Histone tails: Directing the chromatin response to DNA damage

被引:25
|
作者
Greenberg, Roger A. [1 ,2 ]
机构
[1] Univ Penn, Abramson Family Canc Res Inst, Sch Med, Dept Canc Biol, Philadelphia, PA 19104 USA
[2] Univ Penn, Abramson Family Canc Res Inst, Sch Med, Dept Pathol, Philadelphia, PA 19104 USA
关键词
DNA damage response; Histones; Chromatin; Genome stability; DOUBLE-STRAND BREAKS; HOMOLOGOUS RECOMBINATION REPAIR; INDUCED NUCLEAR FOCI; GENOMIC INSTABILITY; POLY(ADP-RIBOSE) POLYMERASE; IONIZING-RADIATION; UBIQUITIN-BINDING; H2AX PHOSPHORYLATION; BRCA1; DEFICIENCY; MAMMALIAN GENOME;
D O I
10.1016/j.febslet.2011.05.037
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
Considerable energetic investment is devoted to altering large stretches of chromatin adjacent to DNA double strand breaks (DSBs). Immediately ensuing DSB formation, a myriad of histone modifications are elicited to create a platform for inducible and modular assembly of DNA repair protein complexes in the vicinity of the DNA lesion. This complex signaling network is critical to repair DNA damage and communicate with cellular processes that occur in cis and in trans to the genomic lesion. Failure to properly execute DNA damage inducible chromatin changes is associated with developmental abnormalities, immunodeficiency, and malignancy in humans and in genetically engineered mouse models. This review will discuss current knowledge of DNA damage responsive histone changes that occur in mammalian cells, highlighting their involvement in the maintenance of genome integrity. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:2883 / 2890
页数:8
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