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
相关论文
共 48 条
[1]   DIVERSITY OF HUMAN P53 MUTANTS REVEALED BY COMPLEX-FORMATION TO SV40 T-ANTIGEN [J].
BARTEK, J ;
VOJTESEK, B ;
LANE, DP .
EUROPEAN JOURNAL OF CANCER, 1993, 29A (01) :101-107
[2]  
BEASLEY RP, 1981, LANCET, V2, P1129
[3]   SELECTIVE G-MUTATION TO T-MUTATION OF P53 GENE IN HEPATOCELLULAR-CARCINOMA FROM SOUTHERN AFRICA [J].
BRESSAC, B ;
KEW, M ;
WANDS, J ;
OZTURK, M .
NATURE, 1991, 350 (6317) :429-431
[4]   DNA-REPAIR AND TRANSCRIPTION - THE HELICASE CONNECTION [J].
BURATOWSKI, S .
SCIENCE, 1993, 260 (5104) :37-38
[5]   TRANSACTIVATION BY HEPATITIS-B VIRUS X-PROTEIN IS PROMISCUOUS AND DEPENDENT ON MITOGEN-ACTIVATED CELLULAR SERINE THREONINE KINASES [J].
CROSS, JC ;
WEN, P ;
RUTTER, WJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (17) :8078-8082
[6]   GAIN OF FUNCTION MUTATIONS IN P53 [J].
DITTMER, D ;
PATI, S ;
ZAMBETTI, G ;
CHU, S ;
TERESKY, AK ;
MOORE, M ;
FINLAY, C ;
LEVINE, AJ .
NATURE GENETICS, 1993, 4 (01) :42-46
[7]   INHIBITION OF DNA-REPLICATION FACTOR RPA BY P53 [J].
DUTTA, A ;
RUPPERT, JM ;
ASTER, JC ;
WINCHESTER, E .
NATURE, 1993, 365 (6441) :79-82
[8]   THE HUMAN PAPILLOMA VIRUS-16 E7-ONCOPROTEIN IS ABLE TO BIND TO THE RETINOBLASTOMA GENE-PRODUCT [J].
DYSON, N ;
HOWLEY, PM ;
MUNGER, K ;
HARLOW, E .
SCIENCE, 1989, 243 (4893) :934-937
[9]   WAF1, A POTENTIAL MEDIATOR OF P53 TUMOR SUPPRESSION [J].
ELDEIRY, WS ;
TOKINO, T ;
VELCULESCU, VE ;
LEVY, DB ;
PARSONS, R ;
TRENT, JM ;
LIN, D ;
MERCER, WE ;
KINZLER, KW ;
VOGELSTEIN, B .
CELL, 1993, 75 (04) :817-825
[10]  
FEITELSON MA, 1993, ONCOGENE, V8, P1109
12345