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

被引：93

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

页码：235 / 251

页数：17

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