Mechanisms of non-canonical activation of ataxia telangiectasia mutated
- Authors: Khoronenkova S.V.1,2
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Affiliations:
- Department of Biochemistry
- Department of Chemistry
- Issue: Vol 81, No 13 (2016)
- Pages: 1669-1675
- Section: Review
- URL: https://journals.rcsi.science/0006-2979/article/view/151182
- DOI: https://doi.org/10.1134/S0006297916130058
- ID: 151182
Cite item
Abstract
ATM is a master regulator of the cellular response to DNA damage. The classical mechanism of ATM activation involves its monomerization in response to DNA double-strand breaks, resulting in ATM-dependent phosphorylation of more than a thousand substrates required for cell cycle progression, DNA repair, and apoptosis. Here, new experimental evidence for non-canonical mechanisms of ATM activation in response to stimuli distinct from DNA double-strand breaks is discussed. It includes cytoskeletal changes, chromatin modifications, RNA–DNA hybrids, and DNA single-strand breaks. Noncanonical ATM activation may be important for the pathology of the multisystemic disease Ataxia Telangiectasia.
About the authors
S. V. Khoronenkova
Department of Biochemistry; Department of Chemistry
Author for correspondence.
Email: sk870@cam.ac.uk
United Kingdom, Cambridge, CB2 1GA; Moscow, 119991