Activation and regulation of ATM kinase activity in response to DNA double-strand breaks
The ataxia–telangiectasia-mutated (ATM) protein kinase is rapidly and specifically activated
in response to DNA double-strand breaks in eukaryotic cells. In this review, we summarize
recent insights into the mechanism of ATM activation, focusing on the role of the
Mre11/Rad50/Nbs1 (MRN) complex in this process. We also compare observations of the
ATM activation process in different biological systems and highlight potential candidates for
cellular factors that may participate in regulating ATM activity in human cells.
in response to DNA double-strand breaks in eukaryotic cells. In this review, we summarize
recent insights into the mechanism of ATM activation, focusing on the role of the
Mre11/Rad50/Nbs1 (MRN) complex in this process. We also compare observations of the
ATM activation process in different biological systems and highlight potential candidates for
cellular factors that may participate in regulating ATM activity in human cells.
Abstract
The ataxia–telangiectasia-mutated (ATM) protein kinase is rapidly and specifically activated in response to DNA double-strand breaks in eukaryotic cells. In this review, we summarize recent insights into the mechanism of ATM activation, focusing on the role of the Mre11/Rad50/Nbs1 (MRN) complex in this process. We also compare observations of the ATM activation process in different biological systems and highlight potential candidates for cellular factors that may participate in regulating ATM activity in human cells.
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