Chen Jun, Siddiqui Aleem
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.
J Virol. 2007 Jun;81(12):6757-60. doi: 10.1128/JVI.00172-07. Epub 2007 Apr 11.
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.
人类乙型肝炎病毒（HBV）X蛋白（HBx）在病毒生命周期中发挥关键作用，并促使肝细胞癌（HCC）的发生。HBx单独或在全病毒基因组转染的情况下导致Raf-1激酶的线粒体易位。Raf-1的线粒体易位由HBx诱导的氧化应激介导，并分别依赖于p21激活蛋白激酶1和Src激酶对Raf-1丝氨酸338/339和Y340/341残基的磷酸化。这些研究为HBV诱导与肝病发病机制（包括HCC）相关的细胞内事件的机制提供了深入了解。
