Abstract
Wild-type p53 acts as a tumor suppressor gene by protecting cells from deleterious effects of genotoxic agents through the induction of a G1/S arrest or apoptosis as a response to DNA damage. Transforming proteins of several oncogenic DNA viruses inactivate tumor suppressor activity of p53 by blocking this cellular response. To test whether hepatitis B virus displays a similar effect, we studied the p53-mediated cellular response to DNA damage in 2215 hepatoma cells with replicative hepatitis B virus. We demonstrate that hepatitis B virus replication does not interfere with known cellular functions of p53 protein.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Base Sequence
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Cyclin-Dependent Kinase Inhibitor p21
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Cyclins / genetics
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DNA Damage*
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DNA Primers / chemistry
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Doxorubicin / pharmacology
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Gene Expression Regulation, Neoplastic / drug effects
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Gene Expression Regulation, Viral
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Hepatitis B / genetics*
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Hepatitis B virus / genetics
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Humans
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Molecular Sequence Data
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Tumor Cells, Cultured
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Tumor Suppressor Protein p53 / pharmacology*
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Virus Replication
Substances
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CDKN1A protein, human
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Cyclin-Dependent Kinase Inhibitor p21
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Cyclins
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DNA Primers
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Tumor Suppressor Protein p53
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Doxorubicin