Chromatin Remodeling at DNA Double-Strand Breaks

被引:440
|
作者
Price, Brendan D. [1 ]
D'Andrea, Alan D. [1 ]
机构
[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol,Div Genom Stabil & DNA Repair, Boston, MA 02215 USA
关键词
HISTONE H2AX PHOSPHORYLATION; DAMAGE RESPONSE; HOMOLOGOUS RECOMBINATION; KAP-1; PHOSPHORYLATION; H4-K16; ACETYLATION; REPAIR; NUCLEOSOME; VARIANT; PROTEIN; TIP60;
D O I
10.1016/j.cell.2013.02.011
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
DNA double-strand breaks (DSBs) can arise from multiple sources, including exposure to ionizing radiation. The repair of DSBs involves both posttranslational modification of nucleosomes and concentration of DNA-repair proteins at the site of damage. Consequently, nucleosome packing and chromatin architecture surrounding the DSB may limit the ability of the DNA-damage response to access and repair the break. Here, we review early chromatin-based events that promote the formation of open, relaxed chromatin structures at DSBs and that allow the DNA-repair machinery to access the spatially confined region surrounding the DSB, thereby facilitating mammalian DSB repair.
引用
收藏
页码:1344 / 1354
页数:11
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