P53-MEDIATED CELLULAR-RESPONSE TO DNA-DAMAGE IN CELLS WITH REPLICATIVE HEPATITIS-B VIRUS

被引：53
作者：
PUISIEUX, A
JI, JW
GUILLOT, C
LEGROS, Y
SOUSSI, T
ISSELBACHER, K
OZTURK, M
机构：
[1] INSERM,CJF 9302,CTR LEON BERARD,MOLEC ONCOL LAB,F-69008 LYON,FRANCE
[2] INST GENET MOLEC,INSERM,U301,F-75010 PARIS,FRANCE
[3] MASSACHUSETTS GEN HOSP E,CTR CANC,BOSTON,MA 02129
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1995年 / 92卷 / 05期
关键词：
TUMOR SUPPRESSOR GENE/P21(CIP1/WAF1); DNA-DAMAGING AGENT; VIRAL CARCINOGENESIS;
D O I：
10.1073/pnas.92.5.1342
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Wild-type p53 acts as a tumor suppressor gene by protecting cells from deleterious effects of genotoxic agents through the induction of a G(1)/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.
引用
收藏
页码：1342 / 1346
页数：5
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