Abstract
AbstractAtaxia‐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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Dates
Type | When |
---|---|
Created | 20 years, 6 months ago (Feb. 25, 2005, 5:55 a.m.) |
Deposited | 1 year, 10 months ago (Oct. 27, 2023, 6:57 a.m.) |
Indexed | 5 months, 2 weeks ago (March 19, 2025, 12:40 p.m.) |
Issued | 27 years, 11 months ago (Oct. 1, 1997) |
Published | 27 years, 11 months ago (Oct. 1, 1997) |
Published Online | 20 years, 6 months ago (Feb. 5, 2005) |
Published Print | 27 years, 11 months ago (Oct. 1, 1997) |
@article{Rotman_1997, title={Hypothesis: Ataxia‐telangiectasia: Is ATM a sensor of oxidative damage and stress?}, volume={19}, ISSN={1521-1878}, url={http://dx.doi.org/10.1002/bies.950191011}, DOI={10.1002/bies.950191011}, number={10}, journal={BioEssays}, publisher={Wiley}, author={Rotman, Galit and Shiloh, Yosef}, year={1997}, month=oct, pages={911–917} }