ArticleCell cycle (Georgetown, Tex.)2012
ATM-dependent phosphorylation of the checkpoint clamp regulates repair pathways and maintains genomic stability.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- p53 and RAD9, the DNA Damage Response, and Regulation of Transcription Networks.Radiation research · 2017Review
- ALDH1A1 Deficiency in Gorlin Syndrome Suggests a Central Role for Retinoic Acid and ATM Deficits in Radiation Carcinogenesis.Proteomes · 2014Article
- Transcriptome analysis reveals molecular profiles associated with evolving steps of monoclonal gammopathies.Haematologica · 2014Article
- RNA binding protein RBM14 promotes radio-resistance in glioblastoma by regulating DNA repair and cell differentiation.Oncotarget · 2014Article
- The checkpoint clamp protein Rad9 facilitates DNA-end resection and prevents alternative non-homologous end joining.Cell cycle (Georgetown, Tex.) · 2014Article
- DNA damage sensing by the ATM and ATR kinases.Cold Spring Harbor perspectives in biology · 2013Review
- The ATM protein kinase: regulating the cellular response to genotoxic stress, and more.Nature reviews. Molecular cell biology · 2013Review
- Role of the checkpoint clamp in DNA damage response.Biomolecules · 2013Article
- Phenothiazine Inhibitors of TLKs Affect Double-Strand Break Repair and DNA Damage Response Recovery and Potentiate Tumor Killing with Radiomimetic Therapy.Genes & cancer · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Upon genotoxic stress and during normal S phase, ATM phosphorylates the checkpoint clamp protein Rad9 in a manner that depends on Ser272. Ser272 is the only known ATM-dependent phosphorylation site in human Rad9. However, Ser272 phosphorylation is not required for survival or checkpoint activation after DNA damage. The physiological function of Ser272 remains elusive. Here, we show that ATM-dependent Rad9(Ser272) phosphorylation requires the MRN complex and controls repair pathways. Furthermore, the mutant cells accumulate large numbers of chromosome breaks and induce gross chromosomal rearrangements. Our findings establish a new and unexpected role for ATM: it phosphorylates the checkpoint clamp in order to control repair pathways, thereby maintaining genomic integrity during unperturbed cell cycle and upon DNA damage.
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Registered trials
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.