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Cell. 2013 Mar 14;152(6):1344-54. doi: 10.1016/j.cell.2013.02.011.

Chromatin remodeling at DNA double-strand breaks.

Author information

1
Division of Genomic Stability and DNA Repair, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.

Abstract

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.

PMID:
23498941
PMCID:
PMC3670600
DOI:
10.1016/j.cell.2013.02.011
[Indexed for MEDLINE]
Free PMC Article

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