Hepatitis B Virus X Protein Stimulates the Mitochondrial Translocation of Raf-1 via Oxidative Stress
Copyright policy )Hepatitis B Virus X Protein Stimulates the Mitochondrial Translocation of Raf-1 via Oxidative Stress
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 serine 338/339 and Y 340/341 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.
- University of California, San Diego United States
- Central South University China (People's Republic of)
- Second Xiangya Hospital of Central South University China (People's Republic of)
- UNIVERSITY OF CALIFORNIA SAN DIEGO
- University of California, San Diego United States
Liver Diseases, Liver Neoplasms, Biological Transport, Genome, Viral, Protein Serine-Threonine Kinases, Mitochondria, Proto-Oncogene Proteins c-raf, Oxidative Stress, Protein Transport, src-Family Kinases, p21-Activated Kinases, Cell Line, Tumor, Serine, Trans-Activators, Humans, Viral Regulatory and Accessory Proteins, Phosphorylation
Liver Diseases, Liver Neoplasms, Biological Transport, Genome, Viral, Protein Serine-Threonine Kinases, Mitochondria, Proto-Oncogene Proteins c-raf, Oxidative Stress, Protein Transport, src-Family Kinases, p21-Activated Kinases, Cell Line, Tumor, Serine, Trans-Activators, Humans, Viral Regulatory and Accessory Proteins, Phosphorylation
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