p53-mediated cellular response to DNA damage in cells with replicative hepatitis B virus.

AUTOR(ES)

Puisieux, A

RESUMO

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.

Documentos Relacionados

• Human papillomavirus 16 E6 expression disrupts the p53-mediated cellular response to DNA damage.
• Nijmegen breakage syndrome cells fail to induce the p53-mediated DNA damage response following exposure to ionizing radiation.
• WISP-1 attenuates p53-mediated apoptosis in response to DNA damage through activation of the Akt kinase
• The hepatitis B virus X gene induces p53-mediated programmed cell death
• DNA damage and p53-mediated cell cycle arrest: A reevaluation