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HEPATITIS-B-VIRUS-X PROTEIN INHIBITS P53 SEQUENCE-SPECIFIC DNA-BINDING, TRANSCRIPTIONAL ACTIVITY, AND ASSOCIATION WITH TRANSCRIPTION FACTOR ERCC3

被引：629
作者：
WANG, XW
FORRESTER, K
YEH, H
FEITELSON, MA
GU, JR
HARRIS, CC
机构：
[1] NCI,DIV CANC ETIOL,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892
[2] THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT PATHOL & CELL BIOL,PHILADELPHIA,PA 19107
[3] SHANGHAI CANC INST,DEPT MOLEC BIOL & BIOCHEM,SHANGHAI,PEOPLES R CHINA
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1994年 / 91卷 / 06期
关键词：
D O I：
10.1073/pnas.91.6.2230
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：
Chronic active hepatitis caused by infection with hepatitis B virus, a DNA virus, is a major risk factor for human hepatocellular carcinoma. Since the oncogenicity of several DNA viruses is dependent on the interaction of their viral oncoproteins with cellular tumor-suppressor gene products, we investigated the interaction between hepatitis B virus X protein (HBX) and human wild-type p53 protein. HBX complexes with the wild-type p53 protein and inhibits its sequence-specific DNA binding in vitro. HBX expression also inhibits p53-mediated transcriptional activation in vivo and the in vitro association of p53 and ERCC3, a general transcription factor involved in nucleotide excision repair. Therefore, HBX may affect a wide range of p53 functions and contribute to the molecular pathogenesis of human hepatocellular carcinoma.
引用
收藏
页码：2230 / 2234
页数：5
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