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.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Biological Transport
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Cell Line, Tumor
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Genome, Viral
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Humans
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Liver Diseases / pathology
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Liver Neoplasms / metabolism
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Liver Neoplasms / pathology
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Mitochondria / metabolism*
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Oxidative Stress
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Phosphorylation
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Protein Serine-Threonine Kinases / metabolism
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Protein Transport
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Proto-Oncogene Proteins c-raf / metabolism*
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Serine / chemistry
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Trans-Activators / physiology*
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Viral Regulatory and Accessory Proteins
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p21-Activated Kinases
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src-Family Kinases / metabolism
Substances
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Trans-Activators
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Viral Regulatory and Accessory Proteins
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hepatitis B virus X protein
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Serine
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src-Family Kinases
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PAK1 protein, human
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-raf
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p21-Activated Kinases