BRCA1 Accelerates CtIP-Mediated DNA-End Resection

被引：220

作者：

Cruz-Garcia, Andres ^{[1
,2
]}

Lopez-Saavedra, Ana ^{[1
,2
]}

Huertas, Pablo ^{[1
,2
]}

机构：

[1] Ctr Andaluz Biol Mol Med & Regenerat CABIMER, Seville 41092, Spain

[2] Univ Seville, Dept Genet, E-41080 Seville, Spain

来源：

CELL REPORTS | 2014年 / 9卷 / 02期

关键词：

STRAND-BREAK REPAIR; CELL-CYCLE; GENOME; REPLICATION; DAMAGE;

D O I：

10.1016/j.celrep.2014.08.076

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

DNA-end resection is a highly regulated and critical step in the response and repair of DNA double-strand breaks. In higher eukaryotes, CtIP regulates resection by integrating cellular signals via its posttranslational modifications and protein-protein interactions, including cell-cycle-controlled interaction with BRCA1. The role of BRCA1 in DNA-end resection is not clear. Here, we develop an assay to study DNA resection in higher eukaryotes at high resolution. We demonstrate that the BRCA1-CtIP interaction, albeit not essential for resection, modulates the speed at which this process takes place.

引用

页码：451 / 459

页数：9

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