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    ASIA unversity > 醫學暨健康學院 > 期刊論文 >  Item 310904400/6786

    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/6786

    Title: Erk associates with and primes GSK-3β for its inactivation resulting in upregulation of β-catenin
    Authors: Qingqing Ding;Weiya Xia;Jaw-Ching Liu;Jer-Yen Yang;Dung-Fang Lee;Jiahong Xia;Geoffrey Bartholomeusz;Yan Li;Zheng Li;Ralf C. Bargou;Jun Qin;Fuu-Jen Tsai;Chang-Hai Tsai;洪明奇
    Date: 2005
    Issue Date: 2009-12-23 14:22:21 (UTC+8)
    Publisher: Asia University
    Abstract: β-catenin is upregulated in many human cancers and considered to be an oncogene. Hepatocellular carcinoma (HCC) is one of the most prevalent human malignancies, and individuals who are chronic hepatitis B virus (HBV) carriers have a greater than 100-fold increased relative risk of developing HCC. Here we report a mechanism by which HBV-X protein (HBX) upregulates β-catenin. Erk, which is activated by HBX, associates with GSK-3β through a docking motif (291FKFP) of GSK-3β and phosphorylates GSK-3β at the 43Thr residue, which primes GSK-3β for its subsequent phosphorylation at Ser9 by p90RSK, resulting in inactivation of GSK-3β and upregulation of β-catenin. This pathway is a general signal, as it was also observed in cell lines in which Erk-primed inactivation of GSK-3β was regulated by IGF-1, TGF-β, and receptor tyrosine kinase HER2, and is further supported by immunohistochemical staining in different human tumors, including cancers of the liver, breast, kidney, and stomach.
    Relation: MOLECULAR CELL 19 (00): 159-170
    Appears in Collections:[醫學暨健康學院] 期刊論文

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