ATM and ATR: networking cellular responses to DNA damage

Curr Opin Genet Dev. 2001 Feb;11(1):71-7. doi: 10.1016/s0959-437x(00)00159-3.


Maintenance of genome stability depends on the appropriate response to DNA damage. This response is based on complex networks of signaling pathways that activate numerous processes and lead ultimately to damage repair and cellular survival - or apoptosis. The protein kinases ATM and ATR are master controllers of some of these networks, acting either in concert or separately to orchestrate the responses to specific types of DNA damage or stalled replication. Understanding their mode of action is essential to our understanding of how cells cope with genotoxic stress.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Apoptosis
  • Ataxia Telangiectasia Mutated Proteins
  • BRCA1 Protein / genetics
  • BRCA1 Protein / metabolism
  • Cell Cycle Proteins*
  • DNA Damage*
  • DNA Repair*
  • DNA-Binding Proteins
  • Endodeoxyribonucleases*
  • Exodeoxyribonucleases*
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism
  • Humans
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism
  • Protein Serine-Threonine Kinases / physiology*
  • Recombination, Genetic
  • Saccharomyces cerevisiae Proteins*
  • Tumor Suppressor Proteins


  • BRCA1 Protein
  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Fungal Proteins
  • Saccharomyces cerevisiae Proteins
  • Tumor Suppressor Proteins
  • ATM protein, human
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein Serine-Threonine Kinases
  • Endodeoxyribonucleases
  • Exodeoxyribonucleases
  • MRE11 protein, S cerevisiae