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
收藏
页码：188 / 195
页数：8
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