Journal
MOLECULAR CELL
Volume 44, Issue 2, Pages 235-251Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2011.09.002
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Funding
- National Cancer Institute
- Dana-Farber/Harvard Cancer Center
- Breast Cancer Research Foundation
- Susan B. Komen Foundation
- Dana-Farber Cancer Institute
- National Institutes of Health, NHGRI [P50HG004233]
- NINDS [P01NS047572]
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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.
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