BRCA1 Is Required for Postreplication Repair after UV-Induced DNA Damage

被引：90
|
作者：
Pathania, Shailja [1 ,4 ]
Jenna Nguyen [4 ]
Hill, Sarah J. [4 ]
Scully, Ralph [2 ,6 ]
Adelmant, Guillaume O. [3 ,4 ,5 ]
Marto, Jarrod A. [3 ,4 ,5 ]
Feunteun, Jean [7 ]
Livingston, David M. [1 ,4 ]
机构：
[1] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA
[4] Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02215 USA
[5] Dana Farber Canc Inst, Blais Prote Ctr, Boston, MA 02215 USA
[6] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA
[7] Inst Gustave Roussy, UMR8200, Lab Stabilite Genet & Oncogenese, F-94805 Villejuif, France
来源：
MOLECULAR CELL | 2011年 / 44卷 / 02期
基金：
美国国家卫生研究院;
关键词：
NUCLEOTIDE EXCISION-REPAIR; STALLED REPLICATION FORKS; POLYMERASE-ETA; HOMOLOGOUS RECOMBINATION; XERODERMA-PIGMENTOSUM; GENOMIC INSTABILITY; S-PHASE; CHECKPOINT; BREAST; CANCER;
D O I：
10.1016/j.molcel.2011.09.002
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
BRCA1 contributes to the response to UV irradiation. Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excision, suppression of translesion synthesis, and the localization and activation of replication factor C complex (RFC) subunits. The last function, in turn, triggers post-UV checkpoint activation and postreplicative repair. These BRCA1 functions differ from those required for DSBR.
引用
收藏
页码：235 / 251
页数：17
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