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Push back to respond better: regulatory inhibition of the DNA double-strand break response.

Authors: Panier, S  Durocher, D 
Citation: Panier S and Durocher D, Nat Rev Mol Cell Biol. 2013 Oct;14(10):661-72. doi: 10.1038/nrm3659. Epub 2013 Sep 4.
Pubmed: (View Article at PubMed) PMID:24002223
DOI: Full-text: DOI:10.1038/nrm3659

Single DNA lesions such as DNA double-strand breaks (DSBs) can cause cell death or trigger genome rearrangements that have oncogenic potential, and so the pathways that mend and signal DNA damage must be highly sensitive but, at the same time, selective and reversible. When initiated, boundaries must be set to restrict the DSB response to the site of the lesion. The integration of positive and, crucially, negative control points involving post-translational modifications such as phosphorylation, ubiquitylation and acetylation is key for building fast, effective responses to DNA damage and for mitigating the impact of DNA lesions on genome integrity.


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CRRD Object Information
CRRD ID: 8661242
Created: 2014-06-10
Species: All species
Last Modified: 2014-06-10
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.