ArticleThe Journal of experimental medicine2009
Impact of a hypomorphic Artemis disease allele on lymphocyte development, DNA end processing, and genome stability.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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Who cites it
27 citing papers in PubMed.
- 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
- Nonhomologous end joining-the importance of end tethering and beyond.Genes & development · 2026Review
- A novel splice donor mutation inFrontiers in oncology · 2023Article
- Dynamics of the Artemis and DNA-PKcs Complex in the Repair of Double-Strand Breaks.Journal of molecular biology · 2022Review
- Partial deletions of the autoregulatory C-terminal domain of Artemis and their effect on its nuclease activity.DNA repair · 2022Article
- The recent advances in non-homologous end-joining through the lens of lymphocyte development.DNA repair · 2020Review
- CD3εFrontiers in immunology · 2020Article
- MRE11 Promotes Tumorigenesis by Facilitating Resistance to Oncogene-Induced Replication Stress.Cancer research · 2017Article
- Autoinhibition of the Nuclease ARTEMIS Is Mediated by a Physical Interaction between Its Catalytic and C-terminal Domains.The Journal of biological chemistry · 2017Article
- Structure-Specific nuclease activities of Artemis and the Artemis: DNA-PKcs complex.Nucleic acids research · 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
- Not All SCID Pigs Are Created Equally: Two Independent Mutations in the Artemis Gene Cause SCID in Pigs.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Linkage of catalysis and 5' end recognition in ribonuclease RNase J.Nucleic acids research · 2015Article
- Functional analysis of naturally occurring DCLRE1C mutations and correlation with the clinical phenotype of ARTEMIS deficiency.The Journal of allergy and clinical immunology · 2015Article
- The spatial organization of non-homologous end joining: from bridging to end joining.DNA repair · 2014Article
- Repair of double-strand breaks by end joining.Cold Spring Harbor perspectives in biology · 2013Review
- Novel spontaneous deletion of artemis exons 10 and 11 in mice leads to T- and B-cell deficiency.PloS one · 2013Article
- Role of non-homologous end joining in V(D)J recombination.Immunologic research · 2012Review
- Artemis C-terminal region facilitates V(D)J recombination through its interactions with DNA Ligase IV and DNA-PKcs.The Journal of experimental medicine · 2012Article
- Polynucleotide kinase and aprataxin-like forkhead-associated protein (PALF) acts as both a single-stranded DNA endonuclease and a single-stranded DNA 3' exonuclease and can participate in DNA end joining in a biochemical system.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Artemis was initially discovered as the gene inactivated in human radiosensitive T(-)B(-) severe combined immunodeficiency, a syndrome characterized by the absence of B and T lymphocytes and cellular hypersensitivity to ionizing radiation. Hypomorphic Artemis alleles have also been identified in patients and are associated with combined immunodeficiencies of varying severity. We examine the molecular mechanisms underlying a syndrome of partial immunodeficiency caused by a hypomorphic Artemis allele using the mouse as a model system. This mutation, P70, leads to premature translation termination that deletes a large portion of a nonconserved C terminus. We find that homozygous Artemis-P70 mice exhibit reduced numbers of B and T lymphocytes, thereby recapitulating the patient phenotypes. The hypomorphic mutation results in impaired end processing during the lymphoid-specific DNA rearrangement known as V(D)J recombination, defective double-strand break repair, and increased chromosomal instability. Biochemical analyses reveal that the Artemis-P70 mutant protein interacts with the DNA-dependent protein kinase catalytic subunit and retains significant, albeit reduced, exo- and endonuclease activities but does not undergo phosphorylation. Together, our findings indicate that the Artemis C terminus has critical in vivo functions in ensuring efficient V(D)J rearrangements and maintaining genome integrity.
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Registered trials
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