The ubiquitin ligase APC/C(Cdh1) puts the brakes on DNA-end resection.
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.
Institute of Molecular Cancer Research; University of Zurich ; Zurich, Switzerland.
Lorenzo
L
Lafranchi
Institute of Molecular Cancer Research; University of Zurich ; Zurich, Switzerland.
Alessandro A
AA
Sartori
Cdh1; CtIP; DNA damage; DNA double-strand break repair; DNA-end resection; anaphase promoting complex/cyclosome (APC/C); cell cycle; genomic instability; ubiquitin-dependent proteolysis