ArticleNucleic acids research2022
Structural analysis of the basal state of the Artemis:DNA-PKcs complex.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- End processing in NHEJ by Polymerase λ and PNKP is coordinated during short-range synapsis.Nature communications · 2026Article
- DNA-PK driven nucleosome unwrapping enables NHEJ in chromatin.Nature communications · 2026Article
- Review
- Decoding the role of non-coding RNAs in HNSCC radioresistance: molecular mechanisms and clinical implications.Frontiers in oncology · 2026Review
- Downregulation of ZFP36L1 contributes to methotrexate resistance in osteosarcoma through enhanced NHEJ DNA repair mechanisms.Cell death & disease · 2025Article
- Artemis (DCLRE1C) Acts as a Target to Enhance Radiotherapy Response in Triple-Negative Breast Cancer.Cancers · 2025Article
- Targeting Artemis Sensitizes B Cells to Topoisomerase 2 Poisons by Disrupting DNA-PKcs-Dependent Repair.Research square · 2025Article
- Redox regulation: mechanisms, biology and therapeutic targets in diseases.Signal transduction and targeted therapy · 2025Review
- Computational advances in the design and discovery of artemis inhibitors for radiosensitization in cancer therapy.Frontiers in chemistry · 2025Article
- Multivalent interactions of the disordered regions of XLF and XRCC4 foster robust cellular NHEJ and drive the formation of ligation-boosting condensates in vitro.Nature structural & molecular biology · 2024Article
- DNA-PK: A synopsis beyond synapsis.DNA repair · 2024Review
- TRIM24 Cooperates with Ras Mutation to Drive Glioma Progression through snoRNA Recruitment of PHAX and DNA-PKcs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- GCN5 mediates DNA-PKcs crotonylation for DNA double-strand break repair and determining cancer radiosensitivity.British journal of cancer · 2024Article
- DNA-PK controls Apollo's access to leading-end telomeres.Nucleic acids research · 2024Article
- Article
- Myriad factors and pathways influencing tumor radiotherapy resistance.Open life sciences · 2024Review
- PRKDC regulates cGAMP to enhance immune response in lung cancer treatment.Frontiers in immunology · 2024Article
- Structure and mechanism in non-homologous end joining.DNA repair · 2023Article
- Structure and function of the apical PIKKs in double-strand break repair.Current opinion in structural biology · 2023Review
- Artemis inhibition as a therapeutic strategy for acute lymphoblastic leukemia.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Artemis nuclease and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) are key components in nonhomologous DNA end joining (NHEJ), the major repair mechanism for double-strand DNA breaks. Artemis activation by DNA-PKcs resolves hairpin DNA ends formed during V(D)J recombination. Artemis deficiency disrupts development of adaptive immunity and leads to radiosensitive T- B- severe combined immunodeficiency (RS-SCID). An activated state of Artemis in complex with DNA-PK was solved by cryo-EM recently, which showed Artemis bound to the DNA. Here, we report that the pre-activated form (basal state) of the Artemis:DNA-PKcs complex is stable on an agarose-acrylamide gel system, and suitable for cryo-EM structural analysis. Structures show that the Artemis catalytic domain is dynamically positioned externally to DNA-PKcs prior to ABCDE autophosphorylation and show how both the catalytic and regulatory domains of Artemis interact with the N-HEAT and FAT domains of DNA-PKcs. We define a mutually exclusive binding site for Artemis and XRCC4 on DNA-PKcs and show that an XRCC4 peptide disrupts the Artemis:DNA-PKcs complex. All of the findings are useful in explaining how a hypomorphic L3062R missense mutation of DNA-PKcs could lead to insufficient Artemis activation, hence RS-SCID. Our results provide various target site candidates to design disruptors for Artemis:DNA-PKcs complex formation.
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Registered trials
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