Journal
ANTIOXIDANTS
Volume 11, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/antiox11040653
Keywords
ataxia-telangiectasia; ataxia-telangiectasia mutated protein kinase; metabolic stress; mitochondrial dysfunction; anaplerosis
Funding
- Australian A-T Foundation
- BrAshA-T, Children's Hospital Foundation, Australia [RM2018002270]
- Wesley Medical Research Fund [2020-28]
- Medical Research Future Fund [APP1200255]
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The ATM protein kinase has diverse functions in the cell, including protecting DNA, maintaining cellular homeostasis, and safeguarding against external and internal damage.
The ataxia-telangiectasia mutated (ATM) protein kinase is, as the name implies, mutated in the human genetic disorder ataxia-telangiectasia (A-T). This protein has its finger in many pies, being responsible for the phosphorylation of many thousands of proteins in different signaling pathways in its role in protecting the cell against a variety of different forms of stress that threaten to perturb cellular homeostasis. The classical role of ATM is the protection against DNA damage, but it is evident that it also plays a key role in maintaining cell homeostasis in the face of oxidative and other forms of non-DNA damaging stress. The presence of ATM is not only in the nucleus to cope with damage to DNA, but also in association with other organelles in the cytoplasm, which suggests a greater protective role. This review attempts to address this greater role of ATM in protecting the cell against both external and endogenous damage.
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