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• W2979433480 startingPage "1554" @default.
• W2979433480 abstract "Proteasomal activator 28 gamma (PA28γ) is frequently overexpressed in hepatocellular carcinoma; however, its underlying mechanism and role in hepatitis B virus (HBV) replication are largely unknown. Here, we found that HBV X protein (HBx) natural variants containing Ser-101 instead of Pro-101 increase reactive oxygen species levels in the mitochondria and activate the ataxia telangiectasia mutated/checkpoint kinase 2 pathway in the nucleus, resulting in the phosphorylation of p53 at Ser-15 and Ser-20 and the subsequent upregulation of its protein levels. Therefore, HBx variants containing Ser-101 induced p53-dependent activation of PA28γ expression in human hepatoma cells. The elevated PA28γ levels upregulated HBx levels through the inhibition of seven in absentia homologue 1-dependent proteasomal degradation. The self-amplifying ability of HBx variants containing Ser-101 via a positive feedback loop involving p53 and PA28γ was accurately reproduced in both a 1.2-mer HBV replicon and in vitro HBV infection systems, which also provided evidence for the stimulation of HBV replication by these HBx variants. In conclusion, the ability of HBx to upregulate PA28γ levels via p53 activation, in a Ser-101-dependent pathway, is critical for the stimulation of HBV replication." @default.
• W2979433480 created "2019-10-18" @default.
• W2979433480 creator A5006285346 @default.
• W2979433480 creator A5068910926 @default.
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• W2979433480 date "2019-11-01" @default.
• W2979433480 modified "2023-09-26" @default.
• W2979433480 title "HBx natural variants containing Ser-101 instead of Pro-101 evade ubiquitin-dependent proteasomal degradation by activating proteasomal activator 28 gamma expression" @default.
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• W2979433480 doi "https://doi.org/10.1099/jgv.0.001337" @default.
• W2979433480 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31596196" @default.
• W2979433480 hasPublicationYear "2019" @default.
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