期刊
BIOCHEMISTRY-MOSCOW
卷 81, 期 13, 页码 1669-1675出版社
MAIK NAUKA/INTERPERIODICA/SPRINGER
DOI: 10.1134/S0006297916130058
关键词
ATM; Ataxia Telangiectasia mutated; DNA damage; DNA single-strand breaks; DNA double-strand breaks; R-loops
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.
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