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...

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Detalles Bibliográficos
Autores principales: Lafranchi, Lorenzo, Sartori, Alessandro A
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2015
Materias:
Author's View
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4905325/
https://www.ncbi.nlm.nih.gov/pubmed/27308488
http://dx.doi.org/10.1080/23723556.2014.1000696
Descripción
Sumario: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.

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