Hepatitis B virus X protein stimulates the mitochondrial translocation of Raf-1 via oxidative stress |
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Authors: | Chen Jun Siddiqui Aleem |
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Affiliation: | Department of Medicine, SCRB 409, University of California-San Diego, 9500 Gilman Drive, MC0711, La Jolla, CA 92093, USA, and Liver Disease Research Center, Second Xiangya Hospital, Changsha, China. |
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Abstract: | The human hepatitis B virus (HBV) X protein (HBx) plays a crucial role(s) in the viral life cycle and contributes to the onset of hepatocellular carcinoma (HCC). HBx caused the mitochondrial translocation of Raf-1 kinase either alone or in the context of whole-viral-genome transfections. Mitochondrial translocation of Raf-1 is mediated by HBx-induced oxidative stress and was dependent upon the phosphorylation of Raf-1 at the serine338/339 and Y340/341 residues by p21-activated protein kinase 1 and Src kinase, respectively. These studies provide an insight into the mechanisms by which HBV induces intracellular events relevant to liver disease pathogenesis, including HCC. |
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