ArticleNucleic acids research1998
XR-C1, a new CHO cell mutant which is defective in DNA-PKcs, is impaired in both V(D)J coding and signal joint formation.
Article in Nucleic acids research, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 58 citations in OpenAlex.
- Article
- Review
- Impaired NHEJ repair in amyotrophic lateral sclerosis is associated with TDP-43 mutations.Molecular neurodegeneration · 2020Article
- Article
- Restoration of ATM Expression in DNA-PKcs-Deficient Cells Inhibits Signal End Joining.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Functional overlaps between XLF and the ATM-dependent DNA double strand break response.DNA repair · 2014Review
- Functional redundancy between the XLF and DNA-PKcs DNA repair factors in V(D)J recombination and nonhomologous DNA end joining.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Different DNA-PKcs functions in the repair of radiation-induced and spontaneous DSBs within interstitial telomeric sequences.Chromosoma · 2011Article
- Ataxia telangiectasia-mutated protein and DNA-dependent protein kinase have complementary V(D)J recombination functions.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- The DNA-dependent protein kinase catalytic subunit is phosphorylated in vivo on threonine 3950, a highly conserved amino acid in the protein kinase domain.Molecular and cellular biology · 2007Article
- Dynamic assembly of end-joining complexes requires interaction between Ku70/80 and XRCC4.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Autophosphorylation of the catalytic subunit of the DNA-dependent protein kinase is required for efficient end processing during DNA double-strand break repair.Molecular and cellular biology · 2003Article
- Cancer predisposition and hematopoietic failure in Rad50(S/S) mice.Genes & development · 2002Article
- The C-terminal conserved domain of DNA-PKcs, missing in the SCID mouse, is required for kinase activity.Nucleic acids research · 2000Article
- Induction and characterization of human glioma clones with different radiosensitivities.Neoplasia (New York, N.Y.) · 1999Article
- Analysis of variable (diversity) joining recombination in DNAdependent protein kinase (DNA-PK)-deficient mice reveals DNA-PK-independent pathways for both signal and coding joint formation.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Hypersensitivity of Ku-deficient cells toward the DNA topoisomerase II inhibitor ICRF-193 suggests a novel role for Ku antigen during the G2 and M phases of the cell cycle.Molecular and cellular biology · 1998Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
DNA-dependent protein kinase (DNA-PK) plays an important role in DNA double-strand break (DSB) repair and V(D)J recombination. We have isolated a new X-ray-sensitive CHO cell line, XR-C1, which is impaired in DSB repair and which was assigned to complementation group 7, the group that is defective in the XRCC7 / SCID ( Prkdc ) gene encoding the catalytic subunit of DNA-PK (DNA-PKcs). Consistent with this complementation analysis, XR-C1 cells lackeddetectable DNA-PKcs protein, did not display DNA-PK catalytic activity and were complemented by the introduction of a single human chromosome 8 (providing the Prkdc gene). The impact of the XR-C1 mutation on V(D)J recombination was quite different from that found in most rodent cells defective in DNA-PKcs, which are preferentially blocked in coding joint formation, whereas XR-C1 cells were defective in forming both coding and signal joints. These results suggest that DNA-PKcs is required for both coding and signal joint formation during V(D)J recombination and that the XR-C1 mutant cell line may prove to be a useful tool in understanding this pathway.
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