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- W2111326137 abstract "Chronic infection by hepatitis B virus is a leading cause of human liver cancer and liver disease. The hepatitis B virus HBx protein is a regulatory factor that is essential for virus infection in mammals and is implicated in development of liver cancer and liver disease. Among the reported activities of HBx is the ability to stimulate Src tyrosine kinases, Ras-GTPases and transcriptional activation. We now demonstrate that HBx activation of Src tyrosine kinases, but not Ras, promotes a high level of viral replication in cell culture. HBx is shown to stimulate reverse transcription of the viral pregenomic mRNA into genomic DNA through a Src-mediated pathway in tissue culture cells. Targeted inhibition of Src tyrosine kinase activity, mutational inactivation of the HBx gene or retargeting of HBx to the nucleus to abolish cytoplasmic signal transduction activity, are shown to impair viral reverse transcription strongly. These studies implicate HBx stimulation of the Src family of tyrosine kinases in stimulation of viral polymerase activity." @default.
- W2111326137 created "2016-06-24" @default.
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- W2111326137 creator A5083567797 @default.
- W2111326137 date "1999-09-15" @default.
- W2111326137 modified "2023-10-03" @default.
- W2111326137 title "Src kinases involved in hepatitis B virus replication" @default.
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- W2111326137 doi "https://doi.org/10.1093/emboj/18.18.5019" @default.
- W2111326137 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1171573" @default.
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