Search: id:"swepub:oai:prod.swepub.kib.ki.se:133999131" >
A genome-wide scree...
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Lopez-Saavedra, A
(author)
A genome-wide screening uncovers the role of CCAR2 as an antagonist of DNA end resection
- Article/chapterEnglish2016
Publisher, publication year, extent ...
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2016-08-09
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Springer Science and Business Media LLC,2016
Numbers
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LIBRIS-ID:oai:prod.swepub.kib.ki.se:133999131
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http://kipublications.ki.se/Default.aspx?queryparsed=id:133999131URI
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https://doi.org/10.1038/ncomms12364DOI
Supplementary language notes
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Language:English
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Summary in:English
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Classification
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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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.
Added entries (persons, corporate bodies, meetings, titles ...)
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Gomez-Cabello, D
(author)
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Dominguez-Sanchez, MS
(author)
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Mejias-Navarro, F
(author)
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Fernandez-Avila, MJ
(author)
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Dinant, C
(author)
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Martinez-Macias, MI
(author)
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Bartek, JKarolinska Institutet
(author)
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Huertas, P
(author)
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Karolinska Institutet
(creator_code:org_t)
Related titles
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In:Nature communications: Springer Science and Business Media LLC7, s. 12364-2041-1723
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