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The ATM protein kinase: regulating the cellular response to genotoxic stress, and more

Journal

NATURE REVIEWS MOLECULAR CELL BIOLOGY
Volume 14, Issue 4, Pages 197-210

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/nrm3546

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Funding

  1. David and Inez Myers Foundation
  2. Ataxia-Telangiectasia (A-T) Medical Research Foundation
  3. Israel Science Foundation
  4. A-T Ease Foundation
  5. Israel Cancer Research Fund
  6. German-Israeli Foundation for Scientific Research and Development
  7. Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
  8. 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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