國家衛生研究院 NHRI:Item 3990099045/2791
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/2791


    Title: Hepatitis B virus X protein activates a survival signaling by linking Src to phosphatidylinositol 3-kinase
    Authors: Shih, WL;Kuo, ML;Chuang, SE;Cheng, AL;Doong, SL
    Contributors: National Institute of Cancer Research
    Abstract: We have previously shown that transactivation-proficient hepatitis virus B X protein (HBx) protects Hep 3B cells from transforming growth factor-beta (TGF-beta)-induced apoptosis via activation of the phosphatidylinositol 3-kinase ( PI 3-kinase)/Akt signaling pathway. This work further investigated how HBx activates PI 3-kinase. Src activity was elevated in Hep 3B cells following expression of transactivation-proficient HBx or HBx-GFP fusion proteins. The Src family kinase inhibitor PP2 and C-terminal Src kinase (Csk) both alleviated HBx-mediated PI 3-kinase activation and protection from TGF-beta-induced apoptosis. Therefore, HBx activated a survival signal by linking Src to PI 3-kinase. Systemic subcellular fractionation and membrane flotation assays indicated that similar to 1.5% of ectopically expressed HBxGFP was associated with periplasmic membrane where Src was located. However, neither nucleus-targeted nor periplasmic membrane-targeted HBxGFP was able to upregulate Src activity or to augment PI 3-kinase survival signaling pathway.
    Keywords: Biochemistry & Molecular Biology
    Date: 2003-08-22
    Relation: Journal of Biological Chemistry. 2003 Aug;278(34):31807-31813.
    Link to: http://dx.doi.org/10.1074/jbc.M302580200
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1083-351X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000184782100043
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0042357131
    Appears in Collections:[Shuang-En Chuang] Periodical Articles

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