ArticleProceedings of the National Academy of Sciences of the United States of America2005
Artemis-independent functions of DNA-dependent protein kinase in Ig heavy chain class switch recombination and development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The trial behind it
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Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- Ku70-SAP domain has an overlapping function with DNA-PKcs in limiting the lateral movement of the Ku ring along DNA.Nucleic acids research · 2026Article
- Unlocking the Therapeutic Potential of DNA-PKcs in Cancer: Comprehensive Insights into Mechanisms and Clinical Applications.Cancers · 2025Review
- The multifaceted functions of DNA-PKcs: implications for the therapy of human diseases.MedComm · 2024Review
- Phosphorylation of DNA-PKcs at the S2056 cluster ensures efficient and productive lymphocyte development in XLF-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Role of DNA Repair in Genomic Instability of Multiple Myeloma.International journal of molecular sciences · 2022Review
- Review
- The recent advances in non-homologous end-joining through the lens of lymphocyte development.DNA repair · 2020Review
- Programmed DNA breaks in lymphoid cells: repair mechanisms and consequences in human disease.Immunology · 2016Review
- Functional overlaps between XLF and the ATM-dependent DNA double strand break response.DNA repair · 2014Review
- Interaction between HIV-1 Tat and DNA-PKcs modulates HIV transcription and class switch recombination.International journal of biological sciences · 2014Article
- A hypomorphic Artemis human disease allele causes aberrant chromosomal rearrangements and tumorigenesis.Human molecular genetics · 2011Article
- The MRE11 complex: starting from the ends.Nature reviews. Molecular cell biology · 2011Review
- Alternative end-joining catalyzes class switch recombination in the absence of both Ku70 and DNA ligase 4.The Journal of experimental medicine · 2010Article
- Non-homologous end joining in class switch recombination: the beginning of the end.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Review
- Artemis and nonhomologous end joining-independent influence of DNA-dependent protein kinase catalytic subunit on chromosome stability.Molecular and cellular biology · 2009Article
- Involvement of Artemis in nonhomologous end-joining during immunoglobulin class switch recombination.The Journal of experimental medicine · 2008Article
- Review
- DNA-PKcs and Artemis function in the end-joining phase of immunoglobulin heavy chain class switch recombination.The Journal of experimental medicine · 2008Article
- Fixing DNA breaks during class switch recombination.The Journal of experimental medicine · 2008Review
- Beta-catenin expression results in p53-independent DNA damage and oncogene-induced senescence in prelymphomagenic thymocytes in vivo.Molecular and cellular biology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Assembly of Ig genes in B lineage cells involves two distinct DNA rearrangements. In early B cell development, site-specific double strand breaks (DSBs) at germ-line V, D, and J gene segments are joined via nonhomologous end-joining (NHEJ) to form variable region exons. Activated mature B cells can change expressed Ig heavy chain constant region exons by class switch recombination (CSR), which also involves DSB intermediates. Absence of any known NHEJ factor severely impairs joining of cleaved V, D, and J segments. In NHEJ, DNA-dependent protein kinase (DNA-PK), which is comprised of the Ku70/80 end-binding heterodimer and the catalytic subunit (DNA-PKcs), activates Artemis to generate a nuclease that processes DSBs before ligation. Because inactivation of DNA-PKcs components also severely affects CSR, we tested whether DNA-PK also functions in CSR via activation of Artemis. To obviate the requirement for V(D)J recombination, we generated DNA-PKcs- and Artemis-deficient B cells that harbored preassembled Ig heavy chain and kappa-light chain "knock-in" (HL) alleles. We found that Artemis-deficient HL B cells undergo robust CSR, indicating that DNA-PKcs functions in CSR via an Artemis-independent mechanism. To further elucidate potential Artemis-independent functions of DNA-PKcs, we asked whether the embryonic lethality associated with double-deficiency for DNA-PKcs and the related ataxia-telangiectasia-mutated (ATM) kinase was also observed in mice doubly deficient for ATM and Artemis. We found that ATM/Artemis double-deficient mice were viable and born in normal Mendelian numbers. Therefore, we conclude that DNA-PKcs has Artemis-independent functions in CSR and normal development.
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