ArticleProceedings of the National Academy of Sciences of the United States of America1998
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.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 87 citations in OpenAlex.
- Lig3-dependent rescue of mouse viability and DNA double-strand break repair by catalytically inactive Lig4.Nucleic acids research · 2025Article
- New Facets of DNA Double Strand Break Repair: Radiation Dose as Key Determinant of HR versus c-NHEJ Engagement.International journal of molecular sciences · 2023Review
- The DNA binding domain and the C-terminal region of DNA Ligase IV specify its role in V(D)J recombination.PloS one · 2023Article
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- Effects of theGenes and environment : the official journal of the Japanese Environmental Mutagen Society · 2020Article
- Article
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- Specific Roles of XRCC4 Paralogs PAXX and XLF during V(D)J Recombination.Cell reports · 2016Article
- Restoration of ATM Expression in DNA-PKcs-Deficient Cells Inhibits Signal End Joining.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- RAG2's acidic hinge restricts repair-pathway choice and promotes genomic stability.Cell reports · 2013Article
- XRCC4's interaction with XLF is required for coding (but not signal) end joining.Nucleic acids research · 2012Article
- Unique and redundant functions of ATM and DNA-PKcs during V(D)J recombination.Cell cycle (Georgetown, Tex.) · 2011Review
- A hypomorphic Artemis human disease allele causes aberrant chromosomal rearrangements and tumorigenesis.Human molecular genetics · 2011Article
- Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping activities during chromosomal signal joint formation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Roles for NBS1 in alternative nonhomologous end-joining of V(D)J recombination intermediates.Molecular cell · 2009Article
- The catalytic subunit of DNA-dependent protein kinase regulates proliferation, telomere length, and genomic stability in human somatic cells.Molecular and cellular biology · 2008Article
- Aberrant V(D)J recombination in ataxia telangiectasia mutated-deficient lymphocytes is dependent on nonhomologous DNA end joining.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- DNA damage and repair during lymphoid development: antigen receptor diversity, genomic integrity and lymphomagenesis.Immunologic research · 2008Review
- The catalytic subunit of DNA-protein kinase (DNA-PKcs) is not required for Ig class-switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies have suggested that ionizing radiation causes irreparable DNA double-strand breaks in mice and cell lines harboring mutations in any of the three subunits of DNA-dependent protein kinase (DNA-PK) (the catalytic subunit, DNA-PKcs, or one of the DNA-binding subunits, Ku70 or Ku86). In actuality, these mutants vary in their ability to resolve double-strand breaks generated during variable (diversity) joining [V(D)J] recombination. Mutant cell lines and mice with targeted deletions in Ku70 or Ku86 are severely compromised in their ability to form coding and signal joints, the products of V(D)J recombination. It is noteworthy, however, that severe combined immunodeficient (SCID) mice, which bear a nonnull mutation in DNA-PKcs, are substantially less impaired in forming signal joints than coding joints. The current view holds that the defective protein encoded by the murine SCID allele retains enough residual function to support signal joint formation. An alternative hypothesis proposes that DNA-PKcs and Ku perform different roles in V(D)J recombination, with DNA-PKcs required only for coding joint formation. To resolve this issue, we examined V(D)J recombination in DNA-PKcs-deficient (SLIP) mice. We found that the effects of this mutation on coding and signal joint formation are identical to the effects of the SCID mutation. Signal joints are formed at levels 10-fold lower than in wild type, and one-half of these joints are aberrant. These data are incompatible with the notion that signal joint formation in SCID mice results from residual DNA-PKcs function, and suggest a third possibility: that DNA-PKcs normally plays an important but nonessential role in signal joint formation.
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