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Search: id:"swepub:oai:prod.swepub.kib.ki.se:133999131" > A genome-wide scree...

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A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection

Lopez-Saavedra, A (author)
Gomez-Cabello, D (author)
Dominguez-Sanchez, MS (author)
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Mejias-Navarro, F (author)
Fernandez-Avila, MJ (author)
Dinant, C (author)
Martinez-Macias, MI (author)
Bartek, J (author)
Karolinska Institutet
Huertas, P (author)
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 (creator_code:org_t)
2016-08-09
2016
English.
In: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7, s. 12364-
  • Journal article (peer-reviewed)
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  • 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.

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