ArticleThe Journal of biological chemistry2014
Nucleotide excision repair-dependent DNA double-strand break formation and ATM signaling activation in mammalian quiescent cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- DNA repair-associated nucleases induce double-strand breaks following sequential exposure to UVA1 and UVB.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Article
- Review
- Tissue Organoid Cultures Metabolize Dietary Carcinogens Proficiently and Are Effective Models for DNA Adduct Formation.Chemical research in toxicology · 2024Article
- BAP1 promotes the repair of UV-induced DNA damage via PARP1-mediated recruitment to damage sites and control of activity and stability.Cell death and differentiation · 2022Article
- Tracing brain genotoxic stress in Parkinson's disease with a novel single-cell genetic sensor.Science advances · 2022Article
- A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation.eLife · 2021Article
- Skin Abnormalities in Disorders with DNA Repair Defects, Premature Aging, and Mitochondrial Dysfunction.The Journal of investigative dermatology · 2021Review
- RNF8 ubiquitinates RecQL4 and promotes its dissociation from DNA double strand breaks.Oncogenesis · 2021Article
- Exploring the effect of UV-C radiation on earthworm and understanding its genomic integrity in the context of H2AX expression.Scientific reports · 2020Article
- Exploring the effect of UV-C radiation on earthworm and understanding its genomic integrity in the context of H2AX expression.Scientific reports · 2020Article
- Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells.International journal of molecular sciences · 2020Article
- γ-H2AX as a potential indicator of radiosensitivity in colorectal cancer cells.Oncology letters · 2020Article
- Solar ultraviolet-induced DNA damage response: Melanocytes story in transformation to environmental melanomagenesis.Environmental and molecular mutagenesis · 2020Review
- DCTPP1 prevents a mutator phenotype through the modulation of dCTP, dTTP and dUTP pools.Cellular and molecular life sciences : CMLS · 2020Article
- ATR Kinase Activity Limits Mutagenesis and Promotes the Clonogenic Survival of Quiescent Human Keratinocytes Exposed to UVB Radiation.Photochemistry and photobiology · 2020Article
- APOBEC3B reporter myeloma cell lines identify DNA damage response pathways leading to APOBEC3B expression.PloS one · 2020Article
- RHOAming Through the Nucleotide Excision Repair Pathway as a Mechanism of Cellular Response Against the Effects of UV Radiation.Frontiers in cell and developmental biology · 2020Article
- Article
- Spironolactone Depletes the XPB Protein and Inhibits DNA Damage Responses in UVB-Irradiated Human Skin.The Journal of investigative dermatology · 2019Article
- Insulin-like growth factor-1 receptor knockdown enhances radiosensitivity via the HIF-1α pathway and attenuates ATM/H2AX/53BP1 DNA repair activation in human lung squamous carcinoma cells.Oncology letters · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone H2A variant H2AX is phosphorylated at Ser(139) in response to DNA double-strand break (DSB) and single-stranded DNA (ssDNA) formation. UV light dominantly induces pyrimidine photodimers, which are removed from the mammalian genome by nucleotide excision repair (NER). We previously reported that in quiescent G0 phase cells, UV induces ATR-mediated H2AX phosphorylation plausibly caused by persistent ssDNA gap intermediates during NER. In this study, we have found that DSB is also generated following UV irradiation in an NER-dependent manner and contributes to an earlier fraction of UV-induced H2AX phosphorylation. The NER-dependent DSB formation activates ATM kinase and triggers the accumulation of its downstream factors, MRE11, NBS1, and MDC1, at UV-damaged sites. Importantly, ATM-deficient cells exhibited enhanced UV sensitivity under quiescent conditions compared with asynchronously growing conditions. Finally, we show that the NER-dependent H2AX phosphorylation is also observed in murine peripheral T lymphocytes, typical nonproliferating quiescent cells in vivo. These results suggest that in vivo quiescent cells may suffer from NER-mediated secondary DNA damage including ssDNA and DSB.
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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.