ArticleNucleic acids research2013
Clustered DNA damage induces pan-nuclear H2AX phosphorylation mediated by ATM and DNA-PK.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 115 citations in OpenAlex.
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- Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Altered MDC1 Interactions and Dysfunctional DNA Repair in Lobular Breast Cancer Confers Sensitivity to PARP Inhibition.Cancer research · 2026Article
- Base-excision repair increases DNA double-strand break clustering within heavy-ion tracks and modulates repair at δ-electron-induced breaks.Scientific reports · 2026Article
- DNA damage response defects induced by the formation of TDP-43 and mutant FUS cytoplasmic inclusions and their pharmacological rescue.Cell death and differentiation · 2025Article
- Reconstructing EBV reactivation and DNA damage response kinetics in morphologic pseudotime.bioRxiv : the preprint server for biology · 2025Article
- Re-epithelialization of cancer cells increases autophagy and DNA damage: Implications for breast cancer dormancy and relapse.Science signaling · 2025Article
- Synergistic Effects of UVB and Ionizing Radiation on Human Non-Malignant Cells: Implications for Ozone Depletion and Secondary Cosmic Radiation Exposure.Biomolecules · 2025Article
- Genome-wide CRISPR screens identify PKMYT1 as a therapeutic target in pancreatic ductal adenocarcinoma.EMBO molecular medicine · 2024Article
- Tumor targeted alpha particle therapy with an actinium-225 labelled antibody for carbonic anhydrase IX.Chemical science · 2024Article
- DNA Double Strand Break and Response Fluorescent Assays: Choices and Interpretation.International journal of molecular sciences · 2024Review
- Nuclear morphology predicts cell survival to cisplatin chemotherapy.Neoplasia (New York, N.Y.) · 2023Article
- Dissection of DNA damage and repair pathways in live cells by femtosecond laser microirradiation and free-electron modeling.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Transient and tunable CRISPRa regulation of APOBEC/AID genes for targeting hepatitis B virus.Molecular therapy. Nucleic acids · 2023Article
- Article
- Investigating the Functional Roles of Aldehyde Dehydrogenase 3A1 in Human Corneal Epithelial Cells.International journal of molecular sciences · 2023Article
- Radiosensitization of Breast Cancer Cells with a 2-Methoxyestradiol Analogue Affects DNA Damage and Repair Signaling In Vitro.International journal of molecular sciences · 2023Article
- Nanomaterial genotoxicity evaluation using the high-throughput p53-binding protein 1 (53BP1) assay.PloS one · 2023Article
- Let's not take DNA breaks for granted. The importance of direct detection of DNA breaks for the successful development of DDR inhibitors.Frontiers in cell and developmental biology · 2023Review
- Differential Recruitment of DNA Repair Proteins KU70/80 and RAD51 upon Microbeam Irradiation with α-Particles.Biology · 2022Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSB) are considered as the most deleterious DNA lesions, and their repair is further complicated by increasing damage complexity. However, the molecular effects of clustered lesions are yet not fully understood. As the locally restricted phosphorylation of H2AX to form γH2AX is a key step in facilitating efficient DSB repair, we investigated this process after localized induction of clustered damage by ionizing radiation. We show that in addition to foci at damaged sites, H2AX is also phosphorylated in undamaged chromatin over the whole-cell nucleus in human and rodent cells, but this is not related to apoptosis. This pan-nuclear γH2AX is mediated by the kinases ataxia telangiectasia mutated and DNA-dependent protein kinase (DNA-PK) that also phosphorylate H2AX at DSBs. The pan-nuclear response is dependent on the amount of DNA damage and is transient even under conditions of impaired DSB repair. Using fluorescence recovery after photobleaching (FRAP), we found that MDC1, but not 53BP1, binds to the nuclear-wide γH2AX. Consequently, the accumulation of MDC1 at DSBs is reduced. Altogether, we show that a transient dose-dependent activation of the kinases occurring on complex DNA lesions leads to their nuclear-wide distribution and H2AX phosphorylation, yet without eliciting a full pan-nuclear DNA damage response.
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