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Title: A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection.
Authors: López-Saavedra, Ana
Gómez-Cabello, Daniel
Domínguez-Sánchez, María Salud
Mejías-Navarro, Fernando
Fernández-Ávila, María Jesús
Dinant, Christoffel
Martínez-Macías, María Isabel
Bartek, Jiri
Huertas, Pablo
metadata.dc.subject.mesh: Adaptor Proteins, Signal Transducing
Carrier Proteins
Cell Line, Tumor
DNA Damage
DNA End-Joining Repair
Gene Regulatory Networks
Genome, Human
Models, Biological
Nuclear Proteins
Protein Binding
Recombinational DNA Repair
Issue Date: 9-Aug-2016
Abstract: There are two major and alternative pathways to repair DNA double-strand breaks: non-homologous end-joining and homologous recombination. Here we identify and characterize novel factors involved in choosing between these pathways; in this study we took advantage of the SeeSaw Reporter, in which the repair of double-strand breaks by homology-independent or -dependent mechanisms is distinguished by the accumulation of green or red fluorescence, respectively. Using a genome-wide human esiRNA (endoribonuclease-prepared siRNA) library, we isolate genes that control the recombination/end-joining ratio. Here we report that two distinct sets of genes are involved in the control of the balance between NHEJ and HR: those that are required to facilitate recombination and those that favour NHEJ. This last category includes CCAR2/DBC1, which we show inhibits recombination by limiting the initiation and the extent of DNA end resection, thereby acting as an antagonist of CtIP.
metadata.dc.identifier.doi: 10.1038/ncomms12364
Appears in Collections:Producción 2020

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