ArticleNucleic acids research1998
DNA-PK is essential only for coding joint formation in V(D)J recombination.
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 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Single-molecule techniques in studying the molecular mechanisms of DNA synapsis in non-homologous end-joining repair.Biophysics reports · 2025Article
- DNA-PK controls Apollo's access to leading-end telomeres.Nucleic acids research · 2024Article
- Temporally uncoupled signal and coding joint formation in human V(D)J recombination.Molecular immunology · 2020Article
- The molecular basis and disease relevance of non-homologous DNA end joining.Nature reviews. Molecular cell biology · 2020Review
- Preserving genome integrity in human cells via DNA double-strand break repair.Molecular biology of the cell · 2020Review
- DNA-PKcs chemical inhibition versus genetic mutation: Impact on the junctional repair steps of V(D)J recombination.Molecular immunology · 2020Article
- The essential elements for the noncovalent association of two DNA ends during NHEJ synapsis.Nature communications · 2019Article
- Article
- Effects of DNA end configuration on XRCC4-DNA ligase IV and its stimulation of Artemis activity.The Journal of biological chemistry · 2017Article
- Restoration of ATM Expression in DNA-PKcs-Deficient Cells Inhibits Signal End Joining.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Unifying the DNA end-processing roles of the artemis nuclease: Ku-dependent artemis resection at blunt DNA ends.The Journal of biological chemistry · 2015Article
- XRCC4's interaction with XLF is required for coding (but not signal) end joining.Nucleic acids research · 2012Article
- 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
- 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
- Productive and nonproductive complexes of Ku and DNA-dependent protein kinase at DNA termini.Molecular and cellular biology · 1998Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The analysis of the role of DNA-dependent protein kinase (DNA-PK) in DNA double-strand break repair and V(D)J recombination is based primarily on studies of murine scid, in which only the C-terminal 2% of the protein is deleted and the remaining 98% is expressed at levels that are within an order of magnitude of normal. In murine scid, signal joint formation is observed at normal levels, even though coding joint formation is reduced over three orders of magnitude. In contrast, a closely associated protein, Ku, is necessary for both coding and signal joint formation. Based on these observations, a reasonable hypothesis has been that absence of the DNA-PK protein (rather than merely its C-terminal 2% truncation) would ablate signal joint formation along with coding joint formation. In fact, a study of equine SCID, in which there is a much larger truncation of the DNA-PK protein, has suggested that signal joints do fail to form. In our current study, we have analyzed signal and coding joint formation in a malignant glioma cell line, M059J, which was previously shown to be deficient in DNA-PK. Our quantitative analysis shows that full-length protein levels are reduced at least 200-fold, to a level that is undetectable, yet signal joint formation occurs at wild-type levels. This result demonstrates that at least this form of non-homologous DNA end joining can occur in the absence of DNA-PK.
Indexed as
Identifiers
What OpenQuestion holds
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.