Cited by 545DNA Repair MechanismsProtein Kinase Regulation and GTPase SignalingEffects of Radiation Exposure

Activation and regulation of ATM kinase activity in response to DNA double-strand breaks

Lee, J-H, Paull, T T·2007·Oncogene

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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Crossref · 10.1038/sj.onc.1210872

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Authors
Lee, J.-H., & Paull, T. T.
Affiliations
The University of Texas at Austin (US)
Corresponding author
Paull, T T
Venue
Oncogene
Published
2007-12-10
Volume
26
Issue
56
Pages
7741-7748
ISSN
  • 0950-9232 (ISSN-L)
  • 1476-5594
OpenAlex
W2087239831
Cited by
545
References
88
Citations by year
2026: 7 · 2025: 16 · 2024: 24 · 2023: 11 · 2022: 27 · 2021: 35 · 2020: 29 · 2019: 23 · 2018: 23 · 2017: 41 · 2016: 22 · 2015: 30 · 2014: 38 · 2013: 50 · 2012: 34
FWCI
2.46
Type
journal article
Language
en
Open access
closed
Locations
  • Oncogene (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
Keywords
ATM kinase, DNA double-strand breaks, kinase activation, MRN complex, MRE11, RAD50, NBS1, DNA damage response, DNA repair
MeSH terms
MRE11 Homologue Protein, Animals, Ataxia Telangiectasia, DNA Repair, DNA-Binding Proteins, Humans, Nuclear Proteins, Phosphorylation, Protein Serine-Threonine Kinases, Acid Anhydride Hydrolases, Cell Cycle Proteins, Tumor Suppressor Proteins, DNA Repair Enzymes, DNA Breaks, Double-Stranded, Ataxia Telangiectasia Mutated Proteins

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