Mechanisms of Non-canonical Activation of Ataxia Telangiectasia Mutated.
Accepted version
Peer-reviewed
Repository URI
Repository DOI
Change log
Authors
Khoronenkova, SV
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.
Description
Keywords
Animals, Ataxia Telangiectasia, Ataxia Telangiectasia Mutated Proteins, DNA, DNA Repair, DNA, Single-Stranded, Enzyme Activation, Humans, RNA
Journal Title
Biochemistry (Mosc)
Conference Name
Journal ISSN
0006-2979
1608-3040
1608-3040
Volume Title
81
Publisher
Pleiades Publishing Ltd