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• W2155133752 abstract "We recently described a CHO DSBR mutant belonging to the XRCC7 complementation group (XR-C2) that has the interesting phenotype of being radiosensitive, but having only a modest defect in VDJ recombination. This cell line expresses only slightly reduced levels of DNA-PKcs but has undetectable DNA-PK activity. Limited sequence analyses of DNA-PKcs transcripts from XR-C2 revealed a point mutation that results in an amino acid substitution of glutamic acid for glycine six residues from the C-terminus. To determine whether this single substitution was responsible for the phenotype in XR-C2 cells, we introduced the mutation into a DNA-PKcs expression vector. Whereas transfection of this expression vector significantly restores the VDJ recombination deficits in DNA-PKcs-deficient cells, radioresistance is not restored. Thus, expression of this mutant form of DNA-PKcs in DNA-PKcs- deficient cells substantially recapitulates the phenotype observed in XR-C2, and we conclude that this single amino acid substitution is responsible for the non-homologous end joining deficits observed in XR-C2." @default.
• W2155133752 created "2016-06-24" @default.
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• W2155133752 date "2002-12-01" @default.
• W2155133752 modified "2023-09-27" @default.
• W2155133752 title "A single amino acid substitution in DNA-PKcs explains the novel phenotype of the CHO mutant, XR-C2" @default.
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• W2155133752 doi "https://doi.org/10.1093/nar/gkf625" @default.
• W2155133752 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/137947" @default.
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