The DOI matches its Crossref record; 76 of the 76 references it cites were found in a registry or an index.
The controlling role of ATM in homologous recombinational repair of DNA damage
Open accessAbstract
The human genetic disorder ataxia telangiectasia (A-T), caused by mutation in the ATM gene, is characterized by chromosomal instability, radiosensitivity and defective cell cycle checkpoint activation. DNA double-strand breaks (dsbs) persist in A-T cells after irradiation, but the underlying defect is unclear. To investigate ATM's interactions with dsb repair pathways, we disrupted ATM along with other genes involved in the principal, complementary dsb repair pathways of homologous recombination (HR) or non-homologous end-joining (NHEJ) in chicken DT40 cells. ATM(-/-) cells show altered kinetics of radiation-induced Rad51 and Rad54 focus formation. Ku70-deficient (NHEJ(-)) ATM(-/-) chicken DT40 cells show radiosensitivity and high radiation-induced chromosomal aberration frequencies, while Rad54-defective (HR(-)) ATM(-/-) cells show only slightly elevated aberration levels after irradiation, placing ATM and HR on the same pathway. These results reveal that ATM defects impair HR-mediated dsb repair and may link cell cycle checkpoints to HR activation.
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“Both homologous recombination and nonhomologous end-joining pathways of double-strand break repair have been shown to be modulated by the ATM-and Chk2-dependent checkpoint (23)(24)(25).”
From Phosphorylation of Nucleotide Excision Repair Factor Xeroderma Pigmentosum Group A by Ataxia Telangiectasia Mutated and Rad3-Related–Dependent Checkpoint Pathway Promotes Cell Survival in Response to UV Irradiation (2006) · cites this paper as [24]
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ATM and related protein kinases: safeguarding genome integrity
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“A-T cells do show a subtle but distinct defect in DSB repair, which was ascribed to suboptimal assembly and functioning of the RAD51-associated protein complexes in the HR arm of DSB repai”
BackgroundDNA double-strand breaks: signaling, repair and the cancer connection
Khanna, K. K., & Jackson, S. P. (2001) · Nature Genetics · doi:10.1038/85798 · Cited by 2,455
“First, careful analyses of the phenotype of ATM-deficient DT40 cells indicates that ATM is involved in the activation of the recombinational repair pathway in response to IR (ref”
BackgroundCell cycle checkpoint signaling through the ATM and ATR kinases
Abraham, R. T. (2001) · Genes & Development · doi:10.1101/gad.914401 · Cited by 1,966
“A later report from the same research group provided genetic evidence that ATM and the late S–G2 recombinational repair mechanism resided in the same genome maintenance pathway (Morrison et al. 2000).”
BackgroundRegulation of DNA double-strand break repair pathway choice
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“Deficiency in ATM and reduction of ATR kinase activity result in defects in HR (22, 23).”
Background
Metadata
- Authors
- Morrison, C., Sonoda, E., Takao, N., Shinohara, A., Yamamoto, K., & Takeda, S.
- Affiliations
- Kyoto University (JP)
- Kanazawa University (JP)
- University of Chicago (US)
- Corresponding author
- Takeda, Shunichi
- ORCID
- Morrison, Ciaran
- Venue
- The EMBO Journal
- Published
- 2000-02-01
- Volume
- 19
- Issue
- 3
- Pages
- 463-471
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC305583
- OpenAlex
- W2017297714
- Cited by
- 312
- References
- 76
- Citations by year
- 2026: 6 · 2025: 1 · 2024: 10 · 2023: 2 · 2022: 8 · 2021: 6 · 2020: 9 · 2019: 8 · 2018: 9 · 2017: 9 · 2016: 1 · 2015: 12 · 2014: 9 · 2013: 8 · 2012: 15
- FWCI
- 10.74
- Type
- journal article
- Language
- en
- Update notices
- erratum (2000-02-15)
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- QIMR Berghofer Medical Research Institute
- University of Cambridge
- University of Sussex
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Bayer Yakuhin
- Medical Research Council
- Japan Society for the Promotion of Science (CREST)
- Core Research for Evolutional Science and Technology
- 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 › PARP inhibition in cancer therapy
- Keywords
- ATM kinase, ataxia telangiectasia, homologous recombination, non-homologous end joining, DNA double-strand break repair, radiosensitivity, chromosomal instability, cell cycle checkpoints, RAD51, Rad54, Ku70, DT40 cells, chromosomal abnormalities
- MeSH terms
- Ku Autoantigen, Animals, Ataxia Telangiectasia, Cell Division, Cell Line, Chickens, Chromosome Aberrations, DNA Damage, DNA Repair, DNA Helicases, DNA-Binding Proteins, Fluorescent Antibody Technique, Fungal Proteins, Humans, Nuclear Proteins, Radiation Tolerance, Recombination, Genetic, Immunoblotting, Protein Serine-Threonine Kinases, Gene Targeting, Cell Cycle Proteins, Tumor Suppressor Proteins, Saccharomyces cerevisiae Proteins, Avian Proteins, Antigens, Nuclear, DNA Repair Enzymes, Rad51 Recombinase, Ataxia Telangiectasia Mutated Proteins
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