biostudies-literaturePathania SNIAID NIH HHSNHGRI NIH HHSNCI NIH HHSNINDS NIH HHSNIGMS NIH HHS235-51https://www.ebi.ac.uk/biostudies/studies/S-EPMC3200447biostudies-literatureUnknown44(2)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.Molecular cellBRCA1 is required for postreplication repair after UV-induced DNA damage.PMC3200447RC1 CA145867P30 AI060354R01 CA095175R01 GM073894P01NS047572R21 CA144017P50 HG004233R01 CA103920-05T32 GM007753R01 CA103920P50HG004233Scully RAdelmant GOHill SJPathania SLivingston DMMarto JANguyen JFeunteun JfalseBRCA1 is required for postreplication repair after UV-induced DNA damage.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.2011-01-01T00:00:00Z2011 Oct2024-11-20T22:07:10.891Z2019-03-27T00:45:21ZS-EPMC32004472196323910.1016/j.molcel.2011.09.002