Open Accessp53-mediated cellular response to DNA damage in cells with replicative hepatitis B virus.
Author(s) -
Alain Puisieux,
Jingwei Ji,
Céline Guillot,
Yann Legros,
Thierry Soussi,
Kurt J. Isselbacher,
Mehmet Öztürk
Publication year - 1995
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.92.5.1342
Subject(s) - dna damage , biology , dna , virus , dna replication , apoptosis , hepatitis b virus , viral transformation , virology , suppressor , gene , viral replication , dna repair , microbiology and biotechnology , genetics
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.