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

Panier, S.; Durocher, D.

doi:10.1038/nrm3659

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

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Panier, S.
Panier – Genome Instability and Ageing, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/24002223
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Citation

Panier, S., & Durocher, D. (2013). Push back to respond better: regulatory inhibition of the DNA double-strand break response. Nat Rev Mol Cell Biol, 14(10), 661-72. doi:10.1038/nrm3659.

Cite as: https://hdl.handle.net/21.11116/0000-000B-7504-D

Abstract

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.