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  Double-strand break repair: 53BP1 comes into focus

Panier, S., & Boulton, S. J. (2013). Double-strand break repair: 53BP1 comes into focus. Nat Rev Mol Cell Biol, 15(1), 7-18. doi:10.1038/nrm3719.

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Panier, S.1, Author           
Boulton, S. J., Author
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1Panier – Genome Instability and Ageing, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society, ou_3394004              

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Free keywords: Animals Chromatin/genetics/metabolism *DNA Breaks, Double-Stranded *DNA End-Joining Repair DNA Repair Histones/metabolism Humans Intracellular Signaling Peptides and Proteins/*physiology Protein Transport Signal Transduction Tumor Suppressor p53-Binding Protein 1
 Abstract: DNA double-strand break (DSB) signalling and repair is crucial to preserve genomic integrity and maintain cellular homeostasis. p53-binding protein 1 (53BP1) is an important regulator of the cellular response to DSBs that promotes the end-joining of distal DNA ends, which is induced during V(D)J and class switch recombination as well as during the fusion of deprotected telomeres. New insights have been gained into the mechanisms underlying the recruitment of 53BP1 to damaged chromatin and how 53BP1 promotes non-homologous end-joining-mediated DSB repair while preventing homologous recombination. From these studies, a model is emerging in which 53BP1 recruitment requires the direct recognition of a DSB-specific histone code and its influence on pathway choice is mediated by mutual antagonism with breast cancer 1 (BRCA1).

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 Dates: 2014-012013-12-12
 Publication Status: Published in print
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 Identifiers: Other: 24326623
DOI: 10.1038/nrm3719
ISSN: 1471-0080 (Electronic)1471-0072 (Linking)
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Title: Nat Rev Mol Cell Biol
Source Genre: Journal
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Pages: - Volume / Issue: 15 (1) Sequence Number: - Start / End Page: 7 - 18 Identifier: -