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A genome-wide scree...
A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection
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Lopez-Saavedra, A (författare)
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Gomez-Cabello, D (författare)
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Dominguez-Sanchez, MS (författare)
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Mejias-Navarro, F (författare)
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Fernandez-Avila, MJ (författare)
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Dinant, C (författare)
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Martinez-Macias, MI (författare)
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- Bartek, J (författare)
- Karolinska Institutet
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Huertas, P (författare)
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(creator_code:org_t)
- 2016-08-09
- 2016
- Engelska.
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7, s. 12364-
- Relaterad länk:
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https://www.nature.c...
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http://kipublication...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- 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.
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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