P53 MODULATION OF TFIIH-ASSOCIATED NUCLEOTIDE EXCISION-REPAIR ACTIVITY

被引：505

作者：

WANG, XW

YEH, H

SCHAEFFER, L

ROY, R

MONCOLLIN, V

EGLY, JM

WANG, Z

FRIEDBERG, EC

EVANS, MK

TAFFE, BG

BOHR, VA

WEEDA, G

HOEIJMAKERS, JHJ

FORRESTER, K

HARRIS, CC

机构：

[1] NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892

[2] FAC MED STRASBOURG,INSERM,U184,CNRS,UPR 6520,F-67085 STRASBOURG,FRANCE

[3] UNIV TEXAS,SW MED CTR,DEPT PATHOL,MOLEC PATHOL LAB,DALLAS,TX 75235

[4] NIA,MOLEC GENET LAB,BALTIMORE,MD 21224

[5] ERASMUS UNIV ROTTERDAM,CTR MED GENET,DEPT CELL BIOL & GENET,3000 DR ROTTERDAM,NETHERLANDS

来源：

NATURE GENETICS | 1995年 / 10卷 / 02期

关键词：

D O I：

10.1038/ng0695-188

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

p53 has pleiotropic functions including control of genomic plasticity and integrity. Here we report that p53 can bind to several transcription factor IIH-associated factors, including transcription-repair factors, XPD (Rad3) and XPB, as well as CSB involved in strand-specific DNA repair, via its C-terminal domain. We also found that wild-type, but not Arg273His mutant p53 inhibits XPD (Rad3) and XPB DNA helicase activities. Moreover, repair of UV-induced dimers is slower in Li-Fraumeni syndrome cells (heterozygote p53 mutant) than in normal human cells. Our findings indicate that p53 may play a direct role in modulating nucleotide excision repair pathways.

引用

页码：188 / 195

页数：8

共 61 条

[1] DIFFERENT CYTOTOXIC AND MUTAGENIC RESPONSES INDUCED BY X-RAYS IN 2 HUMAN LYMPHOBLASTOID CELL-LINES DERIVED FROM A SINGLE DONOR [J].