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Chromatin Remodeling at DNA Double-Strand Breaks
被引:441
|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
来源:
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.
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页码:1344 / 1354
页数:11
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