ArticleProceedings of the National Academy of Sciences of the United States of America2008
ATR kinase is required for global genomic nucleotide excision repair exclusively during S phase in human cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 90 citations in OpenAlex.
- The XPA Protein-Life under Precise Control.Cells · 2022Review
- A genome-wide screen identifies SCAI as a modulator of the UV-induced replicative stress response.PLoS biology · 2022Article
- Effects of replication domains on genome-wide UV-induced DNA damage and repair.PLoS genetics · 2022Article
- Bioprospecting the microbiome of Red Sea Atlantis II brine pool for peptidases and biosynthetic genes with promising antibacterial activity.Microbial cell factories · 2022Article
- Article
- ATR prevents CaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Dual Characters of GH-IGF1 Signaling Pathways in Radiotherapy and Post-radiotherapy Repair of Cancers.Frontiers in cell and developmental biology · 2021Review
- ATR Kinase Activity Limits Mutagenesis and Promotes the Clonogenic Survival of Quiescent Human Keratinocytes Exposed to UVB Radiation.Photochemistry and photobiology · 2020Article
- Growth Hormone Induces Colon DNA Damage Independent of IGF-1.Endocrinology · 2019Article
- The Nup84 complex coordinates the DNA damage response to warrant genome integrity.Nucleic acids research · 2019Article
- Antibacterial and anticancer activities of orphan biosynthetic gene clusters from Atlantis II Red Sea brine pool.Microbial cell factories · 2019Article
- Article
- Sirtuin 1-mediated deacetylation of XPA DNA repair protein enhances its interaction with ATR protein and promotes cAMP-induced DNA repair of UV damage.The Journal of biological chemistry · 2018Article
- Roles of UVA radiation and DNA damage responses in melanoma pathogenesis.Environmental and molecular mutagenesis · 2018Review
- Regulation of DNA Repair Mechanisms: How the Chromatin Environment Regulates the DNA Damage Response.International journal of molecular sciences · 2017Review
- Paracrine regulation of melanocyte genomic stability: a focus on nucleotide excision repair.Pigment cell & melanoma research · 2017Review
- Impact of Age and Insulin-Like Growth Factor-1 on DNA Damage Responses in UV-Irradiated Human Skin.Molecules (Basel, Switzerland) · 2017Review
- Insulin-like Growth Factor 1 Receptor Signaling Is Required for Optimal ATR-CHK1 Kinase Signaling in Ultraviolet B (UVB)-irradiated Human Keratinocytes.The Journal of biological chemistry · 2017Article
- Hormonal Regulation of the Repair of UV Photoproducts in Melanocytes by the Melanocortin Signaling Axis.Photochemistry and photobiology · 2017Review
- Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation.Advances in experimental medicine and biology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Global-genomic nucleotide excision repair (GG-NER) is the only pathway available to humans for removal, from the genome overall, of highly genotoxic helix-distorting DNA adducts generated by many environmental mutagens and certain chemotherapeutic agents, e.g., UV-induced 6-4 photoproducts (6-4PPs) and cyclobutane pyrimidine dimers (CPDs). The ataxia telangiectasia and rad-3-related kinase (ATR) is rapidly activated in response to UV-induced replication stress and proceeds to phosphorylate a plethora of downstream effectors that modulate primarily cell cycle checkpoints but also apoptosis and DNA repair. To investigate whether this critical kinase might participate in the regulation of GG-NER, we developed a novel flow cytometry-based DNA repair assay that allows precise evaluation of GG-NER kinetics as a function of cell cycle. Remarkably, inhibition of ATR signaling in primary human lung fibroblasts by treatment with caffeine, or with siRNA specifically targeting ATR, resulted in total inhibition of 6-4PP removal during S phase, whereas cells repaired normally during either G(0)/G(1) or G(2)/M. Similarly striking S-phase-specific defects in GG-NER of both 6-4PPs and CPDs were documented in ATR-deficient Seckel syndrome skin fibroblasts. Finally, among six diverse model human tumor strains investigated, three manifested complete abrogation of 6-4PP repair exclusively in S-phase populations. Our data reveal a highly novel role for ATR in the regulation of GG-NER uniquely during S phase of the cell cycle, and indicate that many human cancers may be characterized by a defect in this regulation.
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