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Disrupted-in-Schizophrenia-1 (DISC1) protein disturbs neural function in multiple disease-risk pathways  期刊论文  

  • 编号:
    e57b1d7d-33c7-477e-a7f0-d6d1f929f183
  • 作者:
    Shao, Lisha#[1,2]Lu, Binyan#[1,3]Wen, Zhexing[4,5,6];Teng, Shaolei[7];Wang, Lingling[1];Zhao, Yi[1];Wang, Liyuan[1];Ishizuka, Koko[8];Xu, Xiufeng(许秀峰)[9]Sawa, Akira[8];Song, Hongjun[4,5,6];Ming, Guoli[4,5,6];Zhong, Yi*[1,10]
  • 语种:
    英文
  • 期刊:
    HUMAN MOLECULAR GENETICS ISSN:0964-6906 2017 年 26 卷 14 期 (2634 - 2648) ; JUL 15
  • 收录:
  • 摘要:

    Although the genetic contribution is under debate, biological studies in multiple mouse models have suggested that the Disrupted-in-Schizophrenia-1 (DISC1) protein may contribute to susceptibility to psychiatric disorders. In the present study, we took the advantages of the Drosophila model to dissect the molecular pathways that can be affected by DISC1 in the context of pathology-related phenotypes. We found that three pathways that include the homologs of Drosophila Dys, Trio, and Shot were downregulated by introducing a C-terminal truncated mutant DISC1. Consistently, these three molecules were downregulated in the induced pluripotent stem cell-derived forebrain neurons from the subjects carrying a frameshift deletion in DISC1 C-terminus. Importantly, the three pathways were underscored in the pathophysiology of psychiatric disorders in bioinformatics analysis. Taken together, our findings are in line with the polygenic theory of psychiatric disorders.

  • 推荐引用方式
    GB/T 7714:
    Shao Lisha,Lu Binyan,Wen Zhexing, et al. Disrupted-in-Schizophrenia-1 (DISC1) protein disturbs neural function in multiple disease-risk pathways [J].HUMAN MOLECULAR GENETICS,2017,26(14):2634-2648.
  • APA:
    Shao Lisha,Lu Binyan,Wen Zhexing,Teng Shaolei,&Zhong Yi.(2017).Disrupted-in-Schizophrenia-1 (DISC1) protein disturbs neural function in multiple disease-risk pathways .HUMAN MOLECULAR GENETICS,26(14):2634-2648.
  • MLA:
    Shao Lisha, et al. "Disrupted-in-Schizophrenia-1 (DISC1) protein disturbs neural function in multiple disease-risk pathways" .HUMAN MOLECULAR GENETICS 26,14(2017):2634-2648.
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