Hypothesis: Ataxia‐telangiectasia: Is ATM a sensor of oxidative damage and stress?

Rotman, Galit; Shiloh, Yosef

doi:10.1002/bies.950191011

Cited by 160DNA Repair MechanismsEffects of Radiation ExposureRedox biology and oxidative stress

Hypothesis: Ataxia‐telangiectasia: Is ATM a sensor of oxidative damage and stress?

Rotman, Galit, Shiloh, Yosef·1997·BioEssays

DOI 10.1002/bies.950191011

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Abstract

Ataxia‐telangiectasia (A‐T) is a pleiotropic recessive disorder characterized cerebellar ataxia, immunodeficiency, specific developmental defects, profound predisposition to cancer and acute radiosensitivity. Functional inactivation of single gene product, ATM, accounts for this compound phenotype. We suggest that ATM acts as a sensor of reactive oxygen species and/or oxidative damage cellular macromolecules, including DNA. In turn, ATM induces signalling through multiple pathways, thereby coordinating acute phase stress responses with cell cycle checkpoint control and repair of oxidative damage. Absence of ATM is proposed to limit the repair of insidious oxidative damage that can occur under normal physiological conditions, ultimately leading to apoptosis of particularly sensitive cells, such as neurons and thymocytes.

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ATM−/− ataxia-telangiectasia fibroblasts are more susceptible to oxidative stress than normal cells, leading to the proposal that ATM is a major sensor of oxidative DNA damage or ROS.
“As A-T fibroblast cells (ATM−/−) are more susceptible to oxidative stress than normal cells, ATM was proposed as a major sensor of oxidative DNA damage or ROS [73].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [73]

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Authors: Rotman, G., & Shiloh, Y.
Affiliations: Tel Aviv University (IL)
Corresponding author: Rotman, Galit
ORCID: Shiloh, Yosef
Venue: BioEssays
Publisher: Wiley
Published: 1997-10
Volume: 19
Issue: 10
Pages: 911-917
ISSN: 0265-9247 (ISSN-L)
1521-1878
DOI: 10.1002/bies.950191011
OpenAlex: W2140913553
Cited by: 160
References: 84
Citations by year: 2026: 1 · 2025: 3 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 6 · 2020: 3 · 2019: 2 · 2018: 3 · 2016: 2 · 2015: 5 · 2014: 6 · 2013: 4 · 2012: 3
FWCI: 0.97
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2684 d)
Locations: BioEssays (publishedVersion)
PubMed (publishedVersion)
Funders: Israel Science Foundation
National Institute of Neurological Disorders and Stroke (R01NS031763, NS 31763)
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
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: ataxia telangiectasia, ATM kinase, oxidative stress, reactive oxygen species, DNA repair, cell cycle checkpoints, apoptosis, radiosensitivity, cancer susceptibility, immunodeficiency, cerebellar ataxia, neurons, thymocytes
MeSH terms: Ataxia Telangiectasia, DNA Damage, DNA-Binding Proteins, Humans, Models, Biological, Neurons, Proteins, T-Lymphocytes, Signal Transduction, Leucine Zippers, Apoptosis, Protein Serine-Threonine Kinases, Oxidative Stress, Cell Cycle Proteins, Tumor Suppressor Proteins, Ataxia Telangiectasia Mutated Proteins

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Hypothesis: Ataxia‐telangiectasia: Is ATM a sensor of oxidative damage and stress?

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