BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ

被引：305

作者：

Litman, R

Peng, M

Jin, Z

Zhang, F

Zhang, JR

Powell, S

Andreassen, PR

Cantor, SB ^{[1
]}

机构：

[1] Univ Massachusetts, Sch Med, Dept Canc Biol, Womens Canc Program,UMass Mem Canc Ctr, Worcester, MA 01605 USA

[2] Univ Cincinnati, Coll Med, Dept Pediat, Cincinnati Childrens Hosp Med Ctr,Div Expt Hemato, Cincinnati, OH 45229 USA

[3] Washington Univ, St Louis, MO 63108 USA

来源：

CANCER CELL | 2005年 / 8卷 / 03期

关键词：

D O I：

10.1016/j.ccr.2005.08.004

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We showed in this study that cells deficient of the BRCA1-associated BACH1 helicase, also known as BRIPi, failed to elicit homologous recombination (HR) after DNA double-stranded breaks (DSBs). BACH1-deficient cells were also sensitive to mitomycin C (MMC) and underwent MMC-induced chromosome instability. Moreover, we identified a homozygous nonsense mutation in BACH1 in a FA-J patient-derived cell line and could not detect BACH1 protein in this cell line. Expression of wild-type BACH1 in this cell line reduced the accumulation of cells at G2/M phases following exposure to DNA crosslinkers, a characteristic of Fanconi anemia (FA) cells. These results support the conclusion that BACH1 is FANCJ.

引用

页码：255 / 265

页数：11

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