53BP1: pro choice in DNA repair

Trends Cell Biol. 2014 Feb;24(2):108-17. doi: 10.1016/j.tcb.2013.09.003. Epub 2013 Oct 4.


The DNA damage response factor 53BP1 functions at the intersection of two major double strand break (DSB) repair pathways--promoting nonhomologous end-joining (NHEJ) and inhibiting homology-directed repair (HDR)--and integrates cellular inputs to ensure their timely execution in the proper cellular contexts. Recent work has revealed that 53BP1 controls 5' end resection at DNA ends, mediates synapsis of DNA ends, promotes the mobility of damaged chromatin, improves DSB repair in heterochromatic regions, and contributes to lethal mis-repair of DSBs in BRCA1-deficient cells. Here we review these aspects of 53BP1 and discuss new data revealing how 53BP1 is loaded onto chromatin and uses its interacting factors Rif1 and PTIP to promote NHEJ and inhibit HDR.

Keywords: 53BP1; BRCA1; CSR; HDR; NHEJ; PARPi; PTIP; Rif1; V(D)J; resection; telomere.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • DNA Repair*
  • Humans
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Tumor Suppressor p53-Binding Protein 1


  • Intracellular Signaling Peptides and Proteins
  • TP53BP1 protein, human
  • Tumor Suppressor p53-Binding Protein 1