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Cells are continually exposed to DNA assaults from exogenous and endogenous sources. To maintain genomic integrity, cells have evolved a highly conserved mechanism for repairing DNA lesions and, in particular, DNA double strand breaks (DSBs). Emerging evidence indicates that DNA repair/signaling machinery acts in an integrated fashion with chromatin structure at damaged sites. This review focuses on the interplay between histone modifications and the chromatin-mediated response to DNA damage.
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