Mechanism of elimination of phosphorylated histone H2AX from chromatin after repair of DNA double-strand breaks

被引：46

作者：

Svetlova, M. P. ^{[1
]}

Solovjeva, L. V. ^{[1
]}

Tomilin, N. V. ^{[1
]}

机构：

[1] Russian Acad Sci, Inst Cytol, St Petersburg 194064, Russia

来源：

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 2010年 / 685卷 / 1-2期

基金：

俄罗斯基础研究基金会;

关键词：

DNA double-strand breaks; Histone phosphorylation; DNA repair; Histone dephosphorylation; EMBRYONIC STEM-CELLS; PROTEIN-KINASE-A; IONIZING-RADIATION; DAMAGE RESPONSE; MAMMALIAN-CELLS; GAMMA-H2AX FOCI; REPLICATION STRESS; OPTIMIZED METHOD; IN-VIVO; ATM;

D O I：

10.1016/j.mrfmmm.2009.08.001

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Covalent modifications of histories in chromatin play an important role in regulation of eukaryotic gene expression and DNA repair. Formation of double-strand breaks (DSBs) in DNA is followed by the rapid local phosphorylation of the C-terminal serine in the replacement histone H2AX in megabase chromatin domains around DSBs and formation of discrete nuclear foci called gamma H2AX foci. This epigenetic modification of chromatin represents the "histone code" for DNA damage signaling and repair and has been extensively studied during last decade. It is known that after DSB rejoining gamma H2AX foci are eliminated from the nucleus, but molecular mechanism of this elimination remains to be established. However, gamma H2AX elimination can serve as a useful marker of DSB repair in normal cells and tissues. In this paper the available data on kinetics and possible mechanisms of gamma H2AX elimination are reviewed. (C) 2009 Elsevier B.V. All rights reserved.

引用

页码：54 / 60

页数：7

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