Mechanisms of Non-canonical Activation of Ataxia Telangiectasia Mutated.
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Authors
Publication Date
2016-12Journal Title
Biochemistry (Mosc)
ISSN
0006-2979
Publisher
Pleiades Publishing Ltd
Volume
81
Issue
13
Pages
1669-1675
Type
Article
This Version
AM
Physical Medium
Print
Metadata
Show full item recordCitation
Khoronenkova, S. (2016). Mechanisms of Non-canonical Activation of Ataxia Telangiectasia Mutated.. Biochemistry (Mosc), 81 (13), 1669-1675. https://doi.org/10.1134/S0006297916130058
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.
Keywords
Animals, Ataxia Telangiectasia, Ataxia Telangiectasia Mutated Proteins, DNA, DNA Repair, DNA, Single-Stranded, Enzyme Activation, Humans, RNA
Identifiers
External DOI: https://doi.org/10.1134/S0006297916130058
This record's URL: https://www.repository.cam.ac.uk/handle/1810/333864
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