, including the important structural protein PSD95, and modulating the surface expression of glutamate receptor 1 (GluR1, ). More generally, knock-down of DISC1 expression leads to an increase in the formation of spines and GluR1-expessing synapses in mature rat neurons, a process dependent on its interaction with kalirin-7 (Kal7, ). Kal7-dependent regulation of spine formation occurs through its activity as a GDP/GTP exchange factor for Rac1, and DISC1 appears to inhibit its activity by binding to Kal7 and PSD95. Activation of NMDA receptors causes dissociation of DISC1, Kal7 and PSD95, making Kal7 available to modulate Rac1 and thus spine structure. Thus DISC1 appears to modulate the formation of PSD complexes and dendritic spines through regulation of TNIK, Kal7 and Rac1.

Other DISC1 interactors of potential importance at the synapse include APP (Young-Pearce et al., 2010), given its involvement in spine formation and enhancement of NMDA receptor activity. Another DISC1 interactor, Activating Transcription Factor 4 (ATF4 or CREB2, ) is known to bind to GABAB receptors in the synapse, and its transport from the synapse to the nucleus, where it acts as a transcriptional repressor, is implicated in long-term depression and memory.

Roles of DISC1-interacting proteins in signalling

Another important theme in DISC1 biology is its role in a wide variety of signalling pathways, including the GSK3β and Akt pathways discussed above in Section 2.2. A third such pathway involves signalling by the ubiquitous secondary messenger molecule cAMP. The phosphodiesterase 4 family of enzymes degrade cAMP (reviewed in ) and isoforms from all four PDE4 subtypes (PDE4A-D) have been demonstrated to interact with DISC1. DISC1 binds PDE4 in a low-activity conformation and PDE4 activity is diminished in mice with a mutation, Q31L, in a PDE4-binding site on DISC1. Downstream effects of DISC1–PDE4 interaction remain to be determined, but are likely to include regulation of the activity of cAMP-dependent Protein Kinase A (PKA), substrates of which include the DISC1-interactors NDE1 and ATF4. In support of this, over-expression of DISC1 exaggerates the repression of CRE-dependent gene transcription caused by ATF4 in response to PKA. PDE4 is the known target for rolipram and other small molecules which have anti-depressant and anti-psychotic activity in rodent models.

Another family of proteins heavily implicated in major mental illness are the neuregulins and the ErbB family of receptors for which cleaved NRG domains act as ligands (reviewed in ). Intriguingly, NRG1 and NRG2 signalling is seen to increase the expression of a specific DISC1 isoform in a process dependant on the activity of BACE to cleave neuregulins, forming extracellular peptide ligands. This pathway appears to be mediated by PI3 K/Akt signalling and is transcription-dependent. Downstream effects of NRG1 signalling include inducing the expression and activity of ATF4. Expression of DISC1 also appears to be upregulated following signalling by the neuropeptide PACAP, which additionally stimulates interaction of DISC1 with DBZ. DISC1 is also implicated in dopamine signalling, which is altered in several DISC1 mouse models. Silencing of DISC1 in rat striatal neurons leads to loss of dopamine receptor-expressing cilia.

In summary, it is increasingly apparent that DISC1 is not simply a scaffold for the formation of protein complexes, but more an active hub for regulating divergent signalling pathways, including PDE4/cAMP, Akt/mTOR and GSK3β/β-catenin that are each well known to impact upon neurodevelopmental and/or psychiatric illness. An interesting side point is the apparent convergence of the DISC1 pathway with proteins involved in Alzheimer’s disease. DISC1 is now known to interact with APP, from which the β-amyloid peptide is derived, along with the related APLP1 protein. DISC1 also inhibits the activity of GSK3β, which is modulated by and may also modulate β-amyloid peptides, and DISC1 levels are indirectly regulated by BACE, the APP-cleaving enzyme. By implication, DISC1 plays a critical role in integrating these otherwise independent pathways, elaborating the details of which represents a key future challenge.

Genetic evidence implicating DISC1 interactors in schizophrenia and related disorders

Several positive genetic association studies have been reported for genes encoding DISC1 interactors (summarised in Table 2), implying that multiple DISC1-related pathways need to be considered as relevant to risk of psychopathology. ATF4, CIT (encoding citron), FEZ1, NDE1, PAFAH1B1 (encoding LIS1), PCNT (encoding pericentrin), PDE4D, TNIK and YWHAE (encoding 14-3-3ɛ) are thus all implicated in schizophrenia, although some of these are single studies or report modest associations that await firm replication, with some studies failing to replicate (Table 3 and references therein). Replication of genetic association between one or more SNPs and major mental illness supports PDE4B, NDEL1 and PCM1 in their own right (Table 2 and references therein).

It is important here also to distinguish between the strict statistical tests for significance that must be applied to gene-wide or genome-wide test of association and the insight which can be gained from specific mutations in individual cases and families. Thus, in much the same way as DISC1 was discovered at a translocation breakpoint, PDE4B was found to be directly disrupted by a t(1:16) translocation in a proband with schizophrenia, who also had an affected cousin. Similarly, both deletions and duplications at chromosomal locus 16p13.1, containing the NDE1 gene, are significantly over-represented in schizophrenia patients in Scottish and other European populations, with a similar deletion also seen in an African–American individual with the condition. Ultra-rare missense mutations in patients with schizophrenia have been reported for APP PCM1, and indeed DISC1. These rare mutations point the finger directly at these genes and associated pathways, and further demonstrate their biological relevance.

Evidence has also been reported of transcripts encoding several of these proteins being either up- or down-regulated in brain tissue of individuals with psychiatric illness, compared to that from healthy controls (Table 4 and references therein). Such differences in mRNA expression could be the result of direct mutation in those genes, or indirectly, due to dysregulation of transcription factors or other modulatory proteins. Additionally, certain DISC1 SNPs are associated with reduced levels of FEZ1, LIS1 and NDEL1 transcripts in the hippocampus.

Additionally, as one would predict biologically, evidence for epistatic interaction is emerging: three-way interaction between specific SNPs in CIT, DISC1 and NDEL1 has been reported for schizophrenia; there is strong statistical interplay between the HEP3 haplotype and NDE1 in the Finnish population and haplotypes of NDE1 and NDEL1 show association that is dependent on the Ser or Cys variant at position 704 in DISC1.

Although the emphasis of genetic studies to date has been on their potential pathological impact, it is emerging that common variants of DISC1 and its interactors impact on normal variation and intermediate phenotypes, for example memory tasks and in quantitative measures of personality and mood. We have recently reported that common cis-acting variants of DISC1 modulate expression within normal subjects by up to 20%. Moreover, variants in DISC1, PDE4 and NDE1 impact on the expression of genes involved in the cytoskeleton, neurosignalling and sensory perception, and are significantly enriched for current drug development targets in psychiatry.

In a similar vein, the recent demonstration of at least fifty different DISC1 transcripts including an abundance that are specific to foetal development and some for which expression is altered in the hippocampus of those suffering from schizophrenia or carrying DISC1 schizophrenia-risk alleles, raised a whole new series of questions about how DISC1 expression is regulated, and with what effect on neurodevelopment and signalling.

Caveats and limitations

Whereas the growing literature on DISC1 and the DISC1 pathway, as summarised here, provides multiple avenues of promising research to pursue that is relevant to neurodevelopment, signalling and psychopathology, there are gaps and limitations. For example, with respect to the DISC1 interactome derived from yeast-two-hybrid analysis, only a minority of putative DISC1 interactors have been formally tested and confirmed by co-immunoprecipitation or co-localisation in native tissue. Although multiple transcripts and protein isoforms of DISC1 have been described, the functional role of the former and the amino-acid sequence of the later remain to be determined. Evidence from the original family from which DISC1 was identified is consistent with a simple haploinsufficiency model, but in the absence of patient tissue other than lymphoblastoid cell lines, it is not possible to rule out a dominant negative effect of hypothetical truncated or fusion DISC1 protein expression during development or in the adult brain. This family is an example of an ultra rare, in this case unique, genetic event revealing a more general genetic contribution though other genetic variants at the locus. A number of amino-acid substitutions in DISC1 been described and regulatory mutations hypothecated from association evidence, but a comprehensive analysis of all possible mutations awaits the results of large scale resequencing studies. Our understanding of the biological consequences of S704C and L607F, the best studied to date, remain partial. Regarding the cell and animal models used to test for biological effects, these do not as yet model known clinical variants, nor, for obvious reasons, do the models allow testing of psychiatric phenotypes, only at best surrogates and proxies. That said, a still modest, but growing body of evidence is making links between mouse models and human studies through comparative brain histology and imaging (reviewed in ). Thus, despite the remarkable progress, much remains to be done not just in vitro or in model systems, but in clinical studies too.

Summary and conclusions

The complexities of schizophrenia and related psychiatric illness were never likely to yield to single methodologies or models, but a combined genetic and biological approach offers promise. From what might have been viewed as an unlikely start point, the molecular genetic characterisation of a single family with a high loading for psychiatric illness, the insights from the discovery of DISC1 have been manifold and far-reaching, a paradigm for future work. It is now not so much a question of the role of DISC1 per se, but much more about the DISC1 pathway in neurodevelopment and signalling, brought to light through the multiplicity of DISC1-interacting proteins. Mechanistic details remain to be filled in and potential therapeutic targets evaluated. But in the decade since DISC1 was cloned, much progress towards these goals has been made by a combination of genetics, biochemistry, neurobiology and animal models. The next decade promises further exciting prospects to enhance our understanding of the DISC1 pathway to the benefit of patients.

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    Collins D.M., Murdoch H., Dunlop A.J., Charych E., Baillie G.S., Wang Q., Herberg F.W., Brandon N., Prinz A., Houslay M.D. Ndel1 alters its conformation by sequestering cAMP-specific phosphodiesterase-4D3 (PDE4D3) in a manner that is dynamically regulated through Protein Kinase A (PKA). Cell. Signal. 2008;20:2356-2369.

    Not in our library10.1016/j.cellsig.2008.09.017

  23. 23.

    Crepel A., Breckpot J., Fryns J.-P., De la Marche W., Steyaert J., Devriendt K., Peeters H. DISC1 duplication in two brothers with autism and mild mental retardation. Clin. Genet. 2010;77:389-394.

    Not in our library10.1111/j.1399-0004.2009.01318.x

  24. 24.

    Dammermann A., Merdes A. Assembly of centrosomal proteins and microtubule organization depends on PCM-1. J. Cell Biol. 2002;159:255-266.

    Not in our library10.1083/jcb.200204023

  25. 25.

    Datta S.R., McQuillin A., Rizig M., Blaveri E., Thirumalai S., Kalsi G., Lawrence J., Bass N.J., Puri V., Choudhury K., Pimm J., Crombie C., Fraser G., Walker N., Curtis D., Zvelebil M., Pereira A., Kandaswamy R., St Clair D., Gurling H.M.D. A threonine to isoleucine missense mutation in the pericentriolar material 1 gene is strongly associated with schizophrenia. Mol. Psychiatry. 2010;15:615-628.

    Not in our library10.1038/mp.2008.128

  26. 26.

    Delaval B., Doxsey S.J. Pericentrin in cellular function and disease. J. Cell Biol. 2010;188:181-190.

    Not in our library10.1083/jcb.200908114

  27. 27.

    Di Giorgio A., Blasi G., Sambataro F., Rampino A., Papazacharias A., Gambi F., Romano R., Caforio G., Rizzo M., Latorre V., Popolizio T., Kolachana B., Callicott J.H., Nardini M., Weinberger D.R., Bertolino A. Association of the Ser704Cys DISC1 polymorphism with human hippocampal formation gray matter and function during memory encoding. Eur. J. Neurosci. 2008;28:2129-2136.

    Not in our library10.1111/j.1460-9568.2008.06482.x

  28. 28.

    Duan X., Chang J.H., Ge S., Faulkner R.L., Kim J.Y., Kitabatake Y., Liu X.-b., Yang C.-H., Jordan J.D., Ma D.K., Liu C.Y., Ganesan S., Cheng H.-J., Ming G.-l., Lu B., Song H. Disrupted-in-schizophrenia 1 regulates integration of newly generated neurons in the adult brain. Cell. 2007;130:1146-1158.

    Not in our library10.1016/j.cell.2007.07.010

  29. 29.

    Eastwood S.L., Walker M., Hyde T.M., Kleinman J.E., Harrison P.J. The DISC1 Ser704Cys substitution affects centrosomal localization of its binding partner PCM1 in glia in human brain. Hum. Mol. Genet. 2010;19:2487-2496.

    Not in our library10.1093/hmg/ddq130

  30. 30.

    Elefteriou F., Ahn J.D., Takeda S., Starbuck M., Yang X., Liu X., Kondo H., Richards W.G., Bannon T.W., Noda M., Clement K., Vaisse C., Karsenty G. Leptin regulation of bone resorption by the sympathetic nervous system and CART. Nature. 2005;434:514-520.

    Not in our library10.1038/nature03398

  31. 31.

    Enomoto A., Asai N., Namba T., Wang Y., Kato T., Tanaka M., Tatsumi H., Taya S., Tsuboi D., Kuroda K., Kaneko N., Sawamoto K., Miyamoto R., Jijiwa M., Murakumo Y., Sokabe M., Seki T., Kaibuchi K., Takahashi M. Roles of disrupted-in-schizophrenia 1-interacting protein girdin in postnatal development of the dentate gyrus. Neuron. 2009;63:774-787.

    Not in our library10.1016/j.neuron.2009.08.015

  32. 32.

    Ewing R.M., Chu P., Elisma F., Li H., Taylor P., Climie S., McBroom-Cerajewski L., Robinson M.D., O’Connor L., Li M., Taylor R., Dharsee M., Ho Y., Heilbut A., Moore L., Zhang S., Ornatsky O., Bukhman Y.V., Ethier M., Sheng Y., Vasilescu J., Abu-Farha M., Lambert J.-P., Duewel H.S., Stewart I.I., Kuehl B., Hogue K., Colwill K., Gladwish K., Muskat B., Kinach R., Adams S.-L., Moran M.F., Morin G.B., Topaloglou T., Figeys D. Large-scale mapping of human protein–protein interactions by mass spectrometry. Mol. Syst. Biol. 2007;3:89.

    Not in our library10.1038/msb4100134

  33. 33.

    Fatemi S.H., King D.P., Reutiman T.J., Folsom T.D., Laurence J.A., Lee S., Fan Y.-T., Paciga S.A., Conti M., Menniti F.S. PDE4B polymorphisms and decreased PDE4B expression are associated with schizophrenia. Schizophr. Res. 2008;101:36-49.

    Not in our library10.1016/j.schres.2008.01.029

  34. 34.

    Fatemi S.H., Folsom T.D., Reutiman T.J., Vazquez G. Phosphodiesterase signaling system is disrupted in the cerebella of subjects with schizophrenia, bipolar disorder, and major depression. Schizophr. Res. 2010;119:266-267.

    Not in our library10.1016/j.schres.2010.02.1055

  35. 35.

    Faulkner N.E., Dujardin D.L., Tai C.-Y., Vaughan K.T., O’Connell C.B., Wang Y.-l., Vallee R.B. A role for the lissencephaly gene LIS1 in mitosis and cytoplasmic dynein function. Nat. Cell Biol. 2000;2:784-791.

    Not in our library10.1038/35041020

  36. 36.

    Feng Y., Walsh C.A. Mitotic spindle regulation by Nde1 controls cerebral cortical size. Neuron. 2004;44:279-293.

    Not in our library10.1016/j.neuron.2004.09.023

  37. 37.

    Feng Y., Olson E.C., Stukenberg P.T., Flanagan L.A., Kirschner M.W., Walsh C.A. LIS1 regulates CNS lamination by interacting with mNudE, a central component of the centrosome. Neuron. 2000;28:665-679.

    Not in our library10.1016/s0896-6273(00)00145-8

  38. 38.

    Fu C.A., Shen M., Huang B.C.B., Lasaga J., Payan D.G., Luo Y. TNIK, a novel member of the germinal center kinase family that activates the c-Jun N-terminal kinase pathway and regulates the cytoskeleton. J. Biol. Chem. 1999;274:30729-30737.

    Not in our library10.1074/jbc.274.43.30729

  39. 39.

    Fujita T., Maturana A.D., Ikuta J., Hamada J., Walchli S., Suzuki T., Sawa H., Wooten M.W., Okajima T., Tatematsu K., Tanizawa K., Kuroda i S. Axonal guidance protein FEZ1 associates with tubulin and kinesin motor protein to transport mitochondria in neurites of NGF-stimulated PC12 cells. Biochem. Biophysical Res. Commun. 2007;361:605-610.

    Not in our library10.1016/j.bbrc.2007.07.050

  40. 40.

    Fukuda S., Hashimoto R., Ohi K., Yamaguti K., Nakatomi Y., Yasuda Y., Kamino K., Takeda M., Tajima S., Kuratsune H., Nishizawa Y., Watanabe Y. A functional polymorphism in the disrupted-in schizophrenia 1 gene is associated with chronic fatigue syndrome. Life Sci. 2010;86:722-725.

    Not in our library10.1016/j.lfs.2010.03.007

  41. 41.

    Furuyashiki T., Fujisawa K., Fujita A., Madaule P., Uchino S., Mishina M., Bito H., Narumiya S. Citron, a rho-target, interacts with PSD-95/SAP-90 at glutamatergic synapses in the thalamus. J. Neurosci. 1999;19:109-118.

    Not in our library10.1523/jneurosci.19-01-00109.1999

  42. 42.

    Ge X., Frank C.L., Calderon de Anda F., Tsai L.-H. Hook3 interacts with PCM1 to regulate pericentriolar material assembly and the timing of neurogenesis. Neuron. 2010;65:191-203.

    Not in our library10.1016/j.neuron.2010.01.011

  43. 43.

    Glatt S.J., Everall I.P., Kremen W.S., Corbeil J., Sasik R., Khanlou N., Han M., Liew C.-C., Tsuang M.T. Comparative gene expression analysis of blood and brain provides concurrent validation of SELENBP1 up-regulation in schizophrenia. Proc. Natl. Acad. Sci. USA. 2005;102:15533-15538.

    Not in our library10.1073/pnas.0507666102

  44. 44.

    Griffith E., Walker S., Martin C.-A., Vagnarelli P., Stiff T., Vernay B., Al Sanna N., Saggar A., Hamel B., Earnshaw W.C., Jeggo P.A., Jackson A.P., O’Driscoll M. Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling. Nat. Genet. 2008;40:232-236.

    Not in our library10.1038/ng.2007.80

  45. 45.

    Guo J., Yang Z., Song W., Chen Q., Wang F., Zhang Q., Zhu X. Nudel contributes to microtubule anchoring at the mother centriole and is involved in both dynein-dependent and -independent centrosomal protein assembly. Mol. Biol. Cell. 2006;17:680-689.

    Not in our library10.1091/mbc.e05-04-0360

  46. 46.

    Gurling H.M.D., Critchley H., Datta S.R., McQuillin A., Blaveri E., Thirumalai S., Pimm J., Krasucki R., Kalsi G., Quested D., Lawrence J., Bass N., Choudhury K., Puri V., O’Daly O., Curtis D., Blackwood D., Muir W., Malhotra A.K., Buchanan R.W., Good C.D., Frackowiak R.S.J., Dolan R.J. Genetic association and brain morphology studies and the chromosome 8p22 pericentriolar material 1 (PCM1) gene in susceptibility to schizophrenia. Arch. Gen. Psychiatry. 2006;63:844-854.

    Not in our library10.1001/archpsyc.63.8.844

  47. 47.

    Harris S.E., Hennah W., Thomson P.A., Luciano M., Starr J.M., Porteous D.J., Deary I.J. Variation in DISC1 is associated with anxiety, depression and emotional stability in elderly women. Mol. Psychiatry. 2010;15:232-234.

    Not in our library10.1038/mp.2009.88

  48. 48.

    Hashimoto R., Numakawa T., Ohnishi T., Kumamaru E., Yagasaki Y., Ishimoto T., Mori T., Nemoto K., Adachi N., Izumi A., Chiba S., Noguchi H., Suzuki T., Iwata N., Ozaki N., Taguchi T., Kamiya A., Kosuga A., Tatsumi M., Kamijima K., Weinberger D.R., Sawa A., Kunugi H. Impact of the DISC1 Ser704Cys polymorphism on risk for major depression, brain morphology, and ERK signaling. Hum. Mol. Genet. 2006;15:3024-3033.

    Not in our library10.1093/hmg/ddl244

  49. 49.

    Hattori T., Baba K., Matsuzaki S., Honda A., Miyoshi K., Inoue K., Taniguchi M., Hashimoto H., Shintani N., Baba A., Shimizu S., Yukioka F., Kumamoto N., Yamaguchi A., Tohyama M., Katayama T. A novel DISC1-interacting partner DISC1-binding zinc-finger protein: implication in the modulation of DISC1-dependent neurite outgrowth. Mol. Psychiatry. 2007;12:398-407.

    Not in our library10.1038/sj.mp.4001945

  50. 50.

    Hayashi M.A.F., Portaro F.C.V., Bastos M.F., Guerreiro J.R., Oliveira V., Gorrao S.S., Tambourgi D.V., Sant’Anna O.A., Whiting P.J., Camargo L.M., Konno K., Brandon N.J., Camargo A.C.M. Inhibition of NUDEL (nuclear distribution element-like)-oligopeptidase activity by disrupted-in-schizophrenia 1. Proc. Natl. Acad. Sci. USA. 2005;102:3828-3833.

    Not in our library10.1073/pnas.0500330102

  51. 51.

    Hayashi M.A.F., Guerreiro J.R., Charych E., Kamiya A., Barbosa R.L., Machado M.F., Campeiro J.D., Oliveira V., Sawa A., Camargo A.C.M., Brandon N.J. Assessing the role of endooligopeptidase activity of Ndel1 (nuclear-distribution gene E homolog like-1) in neurite outgrowth. Mol. Cell. Neurosci. 2010;44:353-361.

    Not in our library10.1016/j.mcn.2010.04.006

  52. 52.

    Hayashi-Takagi A., Takaki M., Graziane N., Seshadri S., Murdoch H., Dunlop A.J., Makino Y., Seshadri A.J., Ishizuka K., Srivastava D.P., Xie Z., Baraban J.M., Houslay M.D., Tomoda T., Brandon N.J., Kamiya A., Yan Z., Penzes P., Sawa A. Disrupted-in-schizophrenia 1 (DISC1) regulates spines of the glutamate synapse via Rac1. Nat. Neurosci. 2010;13:327-332.

    Not in our library10.1038/nn.2487

  53. 53.

    Hennah W., Porteous D. The DISC1 pathway modulates expression of neurodevelopmental, synaptogenic and sensory perception genes. PLOS One. 2009;4:e4906.

    Not in our library10.1371/journal.pone.0004906

  54. 54.

    Hennah W., Tuulio-Henriksson A., Paunio T., Ekelund J., Varilo T., Partonen T., Cannon T.D., Lonnqvist J., Peltonen L. A haplotype within the DISC1 gene is associated with visual memory functions in families with a high density of schizophrenia. Mol. Psychiatry. 2005;10:1097-1103.

    Not in our library10.1038/sj.mp.4001731

  55. 55.

    Hennah W., Tomppo L., Hiekkalinna T., Palo O.M., Kilpinen H., Ekelund J., Tuulio-Henriksson A., Silander K., Partonen T., Paunio T., Terwilliger J.D., Lonnqvist J., Peltonen L. Families with the risk allele of DISC1 reveal a link between schizophrenia and another component of the same molecular pathway, NDE1. Hum. Mol.Genet. 2007;6:453-462.

    Not in our library10.1093/hmg/ddl462

  56. 56.

    Hennah W., Thomson P., McQuillin A., Bass N., Loukola A., Anjorin A., Blackwood D., Curtis D., Deary I.J., Harris S.E., Isometsa E.T., Lawrence J., Lonnqvist J., Muir W., Palotie A., Partonen T., Paunio T., Pylkko E., Robinson M., Soronen P., Suominen K., Suvisaari J., Thirumalai S., St Clair D., Gurling H., Peltonen L., Porteous D. DISC1 association, heterogeneity and interplay in schizophrenia and bipolar disorder. Mol. Psychiatry. 2009;14:865-873.

    Not in our library10.1038/mp.2008.22

  57. 57.

    Hernández F., Gómez de Barreda E., Fuster-Matanzo A., Lucas J.J., Avila J. GSK3: a possible link between beta amyloid peptide and tau protein. Exp. Neurol. 2010;223:322-325.

    Not in our library10.1016/j.expneurol.2009.09.011

  58. 58.

    Higginbotham H.R., Gleeson J.G. The centrosome in neuronal development. Trends Neurosci. 2007;30:276-283.

    Not in our library10.1016/j.tins.2007.04.001

  59. 59.

    Hirohashi Y., Wang Q., Liu Q., Li B., Du X., Zhang H., Furuuchi K., Masuda K., Sato N., Greene M.I. Centrosomal proteins Nde1 and Su48 form a complex regulated by phosphorylation. Oncogene. 2006;25:6048-6055.

    Not in our library10.1038/sj.onc.1209637

  60. 60.

    Hodgkinson C.A., Goldman D., Ducci F., DeRosse P., Caycedo D.A., Newman E.R., Kane J.M., Roy A., Malhotra A.K. The FEZ1 gene shows no association to schizophrenia in Caucasian or African American populations. Neuropsychopharmacology. 2007;32:190-196.

    Not in our library10.1038/sj.npp.1301177

  61. 61.

    Hoe H.-S., Fu Z., Makarova A., Lee J.-Y., Lu C., Feng L., Pajoohesh-Ganji A., Matsuoka Y., Hyman B.T., Ehlers M.D., Vicini S., Pak D.T.S., Rebeck G.W. The effects of amyloid precursor protein on postsynaptic composition and activity. J. Biol. Chem. 2009;284:8495-8506.

    Not in our library10.1074/jbc.m900141200

  62. 62.

    Holliday E.G., Nyholt D.R., Tirupati S., John S., Ramachandran P., Ramamurti M., Ramadoss A.J., Jeyagurunathan A., Kottiswaran S., Smith H.J., Filippich C., Nertney D.A., Nancarrow D.J., Hayward N.K., Watkins W.S., Jorde L.B., Thara R., Mowry B.J. Strong evidence for a novel schizophrenia risk locus on chromosome 1p31.1 in homogeneous pedigrees from Tamil Nadu, India. Am. J. Psychiatry. 2009;166:206-215.

    Not in our library10.1176/appi.ajp.2008.08030442

  63. 63.

    Houlihan L.M., Harris S.E., Luciano M., Gow A.J., Starr J.M., Visscher P.M., Deary I.J. Replication study of candidate genes for cognitive abilities: the Lothian Birth Cohort 1936. Genes Brain Behav. 2009;8:238-247.

    Not in our library10.1111/j.1601-183x.2008.00470.x

  64. 64.

    Houslay M.D., Adams D.R. PDE4 cAMP phosphodiesterases: modular enzymes that orchestrate signalling cross-talk, desensitization and compartmentalization. Biochem. J. 2003;370:1-18.

    Not in our library10.1042/bj20021698

  65. 65.

    Hutchins J.R.A., Toyoda Y., Hegemann B., Poser I., Heriche J.-K., Sykora M.M., Augsburg M., Hudecz O., Buschhorn B.A., Bulkescher J., Conrad C., Comartin D., Schleiffer A., Sarov M., Pozniakovsky A., Slabicki M.M., Schloissnig S., Steinmacher I., Leuschner M., Ssykor A., Lawo S., Pelletier L., Stark H., Nasmyth K., Ellenberg J., Durbin R., Buchholz F., Mechtler K., Hyman A.A., Peters J.-M. Systematic analysis of human protein complexes identifies chromosome segregation proteins. Science. 2010;328:593-599.

    Not in our library10.1126/science.1181348

  66. 66.

    Ikeda M., Hikita T., Taya S., Uraguchi-Asaki J., Toyo-oka K., Wynshaw-Boris A., Ujike H., Inada T., Takao K., Miyakawa T., Ozaki N., Kaibuchi K., Iwata N. Identification of YWHAE, a gene encoding 14-3-3epsilon, as a possible susceptibility gene for schizophrenia. Hum. Mol. Genet. 2008;17:3212-3222.

    Not in our library10.1093/hmg/ddn217

  67. 67.

    Ikuta J., Maturana A., Fujita T., Okajima T., Tatematsu K., Tanizawa K., Kuroda i S. Fasciculation and elongation protein zeta-1 (FEZ1) participates in the polarization of hippocampal neuron by controlling the mitochondrial motility. Biochem. Biophysical Res. Commun. 2007;353:127-132.

    Not in our library10.1016/j.bbrc.2006.11.142

  68. 68.

    Ingason A., Rujescu D., Cichon S., Sigurdsson E., Sigmundsson T., Pietilainen O.P.H., Buizer-Voskamp J.E., Strengman E., Francks C., Muglia P., Gylfason A., Gustafsson O., Olason P.I., Steinberg S., Hansen T., Jakobsen K.D., Rasmussen H.B., Giegling I., Moller H.-J., Hartmann A., Crombie C., Fraser G., Walker N., Lonnqvist J., Suvisaari J., Tuulio-Henriksson A., Bramon E., Kiemeney L.A., Franke B., Murray R., Vassos E., Toulopoulou T., Muhleisen T.W., Tosato S., Ruggeri M., Djurovic S., Andreassen O.A., Zhang Z., Werge T., Ophoff R.A., GROUP Invesitgators, Rietschel M., Nothen M.M., Petursson H., Stefansson H., Peltonen L., Collier D., Stefansson K., St. Clair D.M. Copy number variations of chromosome 16p13.1 region associated with schizophrenia. Mol Psychiatry. 2011;16:17-25.

    Not in our library10.1038/mp.2009.101

  69. 69.

    James R., Adams R.R., Christie S., Buchanan S.R., Porteous D.J., Millar J.K. Disrupted in schizophrenia 1 (DISC1) is a multicompartmentalized protein that predominantly localizes to mitochondria. Mol. Cell. Neurosci. 2004;16:112-122.

    Not in our library10.1016/j.mcn.2004.01.013

  70. 70.

    Johnstone M., Thomson P.A., Hall J., McIntosh A.M., Lawrie S.M., Porteous D.J. DISC1 in schizophrenia: genetic mouse models and human genomic imaging. Schizophr. Bull. 2010.

    Not in our library10.1093/schbul/sbq135

  71. 71.

    Jones C.T., Morris S., Yates C.M., Moffoot A., Sharpe C., Brock D.J.H., St. Clair D. Mutation in codon 713 of the b amyloid precursor protein gene presenting with schizophrenia. Nat. Genet. 1992;1:306-309.

    Not in our library10.1038/ng0792-306

  72. 72.

    Kähler A.K., Djurovic S., Kulle B., Jönsson E.G., Agartz I., Hall H., Opjordsmoen S., Jakobsen K.D., Hansen T., Melle I., Werge T., Steen V.M., Andreassen O.A. Association analysis of schizophrenia on 18 genes involved in neuronal migration: MDGA1 as a new susceptibility gene. Am. J. Med. Genet. B. Neuropsychiatr. Genet. 2008;147B:1089-1100.

    Not in our library10.1002/ajmg.b.30726

  73. 73.

    Kähler A.K., Otnæss M.K., Wirgenes K.V., Hansen T., Jönsson E.G., Agartz I., Hall H., Werge T., Morken G., Mors O., Mellerup E., Dam H., Koefod P., Melle I., Steen V.M., Andreassen O.A., Djurovic S. Association study of PDE4B gene variants in Scandinavian schizophrenia and bipolar disorder multicenter case–control samples. Am. J. Med. Genet. B. Neuropsychiatr. Genet. 2009;153B:86-96.

    Not in our library10.1002/ajmg.b.30958

  74. 74.

    Kakiuchi C., Ishiwata M., Nanko S., Kunugi H., Minabe Y., Nakamura K., Mori N., Fujii K., Yamada K., Yoshikawa T., Kato T. Association analysis of ATF4 and ATF5, genes for interacting-proteins of DISC1, in bipolar disorder. Neurosci. Lett. 2007;417:316-321.

    Not in our library10.1016/j.neulet.2007.02.054

  75. 75.

    Kamiya A., Kubo K.-i., Tomoda T., Takaki M., Youn R., Ozeki Y., Sawamura N., Park U., Kudo C., Okawa M., Ross C.A., Hatten M.E., Nakajima K., Sawa A. A schizophrenia-associated mutation of DISC1 perturbs cerebral cortex development. Nat. Cell Biol. 2005;7:1167-1178.

    Not in our library10.1038/ncb1328

  76. 76.

    Kamiya A., Tomoda T., Chang J., Takaki M., Zhan C., Morita M., Cascio M.B., Elashvili S., Koizumi H., Takanezawa Y., Dickerson F., Yolken R., Arai H., Sawa A. DISC1-NDEL1/NUDEL protein interaction, an essential component for neurite outgrowth, is modulated by genetic variations of DISC1. Hum. Mol. Genet. 2006;15:3313-3323.

    Not in our library10.1093/hmg/ddl407

  77. 77.

    Kamiya A., Tan P.L., Kubo K., Engelhard C., Ishizuka K., Kubo A., Tsukita S., Pulver A.E., Nakajima K., Cascella N.G., Katsanis N., Sawa A. Recruitment of PCM1 to the centrosome by the cooperative action of DISC1 and BBS4: a candidate for psychiatric illnesses. Arch. Gen. Psychiatry. 2008;65:996-1006.

    Not in our library10.1001/archpsyc.65.9.996

  78. 78.

    Kanes S.J., Tokarczyk J., Siegel S.J., Bilker W., Abel T., Kelly M.P. Rolipram: a specific phosphodiesterase 4 inhibitor with potential antipsychotic activity. Neuroscience. 2007;144:239-246.

    Not in our library10.1016/j.neuroscience.2006.09.026

  79. 79.

    Karpinski B.A., Morle G.D., Huggenvik J., Uhler M.D., Leiden J.M. Molecular cloning of human CREB-2: an ATF/CREB transcription factor that can negatively regulate transcription from the cAMP response element. Proc. Natl. Acad. Sci. U.S.A. 1992;89:4820-4824.

    Not in our library10.1073/pnas.89.11.4820

  80. 80.

    Kilpinen H., Ylisaukko-oja T., Hennah W., Palo O.M., Varilo T., Vanhala R., Nieminen-von Wendt T., von Wendt L., Paunio T., Peltonen L. Association of DISC1 with autism and Asperger syndrome. Mol. Psychiatry. 2008;13:187-196.

    Not in our library10.1038/sj.mp.4002031

  81. 81.

    Kim J.C., Badano J.L., Sibold S., Esmail M.A., Hill J., Hoskins B.E., Leitch C.C., Venner K., Ansley S.J., Ross A.J., Leroux M.R., Katsanis N., Beales P.L. The Bardet–Biedl protein BBS4 targets cargo to the pericentriolar region and is required for microtubule anchoring and cell cycle progression. Nat. Genet. 2004;36:462-470.

    Not in our library10.1038/ng1352

  82. 82.

    Kim H.-J., Park H.J., Jung K.H., Ban J.Y., Ra J., Kim J.W., Park J.K., Choe B.-K., Yim S.V., Kwon Y.K., Chung J.-H. Association study of polymorphisms between DISC1 and schizophrenia in a Korean population. Neurosci. Lett. 2008;430:60-63.

    Not in our library10.1016/j.neulet.2007.10.010

  83. 83.

    Kim J., Krishnaswami S.R., Gleeson J.G. CEP290 interacts with the centriolar satellite component PCM-1 and is required for Rab8 localization to the primary cilium. Hum. Mol. Genet. 2008;17:3796-3805.

    Not in our library10.1093/hmg/ddn277

  84. 84.

    Kim J.Y., Duan X., Liu C.Y., Jang M.-H., Guo J.U., Pow-anpongkul N., Kang E., Song H., Ming G.-l. DISC1 regulates new neuron development in the adult brain via modulation of AKT-mTOR signaling through KIAA1212. Neuron. 2009;63:761-773.

    Not in our library10.1016/j.neuron.2009.08.008

  85. 85.

    Kirkpatrick B., Xu L., Cascella N., Ozeki Y., Sawa A., Roberts R.C. DISC1 immunoreactivity at the light and ultrastructural level in the human neocortex. J. Comp. Neurol. 2006;497:436-450.

    Not in our library10.1002/cne.21007

  86. 86.

    Kitagawa M., Umezu M., Aoki J., Koizumi H., Arai H., Inoue K. Direct association of LIS1, the lissencephaly gene product, with a mammalian homologue of a fungal nuclear distribution protein, rNUDE. FEBS Lett. 2000;479:57-62.

    Not in our library10.1016/s0014-5793(00)01856-1

  87. 87.

    Koga M., Ishiguro H., Horiuchi Y., Albalushi T., Inada T., Iwata N., Ozaki N., Ujike H., Muratake T., Someya T., Arinami T. Failure to confirm the association between the FEZ1 gene and schizophrenia in a Japanese population. Neurosci. Lett. 2007;417:326-329.

    Not in our library10.1016/j.neulet.2007.02.055

  88. 88.

    Lai K.-O., Zhao Y., Ch’ng T.H., Martin K.C. Importin-mediated retrograde transport of CREB2 from distal processes to the nucleus in neurons. Proc. Natl. Acad. Sci. U.S.A. 2008;105:17175-17180.

    Not in our library10.1073/pnas.0803906105

  89. 89.

    Lee K.J., Moussa C.E.H., Lee Y., Sung Y., Howell B.W., Turner R.S., Pak D.T.S., Hoe H.S. Beta amyloid-independent role of amyloid precursor protein in generation and maintenance of dendritic spines. Neuroscience. 2009;169:344-356.

    Not in our library10.1016/j.neuroscience.2010.04.078

  90. 90.

    Lepagnol-Bestel A.-M., Dubertret C., Benmessaoud D., Simonneau M., Adès J., Kacha F., Hamdani N., Gorwood P., Ramoz N. Association of DISC1 gene with schizophrenia in families from two distinct French and Algerian populations. Psychiatr. Genet. 2010;20:298-303.

    Not in our library10.1097/ypg.0b013e32833aa5c4

  91. 91.

    Lim S.M., Kim H.-J., Nam M., Chung J.-H., Park Y.H. Association study of DISC1 in Korean population with autism spectrum disorders. Psychiatr. Genet. 2009;19:160.

    Not in our library10.1097/ypg.0b013e32832a9bd1

  92. 92.

    Lipina T.V., Kaidanovich-Beilin O., Patel S., Wang M., Clapcote S.J., Liu F., Woodgett J.R., Roder J.C. Genetic and pharmacological evidence for schizophrenia-related Disc1 interaction with GSK-3. Synapse. 2010.

    Not in our library10.1002/syn.20839

  93. 93.

    Lipina T.V., Niwa M., Jaaro-Peled H., Fletcher P.J., Seeman P., Sawa A., Roder J.C. Enhanced dopamine function in DISC1-L100P mutant mice: implications for schizophrenia. Genes Brain Behav. 2010;9:777-789.

    Not in our library10.1111/j.1601-183x.2010.00615.x

  94. 94.

    Lipska B.K., Peters T., Hyde T.M., Halim N., Horowitz C., Mitkus S., Weickert C.S., Matsumoto M., Sawa A., Straub R.E., Vakkalanka R., Herman M.M., Weinberger D.R., Kleinman J.E. Expression of DISC1 binding partners is reduced in schizophrenia and associated with DISC1 SNPs. Hum. Mol. Genet. 2006;15:1245-1258.

    Not in our library10.1093/hmg/ddl040

  95. 95.

    Lyons-Warren A., Chang J.J., Balkissoon R., Kamiya A., Garant M., Nurnberger J., Scheftner W., Reich T., McMahon F., Kelsoe J., Gershon E., Coryell W., Byerley W., Berrettini W., DePaulo R., McInnis M., Sawa A. Evidence of association between bipolar disorder and Citron on chromosome 12q24. Mol. Psychiatry. 2005;10:807-809.

    Not in our library10.1038/sj.mp.4001703

  96. 96.

    Mao Y., Ge X., Frank C.L., Madison J.M., Koehler A.N., Doud M.K., Tassa C., Berry E.M., Soda T., Singh K.K., Biechele T., Petryshen T.L., Moon R.T., Haggarty S.J., Tsai L.-H. Disrupted in schizophrenia 1 regulates neuronal progenitor proliferation via modulation of GSK3b/b-catenin signaling. Cell. 2009;136:1017-1031.

    Not in our library10.1016/j.cell.2008.12.044

  97. 97.

    Marley A., von Zastrow M. DISC1 regulates primary cilia that display specific dopamine receptors. PLOS One. 2010;5:e10902.

    Not in our library10.1371/journal.pone.0010902

  98. 98.

    Matigian N., Windus L., Smith H., Filippich C., Pantelis C., McGrath J., Mowry B., Hayward N. Expression profiling in monozygotic twins discordant for bipolar disorder reveals dysregulation of the WNT signalling pathway. Mol. Psychiatry. 2007;12:815-825.

    Not in our library10.1038/sj.mp.4001998

  99. 99.

    Maxwell C.R., Kanes S.J., Abel T., Siegel S.J. Phosphodiesterase inhibitors: a novel mechanism for receptor-independent antipsychotic medications. Neuroscience. 2004;129:101-107.

    Not in our library10.1016/j.neuroscience.2004.07.038

  100. 100.

    McCahill A., McSorley T., Huston E., Hill E.V., Lynch M.J., Gall I., Keryer G., Lygren B., Tasken K., van Heeke G., Houslay M.D. In resting COS1 cells a dominant negative approach shows that specific, anchored PDE4 cAMP phosphodiesterase isoforms gate the activation, by basal cyclic AMP production, of AKAP-tethered protein kinase A type II located in the centrosomal region. Cell. Sig. 2005;17:1158-1173.

    Not in our library10.1016/j.cellsig.2005.04.003

  101. 101.

    Millar J.K., Wilson-Annan J.C., Anderson S., Christie S., Taylor M.S., Semple C.A.M., Devon R.S., St Clair D.M., Muir W.J., Blackwood D.H.R., Porteous D.J. Disruption of two novel genes by a translocation co-segregating with schizophrenia. Hum. Mol. Genet. 2000;9:1415-1425.

    Not in our library10.1093/hmg/9.9.1415

  102. 102.

    Millar J.K., Christie S., Porteous D.J. Yeast two-hybrid screens implicate DISC1 in brain development and function. Biochem. Biophysical Res. Commun. 2003;311:1019-1025.

    Not in our library10.1016/j.bbrc.2003.10.101

  103. 103.

    Millar J.K., Pickard B.S., Mackie S., James R., Christie S., Buchanan S.R., Malloy M.P., Chubb J.E., Huston E., Baille G.S., Hill E.V., Houslay M.D., Brandon N.J., Rain J.-C., Camargo L.M., Whiting P.J., Blackwood D.H.R., Muir W.J., Porteous D.J. DISC1 and PDE4B are interacting genetic factors in schizophrenia that regulate cAMP signalling. Science. 2005;310:1187-1191.

    Not in our library10.1126/science.1112915

  104. 104.

    Mitchell K.J., Porteous D.J. GWAS for psychiatric disease: is the framework built on a solid foundation? Mol. Psychiatry. 2009;14:740-741.

    Not in our library10.1038/mp.2009.17

  105. 105.

    Miyoshi K., Honda A., Baba K., Taniguchi M., Oono K., Fujita T., Kuroda S., Katayama T., Tohyama M. Disrupted-in-Schizophrenia 1, a candidate gene for schizophrenia, participates in neurite outgrowth. Mol. Psychiatry. 2003;8:685-694.

    Not in our library10.1038/sj.mp.4001352

  106. 106.

    Miyoshi K., Asanuma M., Miyazaki I., Diaz-Corrales F.J., Katayama T., Tohyama M., Ogawa N. DISC1 localizes to the centrosome by binding to kendrin. Biochem. Biophysical Res. Commun. 2004;317:1195-1199.

    Not in our library10.1016/j.bbrc.2004.03.163

  107. 107.

    Moens L.N., Ceulemans S., Alaerts M., Van Den Bossche M.J., Lenaerts A.-S., De Zutter S., Norrback K.-F., Adolfsson R., Del-Favero J. PCM1 and schizophrenia: a replication study in the Northern Swedish population. Am. J. Med. Genet. B. Neuropsychiatr. Genet. 2010;153B:1240-1243.

    Not in our library10.1002/ajmg.b.31088

  108. 108.

    Morris J.A., Kandpal G., Ma L., Austin C.P. DISC1 (Disrupted-In-Schizophrenia 1) is a centrosome-associated protein that interacts with MAP1A, MIPT3, ATF4/5 and NUDEL: regulation and loss of interaction with mutation. Hum. Mol. Genet. 2003;12:1591-1608.

    Not in our library10.1093/hmg/ddg162

  109. 109.

    Mouaffak F., Kebir O., Chayet M., Tordjman S., Vacheron M.N., Millet B., Jaafari N., Bellon A., Olie J.P., Krebs M.-O. Association of disrupted in schizophrenia 1 (DISC1) missense variants with ultra-resistant schizophrenia. Pharmacogenomics J. 2010.

    Not in our library10.1038/tpj.2010.40

  110. 110.

    Murdoch H., Mackie S., Collins D.M., Hill E.V., Bolger G.B., Klussmann E., Porteous D.J., Millar J.K., Houslay M.D. Isoform-selective susceptibility of DISC1/phosphodiesterase-4 complexes to dissociation by elevated intracellular cAMP levels. J. Neurosci. 2007;27:9513-9524.

    Not in our library10.1523/jneurosci.1493-07.2007

  111. 111.

    Nakata K., Lipska B.K., Hyde T.M., Ye T., Newburn E.N., Morita Y., Vakkalanka R., Barenboim M., Sei Y., Weinberger D.R., Kleinman J.E. DISC1 splice variants are upregulated in schizophrenia and associated with risk polymorphisms. Proc. Natl. Acad. Sci. USA. 2009;106:15873-15878.

    Not in our library10.1073/pnas.0903413106

  112. 112.
    A Genome-Wide Investigation of SNPs and CNVs in Schizophrenia · 2009
    Corrected
  113. 113.

    Nehring R.B., Horikawa H.P.M., El Far O., Kneussel M., Brandstatter J.H., Stamm S., Wischmeyer E., Betz H., Karschin A. The metabotropic GABAB receptor directly interacts with the activating transcription factor 4. J. Biol. Chem. 2000;275:35185-35191.

    Not in our library10.1074/jbc.m002727200

  114. 114.

    Newton S.S., Collier E.F., Bennett A.H., Russell D.S., Duman R.S. Regulation of growth factor receptor bound 2 by electroconvulsive seizure. Mol. Brain Res. 2004;129:185-188.

    Not in our library10.1016/j.molbrainres.2004.06.032

  115. 115.

    Nicodemus K.K., Callicott J.H., Higier R.G., Luna A., Nixon D.C., Lipska B.K., Vakkalanka R., Giegling I., Rujescu D., St Clair D., Muglia P., Shugart Y.Y., Weinberger D.R. Evidence of statistical epistasis between DISC1, CIT and NDEL1 impacting risk for schizophrenia: biological validation with functional neuroimaging. Hum. Genet. 2010.

    Not in our library10.1007/s00439-009-0782-y

  116. 116.

    Niethammer M., Smith D.S., Ayala R., Peng J., Ko J., Lee M.-S., Morabito M., Tsai L.-H. NUDEL is a novel Cdk5 substrate that associates with LIS1 and cytoplasmic dynein. Neuron. 2000;28:697-711.

    Not in our library10.1016/s0896-6273(00)00147-1

  117. 117.

    Niwa M., Kamiya A., Murai R., Kubo K.-i., Gruber A.J., Tomita K., Lu L., Tomisato S., Jaaro-Peled H., Seshadri S., Hiyama H., Huang B., Kohda K., Noda Y., O’Donnell P., Nakajima K., Sawa A., Nabeshima T. Knockdown of DISC1 by in utero gene transfer disturbs postnatal dopaminergic maturation in the frontal cortex and leads to adult behavioral deficits. Neuron. 2010;65:480-489.

    Not in our library10.1016/j.neuron.2010.01.019

  118. 118.

    Numata S., Ueno S.-i., Iga J.-i., Hongwei S., Nakataki M., Tayoshi S.Y., Sumitani S., Tomotake M., Itakura M., Sano A., Ohmori T. Positive association of the PDE4B (phosphodiesterase 4B) gene with schizophrenia in the Japanese population. J. Psychiatr. Res. 2008;43:7-12.

    Not in our library10.1016/j.jpsychires.2008.01.013

  119. 119.

    Numata S., Ueno S.-i., Iga J.-i., Nakataki M., Tanahashi T., Itakura M., Sano A., Ohi K., Hashimoto R., Takeda M., Ohmori T. No association between the NDE1 gene and schizophrenia in the Japanese population. Schizophr. Res. 2008;99:367-369.

    Not in our library10.1016/j.schres.2007.10.032

  120. 120.

    Numata S., Iga J.-I., Nakataki M., Tayoshi S., Taniguchi K., Sumitani S., Tomotake M., Tanahashi T., Itakura M., Kamegaya Y., Tatsumi M., Sano A., Asada T., Kunugi H., Ueno S.-I., Ohmori T. Gene expression and association analyses of the phosphodiesterase 4B (PDE4B) gene in major depressive disorder in the Japanese population. Am. J. Med. Genet. B. 2009;150B:527-534.

    Not in our library10.1002/ajmg.b.30852

  121. 121.

    Numata S., Iga J., Nakataki M., Tayoshi S., Tanahashi T., Itakura M., Ueno S., Ohmori T. Positive association of the pericentrin (PCNT) gene with major depressive disorder in the Japanese population. J. Psychiatry Neurosci. 2009;34:195-198.

    Not in our library

  122. 122.

    Numata S., Nakataki M., Iga J.-i., Tanahashi T., Nakadoi Y., Ohi K., Hashimoto R., Takeda M., Itakura M., Ueno S.-i., Ohmori T. Association study between the pericentrin (PCNT) gene and schizophrenia. Neuromolecular Med. 2010;12:243-247.

    Not in our library10.1007/s12017-009-8106-x

  123. 123.

    O’Donnell J.M., Zhang H.-T. Antidepressant effects of inhibitors of cAMP phosphodiesterase (PDE4). Trends Pharmacol. Sci. 2004;25:158-163.

    Not in our library10.1016/j.tips.2004.01.003

  124. 124.

    Ogawa F., Kasai M., Akiyama T. A functional link between disrupted-in-schizophrenia 1 and the eukaryotic translation initiation factor 3. Biochem. Biophysical Res. Commun. 2005;338:771-776.

    Not in our library10.1016/j.bbrc.2005.10.013

  125. 125.

    Okuda A., Kishi T., Okochi T., Ikeda M., Kitajima T., Tsunoka T., Okumukura T., Fukuo Y., Kinoshita Y., Kawashima K., Yamanouchi Y., Inada T., Ozaki N., Iwata N. Translin-associated factor X gene (TSNAX) may be associated with female major depressive disorder in the Japanese population. Neuromol. Med. 2010;12:78-85.

    Not in our library10.1007/s12017-009-8090-1

  126. 126.

    Ozeki Y., Tomoda T., Kleiderlein J., Kamiya A., Bord L., Fujii K., Okawa M., Yamada N., Hatten M.E., Snyder S.H., Ross C.A., Sawa A. Disrupted-in-schizophrenia-1 (DISC-1): mutant truncation prevents binding to NudE-like (NUDEL) and inhibits neurite outgrowth. Proc. Natl. Acad. Sci. USA. 2003;100:289-294.

    Not in our library10.1073/pnas.0136913100

  127. 127.

    Palo O.M., Antila M., Silander K., Hennah W., Kilpinen H., Soronen P., Tuulio-Henriksson A., Kieseppa T., Partonen T., Lonnqvist J., Peltonen L., Paunio T. Association of distinct allelic haplotypes of DISC1 with psychotic and bipolar spectrum disorders and with underlying cognitive impairments. Hum. Mol.Genet. 2007;16:2517-2528.

    Not in our library10.1093/hmg/ddm207

  128. 128.

    Perlis R.H., Purcell S., Fagerness J., Kirby A., Petryshen T.L., Fan J., Sklar P. Family-based association study of lithium-related and other candidate genes in bipolar disorder. Arch. Gen. Psychiatry. 2008;65:53-61.

    Not in our library10.1001/archgenpsychiatry.2007.15

  129. 129.

    Pickard B.S., Thomson P.A., Christoforou A., Evans K.L., Morris S.W., Porteous D.J., Blackwood D.H.R., Muir W.J. The PDE4B gene confers sex-specific protection against schizophrenia. Psychiatr. Genet. 2007;17:129-133.

    Not in our library10.1097/ypg.0b013e328014492b

  130. 130.

    Porteous D., Millar K. How DISC1 regulates postnatal brain development: girdin gets in on the AKT. Neuron. 2009;63:711-713.

    Not in our library10.1016/j.neuron.2009.09.017

  131. 131.

    Porteous D. Genetic causality in schizophrenia and bipolar disorder: out with the old and in with the new. Curr. Opin. Genet. Dev. 2008;18:229-234.

    Not in our library10.1016/j.gde.2008.07.005

  132. 132.

    Potkin S.G., Turner J.A., Guffanti G., Lakatos A., Fallon J.H., Nguyen D.D., Mathalon D., Ford J., Lauriello J., Macciardi F., FBIRN. A genome-wide association study of schizophrenia using brain activation as a quantitative phenotype. Schizophr. Bull. 2009;35:96-108.

    Not in our library10.1093/schbul/sbn155

  133. 133.

    Prata D.P., Mechelli A., Fu C.H.Y., Picchioni M., Kane F., Kalidindi S., McDonald C., Kravariti E., Toulopoulou T., Miorelli A., Murray R., Collier D.A., McGuire P.K. Effect of disrupted-in-schizophrenia-1 on pre-frontal cortical function. Mol. Psychiatry. 2008;13:915-917.

    Not in our library10.1038/mp.2008.76

  134. 134.

    Purohit A., Tynan S.H., Vallee R., Doxsey S.J. Direct interaction of pericentrin with cytoplasmic dynein light intermediate chain contributes to mitotic spindle organization. J. Cell Biol. 1999;147:481-492.

    Not in our library10.1083/jcb.147.3.481

  135. 135.

    Qu M., Tang F., Wang L., Yan H., Han Y., Yan J., Yue W., Zhang D. Associations of ATF4 gene polymorphisms with schizophrenia in male patients. Am. J. Med. Genet. B. Neuropsychiatr. Genet. 2008;147B:732-736.

    Not in our library10.1002/ajmg.b.30675

  136. 136.

    Rastogi A., Zai C., Likhodi O., Kennedy J.L., Wong A.H. Genetic association and post-mortem brain mRNA analysis of DISC1 and related genes in schizophrenia. Schizophr. Res. 2009;114:39-49.

    Not in our library10.1016/j.schres.2009.06.019

  137. 137.

    Rauch A., Thiel C.T., Schindler D., Wick U., Crow Y.J., Ekici A.B., van Essen A.J., Goecke T.O., Al-Gazali L., Chrzanowska K.H., Zweier C., Brunner H.G., Becker K., Curry C.J., Dallapiccola B., Devriendt K., Dorfler A., Kinning E., Megarbane A., Meinecke P., Semple R.K., Spranger S., Toutain A., Trembath R.C., Voss E., Wilson L., Hennekam R., de Zegher F., Dorr H.-G., Reis A. Mutations in the pericentrin (PCNT) gene cause primordial dwarfism. Science. 2008;319:816-819.

    Not in our library10.1126/science.1151174

  138. 138.

    Ross C.A., Margolis R.L. Schizophrenia: a point of disruption. Nature. 2009;458:976-977.

    Not in our library10.1038/458976a

  139. 139.

    Saetre P., Agartz I., De Franciscis A., Lundmark P., Djurovic S., Kähler A., Andreassen O.A., Jakobsen K.D., Rasmussen H.B., Werge T., Hall H., Terenius L., Jönsson E.G. Association between a disrupted-in-schizophrenia 1 (DISC1) single nucleotide polymorphism and schizophrenia in a combined Scandinavian case–control sample. Schizophr. Res. 2008;106:237-241.

    Not in our library10.1016/j.schres.2008.08.024

  140. 140.

    Sanders A.R., Duan J., Levinson D.F., Shi J., He D., Hou C., Burrell G.J., Rice J.P., Nertney D.A., Olincy A., Rozic P., Vinogradov S., Buccola N.G., Mowry B.J., Freedman R., Amin F., Black D.W., Silverman J.M., Byerley W.F., Crowe R.R., Cloninger C.R., Martinez M., Gejman P.V. No significant association of 14 candidate genes with schizophrenia in a large european ancestry sample: implications for psychiatric genetics. Am. J. Psychiatry. 2008;165:497-506.

    Not in our library10.1176/appi.ajp.2007.07101573

  141. 141.

    Sasaki S., Shionoya A., Ishida M., Gambello M.J., Yingling J., Wynshaw-Boris A., Hirotsune S. A LIS1/NUDEL/cytoplasmic dyenin heavy chain complex in the developing and adult nervous system. Neuron. 2000;28:681-696.

    Not in our library10.1016/s0896-6273(00)00146-x

  142. 142.

    Sasaki S., Mori D., Toyo-oka K., Chen A., Garrett-Beal L., Muramatsu M., Miyagawa S., Hiraiwa N., Yoshiki A., Wynshaw-Boris A., Hirotsune S. Complete loss of Ndel1 results in neuronal migration defects and early embryonic lethality. Mol. Cell. Biol. 2005;25:7812-7827.

    Not in our library10.1128/mcb.25.17.7812-7827.2005

  143. 143.

    Sawamura N., Ando T., Maruyama Y., Fujimuro M., Mochizuki H., Honjo K., Shimoda M., Toda H., Sawamura-Yamamoto T., Makuch L.A., Hayashi A., Ishizuka K., Cascella N.G., Kamiya A., Ishida N., Tomoda T., Hai T., Furukubo-Tokunaga K., Sawa A. Nuclear DISC1 regulates CRE-mediated gene transcription and sleep homeostasis in the fruit fly. Mol. Psychiatry. 2008;13:1138-1148.

    Not in our library10.1038/mp.2008.101

  144. 144.

    Sayer J.A., Otto E.A., O’Toole J.F., Nurnberg G., Kennedy M.A., Becker C., Hennies H.C., Helou J., Attanasio M., Fausett B.V., Utsch B., Khanna H., Liu Y., Drummond I., Kawakami I., Kusakabe T., Tsuda M., Ma L., Lee H., Larson R.G., Allen S.J., Wilkinson C.J., Nigg E.A., Shou C., Lillo C., Williams D.S., Hoppe B., Kemper M.J., Neuhaus T., Parisi M.A., Glass I.A., Petry M., Kispert A., Gloy J., Ganner A., Walz G., Zhu X., Goldman D., Nurnberg P., Swaroop A., Leroux M.R., Hildebrandt F. The centrosomal protein nephrocystin-6 is mutated in Joubert syndrome and activates transcription factor ATF4. Nat. Genet. 2006;38:674-681.

    Not in our library10.1038/ng1786

  145. 145.

    Schmitt A., Parlapani E., Gruber O., Wobrock T., Falkai P. Impact of neuregulin-1 on the pathophysiology of schizophrenia in human post-mortem studies. Eur. Arch. Psychiatry Clin. Neurosci. 2008;258:35-39.

    Not in our library10.1007/s00406-008-5019-x

  146. 146.

    Schosser A., Gaysina D., Cohen-Woods S., Chow P.C., Martucci L., Craddock N., Farmer A., Korszun A., Gunasinghe C., Gray J., Jones L., Tozzi F., Perry J., Muglia P., Owen M.J., Craig I.W., McGuffin P. Association of DISC1 and TSNAX genes and affective disorders in the depression case-control (DeCC) and bipolar affective case-control (BACCS) studies. Mol. Psychiatry. 2010;15:844-849.

    Not in our library10.1038/mp.2009.21

  147. 147.

    Schumacher J., Laje G., Abou Jamra R., Becker T., Mühleisen T.W., Vasilescu C., Mattheisen M., Herms S., Hoffmann P., Hillmer A.M., Georgi A., Herold C., Schulze T.G., Propping P., Rietschel M., McMahon F.J., Nöthen M.M., Cichon S. The DISC locus and schizophrenia: evidence from an association study in a central European sample and from a meta-analysis across different European populations. Hum. Mol. Genet. 2009;18:2719-2727.

    Not in our library10.1093/hmg/ddp204

  148. 148.

    Seshadri S., Kamiya A., Yokota Y., Prikulis I., Kano S.-I., Hayashi-Takagi A., Stanco A., Eom T.-Y., Rao S., Ishizuka K., Wong P., Korth C., Anton E.S., Sawa A. Disrupted-in-schizophrenia-1 expression is regulated by b-site amyloid precursor protein cleaving enzyme-1-neuregulin cascade. Prot. Natl. Acad. Sci. USA. 2010;107:5622-5627.

    Not in our library10.1073/pnas.0909284107

  149. 149.

    Shim S.Y., Samuels B.A., Wang J., Neumayer G., Belzil C., Ayala R., Shi Y., Shi Y., Tsai L.-H., Nguyen M.D. Ndel1 controls the dynein-mediated transport of vimentin during neurite outgrowth. J. Biol. Chem. 2008;283:12232-12240.

    Not in our library10.1074/jbc.m710200200

  150. 150.

    Shimizu S., Matsuzaki S., Hattori T., Kumamoto N., Miyoshi K., Katayama T., Tohyama M. DISC1-kendrin interaction is involved in centrosomal microtubule network formation. Biochem. Biophysical Res. Commun. 2008;377:1051-1056.

    Not in our library10.1016/j.bbrc.2008.10.100

  151. 151.

    Shinoda T., Taya S., Tsuboi D., Hikita T., Matsuzawa R., Kuroda S., Iwamatsu A., Kaibuchi K. DISC1 regulates neurotrophin-induced axon elongation via interaction with Grb2. J. Neurosci. 2007;27:4-14.

    Not in our library10.1523/jneurosci.3825-06.2007

  152. 152.

    Singh K.K., Ge X., Mao Y., Drane L., Meletis K., Samuels B.A., Tsai L.-H. Dixdc1 is a critical regulator of DISC1 and embryonic cortical development. Neuron. 2010;67:33-48.

    Not in our library10.1016/j.neuron.2010.06.002

  153. 153.

    Smith D.S., Niethammer M., Ayala R., Zhou Y., Gambello M.J., Wynshaw-Boris A., Tsai L.-H. Regulation of cytoplasmic dynein behaviour and microtubule organization by mammalian Lis1. Nat. Cell Biol. 2000;2:767-775.

    Not in our library10.1038/35041000

  154. 154.

    Song W., Li W., Feng J., Heston L.L., Scaringe W.A., Sommer S.S. Identification of high risk DISC1 structural variants with a 2% attributable risk for schizophrenia. Biochem. Biophysical Res. Commun. 2008;367:700-706.

    Not in our library10.1016/j.bbrc.2007.12.117

  155. 155.

    Song W., Li W., Noltner K., Yan J., Green E., Grozeva D., Jones I.R., Craddock N., Longmate J., Feng J., Sommer S.S. Identification of high risk DISC1 protein structural variants in patients with bipolar spectrum disorder. Neurosci. Lett. 2010.

    Not in our library10.1016/j.neulet.2010.09.027

  156. 156.

    St Clair D., Blackwood D., Muir W., Carothers A., Walker M., Spowart G., Gosden C., Evans H.J. Association within a family of a balanced autosomal translocation with major mental illness. Lancet. 1990;336:13-16.

    Not in our library10.1016/0140-6736(90)91520-k

  157. 157.

    Stehman S.A., Chen Y., McKenney R.J., Vallee R.B. NudE and NudEL are r. PLoS Genet. 2009;5:e1000373.

    Not in our library

  158. 158.

    Sullivan P.F., Lin D., Tzeng J.-Y., van den Oord E., Perkins D., Stroup T.S., Wagner M., Lee S., Wright F.A., Zou F., Liu W., Downing A.M., Lieberman J., Close S.L. Genomewide association for schizophrenia in the CATIE study: results of stage 1. Mol. Psychiatry. 2008;13:570-584.

    Not in our library10.1038/mp.2008.25

  159. 159.

    Sweeney K.J., Prokscha A., Eichele G. NudE-L, a novel Lis1-interacting protein, belongs to a family of vertebrate coiled-coil proteins. Mech. Dev. 2001;101:21-33.

    Not in our library10.1016/s0925-4773(00)00543-8

  160. 160.

    Szeszko P.R., Hodgkinson C.A., Robinson D.G., DeRosse P., Bilder R.M., Lencz T., Burdick K.E., Napolitano B., Betensky J.D., Kane J.M., Goldman D., Malhotra A.K. DISC1 is associated with prefrontal cortical gray matter and positive symptoms in schizophrenia. Biol. Psychol. 2008;79:103-110.

    Not in our library10.1016/j.biopsycho.2007.10.011

  161. 161.

    Tai C.-Y., Dujardin D.L., Faulkner N.E., Vallee R.B. Role of dynein, dynactin, and CLIP-170 interactions in LIS1 kinetochore function. J. Cell Biol. 2002;156:959-968.

    Not in our library10.1083/jcb.200109046

  162. 162.

    Takahashi M., Yamagiwa A., Nishimura T., Mukai H., Ono Y. Centrosomal proteins CG-NAP and kendrin provide microtubule nucleation sites by anchoring g-tubulin ring complex. Mol. Biol. Cell. 2002;13:3235-3245.

    Not in our library10.1091/mbc.e02-02-0112

  163. 163.

    Takahashi T., Suzuki M., Tsunoda M., Maeno N., Kawasaki Y., Zhou S.-Y., Hagino H., Niu L., Tsuneki H., Kobayashi S., Sasaoka T., Seto H., Kurachi M., Ozaki N. The disrupted-in-schizophrenia-1 Ser704Cys polymorphism and brain morphology in schizophrenia. Psychiatry Res. Neuroimaging. 2009;172:128-135.

    Not in our library10.1016/j.pscychresns.2009.01.005

  164. 164.

    Talukder A.H., Vadlamudi R., Mandal M., Kumar R. Heregulin induces expression, DNA binding activity, and transactivating functions of basic leucine zipper activating transcription factor 4. Cancer Res. 2000;60:276-281.

    Not in our library

  165. 165.

    Taya S., Shinoda T., Tsuboi D., Asaki J., Nagai K., Hikita T., Kuroda S., Kuroda K., Shimizu M., Hirotsune S., Iwamatsu A., Kaibuchi K. DISC1 regulates the transport of the NUDEL/LIS1/14-3-3epsilon complex through kinesin-1. J. Neurosci. 2007;27:15-26.

    Not in our library10.1523/jneurosci.3826-06.2006

  166. 166.

    Tomppo L., Hennah W., Lahermo P., Loukola A., Tuulio-Henriksson A., Suvisaari J., Partonen T., Ekelund J., Lönnqvist J., Peltonen L. Association between genes of disrupted in schizophrenia 1 (DISC1) interactors and schizophrenia supports the role of the DISC1 pathway in the etiology of major mental illnesses. Biol. Psychiatry. 2009;65:1055-1062.

    Not in our library10.1016/j.biopsych.2009.01.014

  167. 167.

    Tomppo L., Hennah W., Miettunen J., Jarvelin M.-R., Veijola J., Ripatti S., Lahermo P., Lichtermann D., Peltonen L., Ekelund J. Association of variants in DISC1 with psychosis-related traits in a large population cohort. Arch. Gen. Psychiatry. 2009;66:134-141.

    Not in our library10.1001/archgenpsychiatry.2008.524

  168. 168.

    Toth C., Shim S.Y., Wang J., Jiang Y., Neumayer G., Belzil C., Liu W.-Q., Martinez J., Zochodne D., Nguyen M.D. Ndel1 promotes axon regeneration via intermediate filaments. PLOS One. 2008;3:e2014.

    Not in our library10.1371/journal.pone.0002014

  169. 169.

    Toyo-oka K., Sasaki S., Yano Y., Mori D., Kobayashi T., Toyoshima Y.Y., Tokuoka S.M., Ishii S., Shimizu T., Muramatsu M., Hiraiwa N., Yoshiki A., Wynshaw-Boris A., Hirotsune S. Recruitment of katanin p60 by phosphorylated NDEL1, an LIS1 interacting protein, is essential for mitotic cell division and neuronal migration. Hum. Mol. Genet. 2005;14:3113-3128.

    Not in our library10.1093/hmg/ddi339

  170. 170.

    Vernon E., Meyer G., Pickard L., Dev K., Molnar E., Collingridge G.L., Henley J.M. GABAB receptors couple directly to the transcription factor ATF4. Mol. Cell. Neurosci. 2001;17:637-645.

    Not in our library10.1006/mcne.2000.0960

  171. 171.

    Wang Q., Du X., Meinkoth J., Hirohashi Y., Zhang H., Liu Q., Richter M., Greene M.I. Characterization of Su48, a centrosome protein essential for cell division. Proc. Natl. Acad. Sci. USA. 2006;103:6512-6517.

    Not in our library10.1073/pnas.0601682103

  172. 172.

    Wang Q., Charych E.I., Pulito V.L., Lee J.B., Graziane N.M., Crozier R.A., Revilla-Sanchez R., Kelly M.P., Dunlop A.J., Murdoch H., Taylor N., Xie Y., Pausch M., Hayashi-Takagi A., Ishizuka K., Seshadri S., Bates B., Kariya K., Sawa A., Weinberg R.J., Moss S.J., Houslay M.D., Yan Z., Brandon N.J. The psychiatric disease risk factors DISC1 and TNIK interact to regulate synapse composition and function. Mol. Psychiatry. 2010.

    Not in our library10.1038/mp.2010.87

  173. 173.
    The GABAB receptor interacts directly with the related transcription factors CREB2 and ATFx · 2000
    Not checked
  174. 174.

    Williams J.M., Beck T.F., Pearson D.M., Proud M.B., Cheung S.W., Scott D.A. A 1q42 deletion involving DISC1, DISC2, and TSNAX in an autism spectrum disorder. Am. J. Med. Genet. A. 2009;149A:1758-1762.

    Not in our library10.1002/ajmg.a.32941

  175. 175.

    Wynshaw-Boris A., Pramparo T., Youn Y.H., Hirotsune S. Lissencephaly: mechanistic insights from animal models and potential therapeutic strategies. Semin. Cell Dev. Biol. 2010.

    Not in our library10.1016/j.semcdb.2010.07.008

  176. 176.

    Xie Z., Srivastava D.P., Photowala H., Kai L., Cahill M.E., Woolfrey K.M., Shum C.Y., Surmeier D.J., Penzes P. Kalirin-7 controls activity-dependent structural and functional plasticity of dendritic spines. Neuron. 2007;56:640-656.

    Not in our library10.1016/j.neuron.2007.10.005

  177. 177.

    Yamada K., Nakamura K., Minabe Y., Iwayama-Shigeno Y., Takao H., Toyota T., Hattori E., Takei N., Sekine Y., Suzuki K., Iwata Y., Miyoshi K., Honda A., Baba K., Katayama T., Tohyama M., Mori N., Yoshikawa T. Association analysis of FEZ1 variants with schizophrenia in Japanese cohorts. Biol. Psychiatry. 2004;56:683-690.

    Not in our library10.1016/j.biopsych.2004.08.015

  178. 178.

    Young-Pearse T.L., Bai J., Chang R., Zheng J.B., LoTurco J.J., Selkoe D.J. A critical function for b-amyloid precursor protein in neuronal nigration revealed by in utero RNA interference. J. Neurosci. 2007;27:14459-14469.

    Not in our library10.1523/jneurosci.4701-07.2007

  179. 179.

    Young-Pearse T.L., Suth S., Luth E.S., Sawa A., Selkoe D.J. Biochemical and functional interaction of disrupted-in-schizophrenia 1 and amyloid precursor protein regulates neuronal migration during mammalian cortical development. J. Neurosci. 2010;30:10431-10440.

    Not in our library10.1523/jneurosci.1445-10.2010

  180. 180.

    Zhang W., Vazquez L., Apperson M., Kennedy M.B. Citron binds to PSD-95 at glutamatergic synapses on inhibitory neurons in the hippocampus. J. Neurosci. 1999;19:96-108.

    Not in our library10.1523/jneurosci.19-01-00096.1999

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