Journal
NATURE REVIEWS MOLECULAR CELL BIOLOGY
Volume 14, Issue 4, Pages 197-210Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrm3546
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Funding
- David and Inez Myers Foundation
- Ataxia-Telangiectasia (A-T) Medical Research Foundation
- Israel Science Foundation
- A-T Ease Foundation
- Israel Cancer Research Fund
- German-Israeli Foundation for Scientific Research and Development
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- Israeli Centers for Research Excellence (I-CORE) Program of the Planning and Budgeting Committee
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The protein kinase ataxia-telangiectasia mutated (ATM) is best known for its role as an apical activator of the DNA damage response in the face of DNA double-strand breaks (DSBs). Following induction of DSBs, ATM mobilizes one of the most extensive signalling networks that responds to specific stimuli and modifies directly or indirectly a broad range of targets. Although most ATM research has focused on this function, evidence suggests that ATM-mediated phosphorylation has a role in the response to other types of genotoxic stress. Moreover, it has become apparent that ATM is active in other cell signalling pathways involved in maintaining cellular homeostasis.
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