ArticleProceedings of the National Academy of Sciences of the United States of America2001
Phosphorylation of serines 635 and 645 of human Rad17 is cell cycle regulated and is required for G(1)/S checkpoint activation in response to DNA damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 67 citations in OpenAlex.
- Article
- ATR and TopBP1 oppose to control dormant origin activity and global replication dynamics, providing a first defense against replication stress.Nucleic acids research · 2026Article
- Association of rare, recurrent nonsynonymous variants in the germline of prostate cancer patients of African ancestry.The Prostate · 2023Article
- Landscape of Genetic Alterations Underlying Hallmark Signature Changes in Cancer RevealsCancer research communications · 2023Article
- Development of a novel and synthetic HematoMiR technology that broadly modulates quiescence of stem cells and enhances HSC expansion.Cellular and molecular life sciences : CMLS · 2021Article
- Critical role of SMG7 in activation of the ATR-CHK1 axis in response to genotoxic stress.Scientific reports · 2021Article
- Measuring Cancer Hallmark Mediation of the TET1 Glioma Survival Effect with Linked Neural-Network Based Mediation Experiments.Scientific reports · 2020Article
- Article
- ATR kinase regulates its attenuation via PPM1D phosphatase recruitment to chromatin during recovery from DNA replication stress signalling.Journal of biosciences · 2018Article
- Fanconi Anemia Signaling and Cancer.Trends in cancer · 2017Review
- Characterization of the interaction between Rfa1 and Rad24 in Saccharomyces cerevisiae.PloS one · 2015Article
- Src family kinases promote silencing of ATR-Chk1 signaling in termination of DNA damage checkpoint.The Journal of biological chemistry · 2014Article
- Translation initiation factor eIF4E is a target for tumor cell radiosensitization.Cancer research · 2012Article
- Disruption of serine/threonine protein phosphatase 5 (PP5:PPP5c) in mice reveals a novel role for PP5 in the regulation of ultraviolet light-induced phosphorylation of serine/threonine protein kinase Chk1 (CHEK1).The Journal of biological chemistry · 2011Article
- Role for casein kinase 1 in the phosphorylation of Claspin on critical residues necessary for the activation of Chk1.Molecular biology of the cell · 2011Article
- Differential hRad17 expression by histologic subtype of ovarian cancer.Journal of ovarian research · 2011Article
- Proteolysis of Rad17 by Cdh1/APC regulates checkpoint termination and recovery from genotoxic stress.The EMBO journal · 2010Article
- Cyclin-dependent kinase 2 dependent phosphorylation of ATRIP regulates the G2-M checkpoint response to DNA damage.Cancer research · 2007Article
- The checkpoint clamp activates Mec1 kinase during initiation of the DNA damage checkpoint.Molecular cell · 2006Article
- Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
ATR [ataxia-telangiectasia-mutated (ATM)- and Rad3-related] is a protein kinase required for both DNA damage-induced cell cycle checkpoint responses and the DNA replication checkpoint that prevents mitosis before the completion of DNA synthesis. Although ATM and ATR kinases share many substrates, the different phenotypes of ATM- and ATR-deficient mice indicate that these kinases are not functionally redundant. Here we demonstrate that ATR but not ATM phosphorylates the human Rad17 (hRad17) checkpoint protein on Ser(635) and Ser(645) in vitro. In undamaged synchronized human cells, these two sites were phosphorylated in late G(1), S, and G(2)/M, but not in early-mid G(1). Treatment of cells with genotoxic stress induced phosphorylation of hRad17 in cells in early-mid G(1). Expression of kinase-inactive ATR resulted in reduced phosphorylation of these residues, but these same serine residues were phosphorylated in ionizing radiation (IR)-treated ATM-deficient human cell lines. IR-induced phosphorylation of hRad17 was also observed in ATM-deficient tissues, but induction of Ser(645) was not optimal. Expression of a hRad17 mutant, with both serine residues changed to alanine, abolished IR-induced activation of the G(1)/S checkpoint in MCF-7 cells. These results suggest ATR and hRad17 are essential components of a DNA damage response pathway in mammalian cells.
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