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Parallel genome-wide screens identify synthetic viable interactions between the BLM helicase complex and Fanconi anemia
M. Moder, G. Velimezi, M. Owusu, A. Mazouzi, M. Wiedner, J. Ferreira da Silva, L. Robinson-Garcia, F. Schischlik, R. Slavkovsky, R. Kralovics, M. Schuster, C. Bock, T. Ideker, SP. Jackson, J. Menche, JI. Loizou,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
NLK
Directory of Open Access Journals
od 2015
Free Medical Journals
od 2010
Nature Open Access
od 2010-12-01
PubMed Central
od 2012
Europe PubMed Central
od 2012
ProQuest Central
od 2010-01-01
Open Access Digital Library
od 2015-01-01
Open Access Digital Library
od 2015-01-01
Medline Complete (EBSCOhost)
od 2012-11-01
Health & Medicine (ProQuest)
od 2010-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2010
Springer Nature OA/Free Journals
od 2010-12-01
- MeSH
- buněčné linie MeSH
- CRISPR-Cas systémy MeSH
- DNA-helikasy genetika MeSH
- Fanconiho anemie genetika MeSH
- haploidie MeSH
- HEK293 buňky MeSH
- helikasy RecQ genetika MeSH
- inzerční mutageneze MeSH
- lidé MeSH
- NAD(P)H dehydrogenasa (chinon) genetika MeSH
- oprava DNA genetika MeSH
- poškození DNA MeSH
- protein FANCC genetika MeSH
- protein FANCD2 genetika MeSH
- proteiny FANC genetika MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
Maintenance of genome integrity via repair of DNA damage is a key biological process required to suppress diseases, including Fanconi anemia (FA). We generated loss-of-function human haploid cells for FA complementation group C (FANCC), a gene encoding a component of the FA core complex, and used genome-wide CRISPR libraries as well as insertional mutagenesis to identify synthetic viable (genetic suppressor) interactions for FA. Here we show that loss of the BLM helicase complex suppresses FANCC phenotypes and we confirm this interaction in cells deficient for FA complementation group I and D2 (FANCI and FANCD2) that function as part of the FA I-D2 complex, indicating that this interaction is not limited to the FA core complex, hence demonstrating that systematic genome-wide screening approaches can be used to reveal genetic viable interactions for DNA repair defects.
Citace poskytuje Crossref.org
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