{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fattah FJ"],"funding":["NIA NIH HHS","National Cancer Institute","NCI NIH HHS","National Institutes of Health","NIGMS NIH HHS"],"pagination":["39-53"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3948327"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15"],"pubmed_abstract":["Classic non-homologous end-joining (C-NHEJ) is required for the repair of radiation-induced DNA double-strand breaks (DSBs) in mammalian cells and plays a critical role in lymphoid V(D)J recombination. A core C-NHEJ component is the DNA ligase IV co-factor, Cernunnos/XLF (hereafter XLF). In patients, mutations in XLF cause predicted increases in radiosensitivity and deficits in immune function, but also cause other less well-understood pathologies including neural disorders. To characterize XLF function(s) in a defined genetic system, we used a recombinant adeno-associated virus-mediated gene targeting strategy to inactivate both copies of the XLF locus in the human HCT116 cell line. Analyses of XLF-null cells (which were viable) showed that they were highly sensitive to ionizing radiation"],"journal":["DNA repair"],"pubmed_title":["A role for XLF in DNA repair and recombination in human somatic cells."],"pmcid":["PMC3948327"],"funding_grant_id":["P30 CA77598","R01 GM088351","R01 CA154461","P30 CA077598","CA154461","T32 AG029796","GM088351"],"pubmed_authors":["Lichter N","Hendrickson EA","Kweon J","Fattah FJ","Lee EH","Wang Y","Weisensel N","Kan Y"],"additional_accession":[]},"is_claimable":false,"name":"A role for XLF in DNA repair and recombination in human somatic cells.","description":"Classic non-homologous end-joining (C-NHEJ) is required for the repair of radiation-induced DNA double-strand breaks (DSBs) in mammalian cells and plays a critical role in lymphoid V(D)J recombination. A core C-NHEJ component is the DNA ligase IV co-factor, Cernunnos/XLF (hereafter XLF). In patients, mutations in XLF cause predicted increases in radiosensitivity and deficits in immune function, but also cause other less well-understood pathologies including neural disorders. To characterize XLF function(s) in a defined genetic system, we used a recombinant adeno-associated virus-mediated gene targeting strategy to inactivate both copies of the XLF locus in the human HCT116 cell line. Analyses of XLF-null cells (which were viable) showed that they were highly sensitive to ionizing radiation","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Mar","modification":"2025-04-20T02:44:56.708Z","creation":"2019-03-27T01:23:10Z"},"accession":"S-EPMC3948327","cross_references":{"pubmed":["24461734"],"doi":["10.1016/j.dnarep.2013.12.006"]}}