ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Restoration of ATM Expression in DNA-PKcs-Deficient Cells Inhibits Signal End Joining.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- Systematic discovery of UFM1 receptors reveals a regulatory module in DNA repair directing non-homologous end-joining.Nature communications · 2026Article
- Nonhomologous end joining-the importance of end tethering and beyond.Genes & development · 2026Review
- Single-molecule imaging reveals the kinetics of non-homologous end-joining in living cells.Nature communications · 2024Article
- ATM and 53BP1 regulate alternative end joining-mediated V(D)J recombination.Science advances · 2024Article
- Single-molecule imaging reveals the kinetics of non-homologous end-joining in living cells.bioRxiv : the preprint server for biology · 2024Article
- Unravelling the complexities of DNA-PK activation by structure-based mutagenesis.Research square · 2023Article
- Efficient high-precision homology-directed repair-dependent genome editing by HDRobust.Nature methods · 2023Article
- Heavy metal ions exchange driven protein phosphorylation cascade functions in genomic instability in spermatocytes and male infertility.Nucleic acids research · 2023Article
- Two distinct long-range synaptic complexes promote different aspects of end processing prior to repair of DNA breaks by non-homologous end joining.Molecular cell · 2023Article
- Catalytically inactive DNA ligase IV promotes DNA repair in living cells.Nucleic acids research · 2022Article
- Cryo-EM of NHEJ supercomplexes provides insights into DNA repair.Molecular cell · 2021Article
- Review
- Structure of an activated DNA-PK and its implications for NHEJ.Molecular cell · 2021Article
- Temporally uncoupled signal and coding joint formation in human V(D)J recombination.Molecular immunology · 2020Article
- Deciphering the role of distinct DNA-PK phosphorylations at collapsed replication forks.DNA repair · 2020Article
- The recent advances in non-homologous end-joining through the lens of lymphocyte development.DNA repair · 2020Review
- ATM antagonizes NHEJ proteins assembly and DNA-ends synapsis at single-ended DNA double strand breaks.Nucleic acids research · 2020Article
- Activation of DNA-PK by hairpinned DNA ends reveals a stepwise mechanism of kinase activation.Nucleic acids research · 2020Article
- Human DNA-PK activates a STING-independent DNA sensing pathway.Science immunology · 2020Article
- Simultaneous precise editing of multiple genes in human cells.Nucleic acids research · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Unlike most DNA-dependent protein kinase, catalytic subunit (DNA-PKcs)-deficient mouse cell strains, we show in the present study that targeted deletion of DNA-PKcs in two different human cell lines abrogates VDJ signal end joining in episomal assays. Although the mechanism is not well defined, DNA-PKcs deficiency results in spontaneous reduction of ATM expression in many cultured cell lines (including those examined in this study) and in DNA-PKcs-deficient mice. We considered that varying loss of ATM expression might explain differences in signal end joining in different cell strains and animal models, and we investigated the impact of ATM and/or DNA-PKcs loss on VDJ recombination in cultured human and rodent cell strains. To our surprise, in DNA-PKcs-deficient mouse cell strains that are proficient in signal end joining, restoration of ATM expression markedly inhibits signal end joining. In contrast, in DNA-PKcs-deficient cells that are deficient in signal end joining, complete loss of ATM enhances signal (but not coding) joint formation. We propose that ATM facilitates restriction of signal ends to the classical nonhomologous end-joining pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.