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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16146


    Title: ARD1 stabilization of TSC2 suppresses tumorigenesis via the mTOR signaling pathway
    Authors: ;Kuo, H-P;Lee, D-F;Chen, C-T;Liu, M;Chou, C-K;Lee, H-J.;Xie, X;Wei, Y.;Xia, W;Zhang, W;Yi, D;Yang, J-Y;Huang, T-H;Yen, C-J;Tan, M;Xing, G;Zhao, Y;Lin, C-H;Tsai, S-F;Fidler, IJ;洪明奇;Hung, Mien-Chie
    Contributors: 生物科技學系
    Date: 2010
    Issue Date: 2012-11-23 17:09:09 (UTC+8)
    Abstract: Mammalian target of rapamycin (mTOR) regulates various cellular functions, including tumorigenesis, and is inhibited by the tuberous sclerosis 1 (TSC1)–TSC2 complex. Here, we demonstrate that arrest-defective protein 1 (ARD1) physically interacts with, acetylates, and stabilizes TSC2, thereby repressing mTOR activity. The inhibition of mTOR by ARD1 inhibits cell proliferation and increases autophagy, thereby inhibiting tumorigenicity. Correlation between ARD1 and TSC2 abundance was apparent in multiple tumor types. Moreover, evaluation of loss of heterozygosity at Xq28 revealed allelic loss in 31% of tested breast cancer cell lines and tumor samples. Together, our findings suggest that ARD1 functions as an inhibitor of the mTOR pathway and that dysregulation of the ARD1-TSC2-mTOR axis may contribute to cancer development.
    Relation: Science Signaling
    Appears in Collections:[生物科技學系] 期刊論文

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