BRCA1 is required for postreplication repair after UV-induced DNA damage

Mol Cell. 2011 Oct 21;44(2):235-51. doi: 10.1016/j.molcel.2011.09.002. Epub 2011 Sep 29.

Abstract

BRCA1 contributes to the response to UV irradiation. Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excision, suppression of translesion synthesis, and the localization and activation of replication factor C complex (RFC) subunits. The last function, in turn, triggers post-UV checkpoint activation and postreplicative repair. These BRCA1 functions differ from those required for DSBR.

Publication types

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

MeSH terms

  • BRCA1 Protein / genetics
  • BRCA1 Protein / metabolism*
  • Cell Line
  • DNA Breaks, Double-Stranded
  • DNA Damage*
  • DNA Repair / physiology
  • DNA Replication
  • Humans
  • Replication Protein C / genetics
  • Replication Protein C / metabolism
  • Ultraviolet Rays*

Substances

  • BRCA1 Protein
  • BRCA1 protein, human
  • Replication Protein C