The ubiquitin ligase APC/C(Cdh1) puts the brakes on DNA-end resection.
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ABSTRACT: DNA double-strand breaks (DSBs) are highly deleterious lesions and their misrepair can promote genomic instability, a hallmark of cancer. DNA-end resection is a cell cycle-regulated mechanism that is required for the faithful repair of DSBs. We recently discovered that the anaphase-promoting complex/cyclosome-Cdh1 (APC/C(Cdh1)) ubiquitin ligase is responsible for the timely degradation of CtBP-interacting protein (CtIP), a key DNA-end resection factor, providing a new layer of regulation of DSB repair in human cells.
SUBMITTER: Lafranchi L
PROVIDER: S-EPMC4905325 | biostudies-other | 2015 Oct-Dec
REPOSITORIES: biostudies-other
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