Abstract
A decade has passed since the first reported connection between RAP80 and BRCA1 in DNA double-strand break repair. Despite the initial identification of RAP80 as a factor localizing BRCA1 to DNA double-strand breaks and potentially promoting homologous recombination, there is increasing evidence that RAP80 instead suppresses homologous recombination to fine-tune the balance of competing DNA repair processes during the S/G2 phase of the cell cycle. RAP80 opposes homologous recombination by inhibiting DNA end-resection and sequestering BRCA1 into the BRCA1-A complex. Ubiquitin and SUMO modifications of chromatin at DNA double-strand breaks recruit RAP80, which contains distinct sequence motifs that recognize ubiquitin and SUMO. Here, we review RAP80’s role in repressing homologous recombination at DNA double-strand breaks and how this role is facilitated by its ability to bind ubiquitin and SUMO modifications.
Original language | English (US) |
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Pages (from-to) | 799-807 |
Number of pages | 9 |
Journal | Journal of Molecular Medicine |
Volume | 95 |
Issue number | 8 |
DOIs | |
State | Published - Aug 1 2017 |
Keywords
- BRCA1
- DNA double-strand break repair
- Homologous recombination
- RAP80
- SUMO
- Ubiquitin
ASJC Scopus subject areas
- Molecular Medicine
- Drug Discovery
- Genetics(clinical)