Expression of DISC1 binding partners is reduced in schizophrenia and associated with DISC1 SNPs

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Expression of DISC1 binding partners is reduced in schizophrenia and associated with DISC1 SNPs.

DISC1 has been identified as a schizophrenia susceptibility gene based on linkage and SNP association studies and clinical data suggesting that risk SNPs impact on hippocampal structure and function. In cell and animal models, C-terminus-truncated DISC1 disrupts intracellular transport, neural architecture and migration, perhaps because it fails to interact with binding partners involved in neu...

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DISC1 Partners with GSK3β in Neurogenesis

The protein DISC1, encoded by a gene implicated in schizophrenia susceptibility, regulates the development of postmitotic neurons. Mao et al. (2009) now report that DISC1 also regulates the proliferation of embryonic and adult neural progenitor cells through the GSK3beta/beta-catenin pathway, providing new insights into how susceptibility genes may contribute to the etiology of psychiatric diso...

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DISC1-binding proteins in neural development, signalling and schizophrenia

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 ...

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Copy Number Variations in DISC1 and DISC1-Interacting Partners in Major Mental Illness

Robust statistical, genetic and functional evidence supports a role for DISC1 in the aetiology of major mental illness. Furthermore, many of its protein-binding partners show evidence for involvement in the pathophysiology of a range of neurodevelopmental and psychiatric disorders. Copy number variants (CNVs) are suspected to play an important causal role in these disorders. In this study, CNV ...

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Two papers address the contribution of DISC1 to neural development and schizophrenia risk in this issue of Neuron. These complementary studies elegantly bridge the gap between genetic and cellular studies of schizophrenia, providing a level of functional validation that is often lacking in the field.

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ژورنال

عنوان ژورنال: Human Molecular Genetics

سال: 2006

ISSN: 1460-2083,0964-6906

DOI: 10.1093/hmg/ddl040