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ATM signaling and 53BP1

Omar Zgheib1, Yentram Huyen, Richard A DiTullio

  • 1The Wistar Institute, USA.

Radiotherapy and Oncology : Journal of the European Society for Therapeutic Radiology and Oncology
|July 19, 2005
PubMed

Insights

The ATM protein kinase signals DNA double-strand breaks (DSBs) by sensing chromatin changes. This review covers ATM activation, substrates, and roles in cell cycle, apoptosis, and DNA repair.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • ATM (Ataxia-Telangiectasia mutated) is a crucial kinase in DNA double-strand break (DSB) signaling in eukaryotes.
  • ATM activation is increasingly understood to be mediated indirectly via DSB-induced chromatin alterations.
  • 53BP1 is a key DNA damage checkpoint protein that senses these chromatin structure changes.

Purpose of the Study:

  • To review the activation mechanisms of ATM in response to DNA DSBs.
  • To highlight key ATM substrates involved in cellular responses.
  • To discuss the role of ATM in cell cycle control, apoptosis, and DNA repair.

Main Methods:

  • Literature review of recent studies on ATM signaling pathways.
  • Analysis of conserved DNA damage checkpoint proteins, including 53BP1 and RAD9.
  • Examination of ATM substrates and their functions in DNA repair and cell fate decisions.

Main Results:

  • ATM activation is linked to indirect sensing of DSBs through chromatin modifications.
  • 53BP1 acts as a critical mediator in sensing these DSB-induced chromatin changes.
  • ATM regulates essential cellular processes including cell cycle arrest, programmed cell death, and DNA repair.

Conclusions:

  • ATM plays a central role in the DNA damage response pathway.
  • Understanding ATM activation and substrate function is vital for comprehending eukaryotic genome stability.
  • This review consolidates current knowledge on ATM's multifaceted roles in response to DNA damage.

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