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The ubiquitin ligase APC/C(Cdh1) puts the brakes on DNA-end resection.

Research paper by Lorenzo L Lafranchi, Alessandro A AA Sartori

Indexed on: 17 Jun '16Published on: 17 Jun '16Published in: Molecular & cellular oncology



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.