乳腺癌1号基因（BRCA1）可加速CtIP介导的DNA末端切除。

BRCA1 accelerates CtIP-mediated DNA-end resection.

作者信息

Cruz-García Andrés, López-Saavedra Ana, Huertas Pablo

机构信息

Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), 41092 Sevilla, Spain; Departamento de Genética, Universidad de Sevilla, 41080, Sevilla, Spain.

出版信息

Cell Rep. 2014 Oct 23;9(2):451-9. doi: 10.1016/j.celrep.2014.08.076. Epub 2014 Oct 9.

DOI:10.1016/j.celrep.2014.08.076

PMID:25310973

Abstract

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.

摘要

DNA 末端切除是 DNA 双链断裂应答和修复过程中一个受到高度调控的关键步骤。在高等真核生物中，CtIP 通过其翻译后修饰和蛋白质-蛋白质相互作用（包括与 BRCA1 的细胞周期控制相互作用）整合细胞信号来调节切除过程。BRCA1 在 DNA 末端切除中的作用尚不清楚。在此，我们开发了一种检测方法，以高分辨率研究高等真核生物中的 DNA 切除。我们证明，BRCA1-CtIP 相互作用虽然对切除不是必需的，但会调节这一过程发生的速度。