The DOI matches its Crossref record; 94 of the 96 references it cites were found in a registry or an index.
The ATM protein is required for sustained activation of NF-κB following DNA damage
Abstract
Cells lacking an intact ATM gene are hypersensitive to ionizing radiation and show multiple defects in the cell cycle-coupled checkpoints. DNA damage usually triggers cell cycle arrest through, among other things, the activation of p53. Another DNA-damage responsive factor is NF-kappaB. It is activated by various stress situations, including oxidative stress, and by DNA-damaging compounds such as topoisomerase poisons. We found that cells from Ataxia Telangiectasia patients exhibit a defect in NF-kappaB activation in response to treatment with camptothecin, a topoisomerase I poison. In AT cells, this activation is shortened or suppressed, compared to that observed in normal cells. Ectopic expression of the ATM protein in AT cells increases the activation of NF-kappaB in response to camptothecin. MO59J glioblastoma cells that do not express the DNA-PK catalytic subunit respond normally to camptothecin. These results support the hypothesis that NF-kappaB is a DNA damage-responsive transcription factor and that its activation pathway by DNA damage shares some components with the one leading to p53 activation.
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“Previous work with AT fibroblasts had shown that the canonical immune transcription factor NF‐kB is activated in an ATM‐dependent manner following treatment with a radiomimetic, ionizing radiation, or topoisomerase inhibitor (Lee et al, 1998; Piret et al, 1999; Li et al, 2001).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Piret et al, 1999
Citations
Cites
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Telomeres shorten during ageing of human fibroblasts
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An Essential Role for NF-κB in Preventing TNF-α-Induced Cell Death
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A Single Ataxia Telangiectasia Gene with a Product Similar to PI-3 Kinase
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TNF- and Cancer Therapy-Induced Apoptosis: Potentiation by Inhibition of NF-κB
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Suppression of TNF-α-Induced Apoptosis by NF-κB
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Cited by
Sorted by citations
Regulation and Function of IKK and IKK-Related Kinases
Häcker, H., & Karin, M. (2006) · Science s STKE · doi:10.1126/stke.3572006re13 · Cited by 1,298
“Genetic evidence shows that the kinase ATM (ataxia telangiectasia mutated) is required for this response, although the mechanism by which it activates NF-κB has been enigmatic (156, 157).”
BackgroundDunphy, G., Flannery, S. M., Almine, J. F., Connolly, D. J., Paulus, C., Jønsson, K. L., Jakobsen, M. R., Nevels, M. M., Bowie, A. G., & Unterholzner, L. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.07.034 · Cited by 648
“…(PMA) Fl uo re sc en ce (x 10 00 rf u) O (legend on next page) 746 Molecular Cell 71, 745–760, September 6, 2018 involves the DNA damage kinase ataxia telangiectasia mutated (ATM) and the enzyme poly(ADP-ribose) polymerase 1 (PARP-1) (Hinz et al., 2010; Piret et al., 1999; Stilmann et al., 2009).”
BackgroundIκB kinase complexes: gateways to NF-κB activation and transcription
Scheidereit, C. (2006) · Oncogene · doi:10.1038/sj.onc.1209934 · Cited by 668
“In transfected cells, CYLD interacts with NEMO and TRAFs, selectively degrades UbLys63 chains from NEMO, TRAF2, TRAF6 or TRAF7, and represses activation of IKK and NF-kB by various stimuli.”
BackgroundInfluentialPoly(ADP-ribose) polymerase-1: what have we learned from the deficient mouse model?
Shall, S., & de MURCIA, G. (2000) · Mutation Research/DNA Repair · doi:10.1016/s0921-8777(00)00016-1 · Cited by 534
Molecular Linkage Between the Kinase ATM and NF-κB Signaling in Response to Genotoxic Stimuli
Wu, Z., Shi, Y., Tibbetts, R. S., & Miyamoto, S. (2006) · Science · doi:10.1126/science.1121513 · Cited by 515
Metadata
- Authors
- Piret, B., Schoonbroodt, S., & Piette, J.
- Affiliations
- University of Liège (BE)
- Venue
- Oncogene
- Published
- 1999-04-01
- Volume
- 18
- Issue
- 13
- Pages
- 2261-2271
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2316716290
- Cited by
- 176
- References
- 96
- Citations by year
- 2025: 4 · 2024: 5 · 2023: 2 · 2022: 6 · 2021: 4 · 2020: 5 · 2019: 2 · 2018: 4 · 2017: 4 · 2016: 10 · 2015: 11 · 2014: 2 · 2013: 5 · 2012: 9
- FWCI
- 3.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- ATM protein, NF-κB activation, DNA damage response, camptothecin, topoisomerase I poisons, ataxia telangiectasia, p53, cell cycle checkpoints, radiosensitivity, DNA-dependent protein kinase, transcription factors
- MeSH terms
- NF-KappaB Inhibitor alpha, Adolescent, Age Factors, Antineoplastic Agents, Phytogenic, Ataxia Telangiectasia, Brain Neoplasms, Camptothecin, Cells, Cultured, Child, Child, Preschool, DNA Damage, DNA-Binding Proteins, Enzyme Inhibitors, Fibroblasts, Gene Expression Regulation, Glioblastoma, Humans, Leupeptins, Nuclear Proteins, Phosphoric Monoester Hydrolases, Protease Inhibitors, Proteins, Radiation Tolerance, Recombinant Fusion Proteins, Transcription, Genetic, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha, Tumor Suppressor Protein p53, NF-kappa B, Protein Serine-Threonine Kinases, Cell Cycle Proteins, I-kappa B Proteins, Tumor Suppressor Proteins, DNA-Activated Protein Kinase, Topoisomerase I Inhibitors, Ataxia Telangiectasia Mutated Proteins
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