DISC1-binding proteins in neural development, signalling and schizophrenia

被引：141

作者：

Bradshaw, Nicholas J. ^{[1
]}

Porteous, David J. ^{[1
]}

机构：

[1] Univ Edinburgh, Western Gen Hosp, Inst Genet & Mol Med, Med Genet Sect,Mol Med Ctr, Edinburgh EH4 2XU, Midlothian, Scotland

来源：

NEUROPHARMACOLOGY | 2012年 / 62卷 / 03期

基金：

英国惠康基金;

关键词：

DISC1; Schizophrenia; Neurodevelopment; Signalling; Synapse; Association studies; AMYLOID PRECURSOR PROTEIN; MAJOR DEPRESSIVE DISORDER; PERICENTRIN PCNT GENE; TRANSCRIPTION FACTOR; NEURONAL MIGRATION; BIPOLAR DISORDER; CENTROSOMAL PROTEINS; ASSOCIATION ANALYSIS; CANDIDATE GENES; GRAY-MATTER;

D O I：

10.1016/j.neuropharm.2010.12.027

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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 (GSK3 beta), neurosignalling (Girdin, GSK3 beta, 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. This article is part of a Special Issue entitled 'Schizophrenia'. (C) 2011 Elsevier Ltd. All rights reserved.

引用

页码：1230 / 1241

页数：12

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