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本文引用的文献

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Loss of dysbindin-1 in mice impairs reward-based operant learning by increasing impulsive and compulsive behavior.小鼠中 dysbindin-1 的缺失通过增加冲动和强迫行为来损害基于奖励的操作性学习。
Behav Brain Res. 2013 Mar 15;241:173-84. doi: 10.1016/j.bbr.2012.12.021. Epub 2012 Dec 20.
2
Pathogenic disruption of DISC1-serine racemase binding elicits schizophrenia-like behavior via D-serine depletion.致病性 DISC1-丝氨酸消旋酶结合破坏通过 D-丝氨酸耗竭引起精神分裂症样行为。
Mol Psychiatry. 2013 May;18(5):557-67. doi: 10.1038/mp.2012.97. Epub 2012 Jul 17.
3
Behavioral alterations associated with targeted disruption of exons 2 and 3 of the Disc1 gene in the mouse.与在小鼠中靶向破坏 Disc1 基因外显子 2 和 3 相关的行为改变。
Hum Mol Genet. 2011 Dec 1;20(23):4666-83. doi: 10.1093/hmg/ddr400. Epub 2011 Sep 8.
4
Convergence of two independent mental disease genes on the protein level: recruitment of dysbindin to cell-invasive disrupted-in-schizophrenia 1 aggresomes.两个独立的精神疾病基因在蛋白质水平上的汇聚：通过募集神经连接蛋白聚糖至分裂素激活激酶相互作用蛋白 1 聚集体，导致细胞侵袭。
Biol Psychiatry. 2011 Oct 1;70(7):604-10. doi: 10.1016/j.biopsych.2011.03.027. Epub 2011 May 4.
5
Dysbindin-1, a schizophrenia-related protein, facilitates neurite outgrowth by promoting the transcriptional activity of p53.神经结合蛋白-1 是一种与精神分裂症相关的蛋白质，通过促进 p53 的转录活性促进神经突生长。
Mol Psychiatry. 2011 Nov;16(11):1105-16. doi: 10.1038/mp.2011.43. Epub 2011 Apr 19.
6
DISC1-dependent switch from progenitor proliferation to migration in the developing cortex.DISC1 依赖性发育皮层祖细胞增殖到迁移的转变。
Nature. 2011 May 5;473(7345):92-6. doi: 10.1038/nature09859. Epub 2011 Apr 6.
7
Dysbindin-1 modulates prefrontal cortical activity and schizophrenia-like behaviors via dopamine/D2 pathways.Dysbindin-1 通过多巴胺/D2 途径调节前额叶皮层活动和类似精神分裂症的行为。
Mol Psychiatry. 2012 Jan;17(1):85-98. doi: 10.1038/mp.2010.106. Epub 2010 Oct 19.
8
CAMDI, a novel disrupted in schizophrenia 1 (DISC1)-binding protein, is required for radial migration.CAMDI，一种新型的精神分裂症 1 （DISC1）结合蛋白，是放射状迁移所必需的。
J Biol Chem. 2010 Dec 24;285(52):40554-61. doi: 10.1074/jbc.M110.179481. Epub 2010 Oct 18.
9
Disrupted-in-schizophrenia 1 (DISC1) plays essential roles in mitochondria in collaboration with Mitofilin.精神分裂症相关蛋白 1（DISC1）与 Mitofilin 协作在细胞器线粒体中发挥重要作用。
Proc Natl Acad Sci U S A. 2010 Oct 12;107(41):17785-90. doi: 10.1073/pnas.1004361107. Epub 2010 Sep 28.
10
Dysbindin-1, WAVE2 and Abi-1 form a complex that regulates dendritic spine formation.Dysbindin-1、WAVE2 和 Abi-1 形成一个复合物，调节树突棘的形成。
Mol Psychiatry. 2010 Oct;15(10):976-86. doi: 10.1038/mp.2010.69. Epub 2010 Jun 8.

精神分裂症相关基因1（DISC1）通过增强dysbindin的稳定性来调节其功能。

Disrupted-in-schizophrenia 1 (DISC1) regulates dysbindin function by enhancing its stability.

作者信息

Lee Seol-Ae, Kim Seong-Mo, Suh Bo Kyoung, Sun Hwa-Young, Park Young-Un, Hong Ji-Ho, Park Cana, Nguyen Minh Dang, Nagata Koh-Ichi, Yoo Joo-Yeon, Park Sang Ki

机构信息

From the Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea.

the Hotchkiss Brain Institute, Departments of Clinical Neurosciences, Cell Biology and Anatomy, and Biochemistry and Molecular Biology, University of Calgary, Calgary T2N 4N1, Canada, and.

出版信息

J Biol Chem. 2015 Mar 13;290(11):7087-96. doi: 10.1074/jbc.M114.614750. Epub 2015 Jan 29.

DOI:10.1074/jbc.M114.614750
PMID:25635053
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4358130/
Abstract

Dysbindin and DISC1 are schizophrenia susceptibility factors playing roles in neuronal development. Here we show that the physical interaction between dysbindin and DISC1 is critical for the stability of dysbindin and for the process of neurite outgrowth. We found that DISC1 forms a complex with dysbindin and increases its stability in association with a reduction in ubiquitylation. Furthermore, knockdown of DISC1 or expression of a deletion mutant, DISC1 lacking amino acid residues 403-504 of DISC1 (DISC1(Δ403-504)), effectively decreased levels of endogenous dysbindin. Finally, the neurite outgrowth defect induced by knockdown of DISC1 was partially reversed by coexpression of dysbindin. Taken together, these results indicate that dysbindin and DISC1 form a physiologically functional complex that is essential for normal neurite outgrowth.

摘要

失调结合蛋白（dysbindin）和精神分裂症相关基因1（DISC1）是在神经元发育过程中发挥作用的精神分裂症易感因素。在此我们表明，失调结合蛋白与DISC1之间的物理相互作用对于失调结合蛋白的稳定性以及神经突生长过程至关重要。我们发现，DISC1与失调结合蛋白形成复合物，并通过减少泛素化作用来提高其稳定性。此外，敲低DISC1或表达缺失氨基酸残基403 - 504的DISC1缺失突变体（DISC1(Δ403 - 504)），可有效降低内源性失调结合蛋白的水平。最后，通过共表达失调结合蛋白，部分逆转了敲低DISC1所诱导的神经突生长缺陷。综上所述，这些结果表明，失调结合蛋白与DISC1形成了一种对正常神经突生长必不可少的生理功能复合物。