The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
An Imperfect G 2 M Checkpoint Contributes to Chromosome Instability Following Irradiation of S and G 2 Phase Cells
Open accessAbstract
DNA double strand break (DSB) repair and checkpoint control represent two major mechanisms that function to reduce chromosomal instability following ionizing irradiation (IR). Ataxia telangiectasia (A-T) cells have long been known to have defective checkpoint responses. Recent studies have shown that they also have a DSB repair defect following IR raising the issue of how ATM's repair and checkpoint functions interplay to maintain chromosomal stability. A-T and Artemis cells manifest an identical and epistatic repair defect throughout the cell cycle demonstrating that ATM's major repair defect following IR represents Artemis-dependent end-processing. Artemis cells show efficient G(2)/M checkpoint induction and a prolonged arrest relative to normal cells. Following irradiation of G(2) cells, this checkpoint is dependent on ATM and A-T cells fail to show checkpoint arrest. In contrast, cells irradiated during S phase initiate a G(2)/M checkpoint which is independent of ATM and, significantly, both Artemis and A-T cells show a prolonged arrest at the G(2)/M checkpoint likely reflecting their repair defect. Strikingly, the G(2)/M checkpoint is released before the completion of repair when approximately 10-20 DSBs remain both for S phase and G(2) phase irradiated cells. This defined sensitivity level of the G(2)/M checkpoint explains the prolonged arrest in repair-deficient relative to normal cells and provides a conceptual framework for the cooperative phenotype between checkpoint and repair functions in maintaining chromosomal stability.
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“Therefore, cells with a low number of DNA breaks can enter mitosis [103,104].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [104]
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Cites
The DNA damage response: putting checkpoints in perspective
Zhou, B.-B. S., & Elledge, S. J. (2000) · Nature · doi:10.1038/35044005 · Cited by 3,213
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
Chromosomal stability and the DNA double-stranded break connection
van Gent, D. C., Hoeijmakers, J. H. J., & Kanaar, R. (2001) · Nature Reviews Genetics · doi:10.1038/35056049 · Cited by 1,219
Pathways 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
DNA damage checkpoints: from initiation to recovery or adaptation
Bartek, J., & Lukas, J. (2007) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2007.02.009 · Cited by 784
DNA damage-induced G2–M checkpoint activation by histone H2AX and 53BP1
Fernández-Capetillo, Ó., Chen, H. T., Celeste, A., Ward, I. M., Romanienko, P. J., Morales, J. C., Naka, K., Xia, Z., Camerini‐Otero, R. D., Motoyama, N., et al. (2002) · Nature Cell Biology · doi:10.1038/ncb884 · Cited by 657
THE GENETIC DEFECT IN ATAXIA-TELANGIECTASIA
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ATM and ATR: networking cellular responses to DNA damage
Shiloh, Y. (2001) · Current Opinion in Genetics & Development · doi:10.1016/s0959-437x(00)00159-3 · Cited by 601
Surviving the Breakup: The DNA Damage Checkpoint
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Research works printed but not linked: 3
- Riballo E, Kuhne M, Rief N, Doherty A, Smith GC, Recio MJ, Reis C, Dahm K, Fricke A, Krempler A, Parker AR, Jackson SP, Gennery A, Jeggo PA, Lobrich M. A pathway of double-strand break rejoining dependent upon ATM, Artemis, and proteins locating to gamma-H2AX foci. Mol Cell 2004; 16:715-24.
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Role of the MDM2/p53 axis in regulating cisplatin response in tumor cells
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Metadata
- Authors
- Krempler, A., Deckbar, D., Jeggo, P. A., & Lobrich, M.
- Affiliations
- Saarland University (DE)
- University of Sussex (GB)
- ORCID
- Jeggo, Penny A.
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2007-07-15
- Volume
- 6
- Issue
- 14
- Pages
- 1682-1686
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- OpenAlex
- W2054949155
- Cited by
- 109
- References
- 32
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 4 · 2022: 3 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 3 · 2017: 2 · 2016: 3 · 2015: 4 · 2014: 8 · 2013: 8 · 2012: 10
- FWCI
- 0.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed (publishedVersion)
- Sussex Research Online (University of Sussex) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Funders
- Wilhelm Sander-Stiftung
- Deutsche Forschungsgemeinschaft (LO 677/4-1/2)
- Bundesministerium für Bildung und Forschung (02S8335, 02S8355)
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- G2/M checkpoint, chromosomal instability, ionizing radiation, DNA double-strand break repair, ATM, ataxia telangiectasia, Artemis, S-phase checkpoint, DNA end processing
- MeSH terms
- Cell Division, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, Endonucleases, Humans, Nuclear Proteins, Radiation, Ionizing, G2 Phase, S Phase, Protein Serine-Threonine Kinases, Cell Cycle Proteins, Tumor Suppressor Proteins, Chromosomal Instability, Ataxia Telangiectasia Mutated Proteins
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