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- W2106861716 startingPage "685" @default.
- W2106861716 abstract "In response to DNA double-strand breaks (DSBs), BRCA1 forms biochemically distinct complexes with certain other DNA damage response proteins. These structures, some of which are required for homologous recombination (HR)-type DSB repair, concentrate at distinct nuclear foci that demarcate sites of genome breakage. Polyubiquitin binding by one of these structures, the RAP80/BRCA1 complex, is required for efficient BRCA1 focal recruitment, but the relationship of this process to the execution of HR has been unclear. We found that this complex actively suppresses otherwise exaggerated, BRCA1-driven HR. By controlling the kinetics by which other BRCA1-interacting proteins that promote HR concentrate together with BRCA1 in nuclear foci, RAP80/BRCA1 complexes suppress excessive DSB end processing, HR-type DSB repair, and overt chromosomal instability. Since chromosomal instability emerges when BRCA1 HR function is either unbridled or absent, active tuning of BRCA1 activity, executed in nuclear foci, is important to genome integrity maintenance." @default.
- W2106861716 created "2016-06-24" @default.
- W2106861716 creator A5014909593 @default.
- W2106861716 creator A5021683017 @default.
- W2106861716 creator A5029032924 @default.
- W2106861716 creator A5039031303 @default.
- W2106861716 creator A5059044712 @default.
- W2106861716 creator A5070645953 @default.
- W2106861716 date "2011-03-15" @default.
- W2106861716 modified "2023-10-16" @default.
- W2106861716 title "RAP80-directed tuning of BRCA1 homologous recombination function at ionizing radiation-induced nuclear foci" @default.
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