ArticleJournal of cell science2023
Live-cell tracking of γ-H2AX kinetics reveals the distinct modes of ATM and DNA-PK in the immediate response to DNA damage.
Article in Journal of cell science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
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- Targeting the Hippo/YAP-TAZ pathway increases X-ray sensitivity in chondrosarcoma spheroids and is associated with autophagic disruption.Journal of bone oncology · 2026Article
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- Mitochondrial-targeted photodynamic therapy combined with TGF-β inhibition potentiates anti-PD-1 therapy in pancreatic ductal adenocarcinoma.Journal of nanobiotechnology · 2025Article
- Engineered chromatin readers track damaged chromatin dynamics in live cells and animals.Nature communications · 2025Article
- Imaging the time course of DNA damage response at a nonrepetitive endogenous locus.Cell reports methods · 2025Article
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- High-dose estrogen impairs demethylation of H3K27me3 by decreasing Kdm6b expression during ovarian hyperstimulation in mice.Journal of Zhejiang University. Science. B · 2025Article
- Melatonin ameliorates zearalenone-induced ovarian damage in mice through antioxidative effects.Frontiers in veterinary science · 2025Article
- Diffusion of activated ATM explains γH2AX and MDC1 spread beyond the DNA damage site.iScience · 2024Article
- ARID1A is involved in DNA double-strand break repair in gastric cancer.Journal of gastrointestinal oncology · 2024Article
- PARP inhibitor synthetic lethality in ATM biallelic mutant cancer cell lines is associated with BRCA1/2 and RAD51 downregulation.Frontiers in oncology · 2024Article
- ATM phosphorylates the FATC domain of DNA-PKcs at threonine 4102 to promote non-homologous end joining.Nucleic acids research · 2023Article
- Dynamics of nuclear architecture during early embryonic development and lessons from liveimaging.Developmental cell · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) are a serious form of DNA damage that can cause genetic mutation. On the induction of DSBs, histone H2AX becomes phosphorylated by kinases, including ataxia telangiectasia-mutated (ATM), ataxia telangiectasia and Rad3-related (ATR) and DNA-dependent protein kinase (DNA-PK). Phosphorylated H2AX (γ-H2AX) can be a platform to recruit DNA repair machinery. Here, we analyzed the immediate early kinetics of γ-H2AX upon laser-induced DNA damage in ATM-proficient and -deficient living cells by using fluorescently labeled antigen-binding fragments specific for γ-H2AX. The accumulation kinetics of γ-H2AX were similar in both ATM-proficient and -deficient cells. However, γ-H2AX accumulation was delayed when the cells were treated with a DNA-PK inhibitor, suggesting that DNA-PK rapidly phosphorylates H2AX at DSB sites. Ku80 (also known as XRCC5), a DNA-PK subunit, diffuses freely in the nucleus without DNA damage, whereas ATM repeatedly binds to and dissociates from chromatin. The accumulation of ATM at damage sites was regulated by the histone H4K16 acetyltransferase MOF (also known as KAT8 in mammals), but its accumulation was not necessarily reflected in the γ-H2AX level. These results suggest distinct actions of ATM and DNA-PK in immediate γ-H2AX accumulation.
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