The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks
Abstract
It is generally thought that the DNA-damage checkpoint kinases, ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR), work independently of one another. Here, we show that ATM and the nuclease activity of meiotic recombination 11 (Mre11) are required for the processing of DNA double-strand breaks (DSBs) to generate the replication protein A (RPA)-coated ssDNA that is needed for ATR recruitment and the subsequent phosphorylation and activation of Chk1. Moreover, we show that efficient ATM-dependent ATR activation in response to DSBs is restricted to the S and G2 cell cycle phases and requires CDK kinase activity. Thus, in response to DSBs, ATR activation is regulated by ATM in a cell-cycle dependent manner.
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In the citing paper
“The situation is somewhat complicated by the finding that ATR can be also recruited to DSBs and this binding depends upon ATM [41,42].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [41]
In the citing paper
“Furthermore, ATM is essential for DSB-induced ATR activation in the S and G2 phases of cell cycle, but not in the G1 phase [140].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [140]
Citations
Cites
Sensing DNA Damage Through ATRIP Recognition of RPA-ssDNA Complexes
Zou, L., & Elledge, S. J. (2003) · Science · doi:10.1126/science.1083430 · Cited by 2,693
ATM and related protein kinases: safeguarding genome integrity
Shiloh, Y. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1011 · Cited by 2,577
Cell cycle checkpoint signaling through the ATM and ATR kinases
Abraham, R. T. (2001) · Genes & Development · doi:10.1101/gad.914401 · Cited by 1,966
Liu, Q., Guntuku, S., Cui, X.-S., Matsuoka, S., Cortez, D., Tamai, K., Luo, G., Carattini-Rivera, S., DeMayo, F., Bradley, A., et al. (2000) · Genes & Development · doi:10.1101/gad.14.12.1448 · Cited by 1,625
Chk1 and Chk2 kinases in checkpoint control and cancer
Bartek, J., & Lukas, J. (2003) · Cancer Cell · doi:10.1016/s1535-6108(03)00110-7 · Cited by 1,513
Self-citationATM Activation by DNA Double-Strand Breaks Through the Mre11-Rad50-Nbs1 Complex
Lee, J.-H., & Paull, T. T. (2005) · Science · doi:10.1126/science.1108297 · Cited by 1,424
Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage
Falck, J., Coates, J., & Jackson, S. P. (2005) · Nature · doi:10.1038/nature03442 · Cited by 1,304
Self-citationHickson, I., Zhao, Y., Richardson, C. J., Green, S. J., Martin, N. M. B., Orr, A. I., Reaper, P. M., Jackson, S. P., Curtin, N. J., & Smith, G. C. M. (2004) · Cancer Research · doi:10.1158/0008-5472.can-04-2727 · Cited by 1,220
Self-citationPathways of DNA Double-Strand Break Repair during the Mammalian Cell Cycle
Rothkamm, K., Krüger, I., Thompson, L. H., & Lübrich, M. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.16.5706-5715.2003 · Cited by 1,187
ATR-Mediated Checkpoint Pathways Regulate Phosphorylation and Activation of Human Chk1
Zhao, H., & Piwnica-Worms, H. (2001) · Molecular and Cellular Biology · doi:10.1128/mcb.21.13.4129-4139.2001 · Cited by 1,091
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ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response
Blackford, A. N., & Jackson, S. P. (2017) · Molecular Cell · doi:10.1016/j.molcel.2017.05.015 · Cited by 2,050
Self-citationATR: an essential regulator of genome integrity
Cimprich, K. A., & Cortez, D. (2008) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2450 · Cited by 1,798
Non-homologous DNA end joining and alternative pathways to double-strand break repair
Chang, H. H. Y., Pannunzio, N. R., Adachi, N., & Lieber, M. R. (2017) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2017.48 · Cited by 1,757
53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA Breaks
Bunting, S. F., Callén, E., Wong, N., Chen, H.-T., Polato, F., Gunn, A., Bothmer, A., Feldhahn, N., Fernandez-Capetillo, O., Cao, L., et al. (2010) · Cell · doi:10.1016/j.cell.2010.03.012 · Cited by 1,671
Playing the End Game: DNA Double-Strand Break Repair Pathway Choice
Chapman, J. R., Taylor, M. R. G., & Boulton, S. J. (2012) · Molecular Cell · doi:10.1016/j.molcel.2012.07.029 · Cited by 1,728
Metadata
- Authors
- Jazayeri, A., Falck, J., Lukas, C., Bartek, J., Smith, G. C. M., Lukas, J., & Jackson, S. P.
- Affiliations
- University of Cambridge (GB)
- Danish Cancer Society (DK)
- Corresponding author
- Jackson, Stephen P.
- Venue
- Nature Cell Biology
- Published
- 2005-12-04
- Volume
- 8
- Issue
- 1
- Pages
- 37-45
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W2062284662
- Cited by
- 1,064
- References
- 47
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 24 · 2023: 17 · 2022: 33 · 2021: 43 · 2020: 35 · 2019: 45 · 2018: 38 · 2017: 41 · 2016: 48 · 2015: 64 · 2014: 56 · 2013: 79 · 2012: 65
- FWCI
- 25.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Keywords
- ATM, ATR, DNA double-strand breaks, DNA damage checkpoint, Mre11 nuclease, Chk1 phosphorylation, cell cycle regulation, meiotic recombination
- MeSH terms
- Checkpoint Kinase 1, MRE11 Homologue Protein, Cell Cycle, Cell Nucleus, DNA Damage, DNA-Binding Proteins, HeLa Cells, Humans, Nuclear Proteins, Phosphorylation, Protein Kinases, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Cyclin-Dependent Kinases, Tumor Suppressor Proteins, Cell Line, Tumor, Replication Protein A, Ataxia Telangiectasia Mutated Proteins
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