53BP1: pro choice in DNA repair

被引：181

作者：

Zimmerman, Michal ^{[1
]}

de Lange, Titia ^{[1
]}

机构：

[1] Rockefeller Univ, Lab Cell Biol & Genet, New York, NY 10065 USA

来源：

TRENDS IN CELL BIOLOGY | 2014年 / 24卷 / 02期

基金：

欧洲研究理事会;

关键词：

53BP1; Rif1; PTIP; NHEJ; HDR; PARPi; telomere; CSR; V(D)J; BRCA1; resection; DOUBLE-STRAND BREAKS; CELLULAR-RESPONSE; DAMAGE-RESPONSE; HOMOLOGOUS RECOMBINATION; END RESECTION; HISTONE H2AX; HUMAN RIF1; PROMOTES; BRCA1; PROTEIN;

D O I：

10.1016/j.tcb.2013.09.003

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The DNA damage response factor 53BP1 functions at the intersection of two major double strand break (DSB) repair pathways - promoting nonhomologous end-joining (NHEJ) and inhibiting homology-directed repair (HDR) - and integrates cellular inputs to ensure their timely execution in the proper cellular contexts. Recent work has revealed that 53BP1 controls 5' end resection at DNA ends, mediates synapsis of DNA ends, promotes the mobility of damaged chromatin, improves DSB repair in heterochromatic regions, and contributes to lethal mis-repair of DSBs in BRCA1-deficient cells. Here we review these aspects of 53BP1 and discuss new data revealing how 53BP1 is loaded onto chromatin and uses its interacting factors Rif1 and PTIP to promote NHEJ and inhibit HDR.

引用

页码：108 / 117

页数：10

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