Homology-directed Fanconi anemia pathway cross-link repair is dependent on DNA replication

被引：60

作者：

Nakanishi, Koji ^{[1
]}

Cavallo, Francesca ^{[2
]}

Perrouault, Loic ^{[3
,4
,5
]}

Giovannangeli, Carine ^{[3
,4
,5
]}

Moynahan, Mary Ellen ^{[6
]}

Barchi, Marco ^{[2
]}

Brunet, Erika ^{[1
,3
,4
,5
]}

Jasin, Maria ^{[1
]}

机构：

[1] Mem Sloan Kettering Canc Ctr, Dev Biol Program, New York, NY 10021 USA

[2] Univ Roma Tor Vergata, Dept Publ Hlth & Cell Biol, Sect Anat, Rome, Italy

[3] Museum Natl Hist Nat, F-75231 Paris, France

[4] CNRS, UMR7196, Paris, France

[5] INSERM, U565, Paris, France

[6] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA

来源：

NATURE STRUCTURAL & MOLECULAR BIOLOGY | 2011年 / 18卷 / 04期

关键词：

TRIPLEX-FORMING OLIGONUCLEOTIDES; DOUBLE-STRAND BREAKS; EPSTEIN-BARR-VIRUS; MAMMALIAN-CELLS; RECOMBINATION; PSORALEN; PROTEIN; DAMAGE; DEFECTS; BRCA1;

D O I：

10.1038/nsmb.2029

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：

Homologous recombination (also termed homology-directed repair, HDR) is a major pathway for the repair of DNA interstrand cross-links (ICLs) in mammalian cells. Cells from individuals with Fanconi anemia (FA) are characterized by extreme ICL sensitivity, but their reported defect in HDR is mild. Here we examined ICL-induced HDR using a GFP reporter and observed a profound defect in ICL-induced HDR in FA cells, but only when the reporter could replicate.

引用

页码：500 / 503

页数：4

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