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

J-H Lee1, T T Paull

  • 1Department of Molecular Genetics and Microbiology, Institute of Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.

Oncogene
|December 11, 2007
PubMed

Insights

The ataxia-telangiectasia-mutated (ATM) protein kinase is activated by DNA double-strand breaks. This review details ATM activation mechanisms, emphasizing the Mre11/Rad50/Nbs1 complex and regulatory factors.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA double-strand breaks (DSBs) are critical DNA lesions.
  • The ataxia-telangiectasia-mutated (ATM) protein kinase is a key sensor of DSBs.
  • ATM activation is essential for maintaining genomic stability.

Purpose of the Study:

  • To review recent advances in understanding ATM activation mechanisms.
  • To highlight the role of the Mre11/Rad50/Nbs1 (MRN) complex in ATM activation.
  • To explore regulatory factors of ATM activity in human cells.

Main Methods:

  • Literature review of recent research on ATM activation.
  • Comparative analysis of ATM activation across different biological systems.
  • Identification and discussion of potential ATM regulatory factors.

Main Results:

  • The Mre11/Rad50/Nbs1 (MRN) complex plays a crucial role in recruiting and activating ATM at DSB sites.
  • ATM activation is a conserved process across eukaryotes, with variations observed in specific systems.
  • Several cellular factors are proposed to modulate ATM activity, though their precise roles require further elucidation.

Conclusions:

  • The MRN complex is central to ATM activation following DNA damage.
  • Understanding ATM regulation is vital for comprehending DNA repair pathways and genomic integrity.
  • Further research is needed to fully characterize the network of factors controlling ATM activity in human cells.

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