Cell-cycle signaling: Atm displays its many talents

Curr Biol. 1997 Dec 1;7(12):R789-92. doi: 10.1016/s0960-9822(06)00406-4.

Abstract

The discovery of multiple signaling cascades downstream of Atm may lead to a clearer understanding of the diverse defects seen in ataxia-telangiectasia. These pathways - which include evolutionarily conserved Chk1 and Atr, and non-conserved p21, p53 and AbI - guard genomic integrity after DNA damage.

Publication types

  • Review

MeSH terms

  • Animals
  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins
  • Cell Cycle*
  • Checkpoint Kinase 1
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / genetics
  • Cyclins / metabolism
  • DNA-Binding Proteins
  • Gamma Rays
  • Humans
  • Phosphorylation
  • Protein Kinases / metabolism
  • Protein-Serine-Threonine Kinases*
  • Proteins / genetics
  • Proteins / metabolism*
  • Proto-Oncogene Proteins c-abl / metabolism
  • Schizosaccharomyces
  • Schizosaccharomyces pombe Proteins
  • Signal Transduction*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Proteins

Substances

  • CDKN1A protein, human
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • DNA-Binding Proteins
  • Proteins
  • Schizosaccharomyces pombe Proteins
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • Protein Kinases
  • Proto-Oncogene Proteins c-abl
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • CHEK1 protein, human
  • Checkpoint Kinase 1
  • Chk1 protein, S pombe
  • Protein-Serine-Threonine Kinases