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Double-strand break repair: 53BP1 comes into focus.

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).
AuthorsStephanie Panier, Simon J Boulton
JournalNature reviews. Molecular cell biology (Nat Rev Mol Cell Biol) Vol. 15 Issue 1 Pg. 7-18 (Jan 2014) ISSN: 1471-0080 [Electronic] England
PMID24326623 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Chromatin
  • Histones
  • Intracellular Signaling Peptides and Proteins
  • TP53BP1 protein, human
  • Tumor Suppressor p53-Binding Protein 1
Topics
  • 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

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