Cellular responses to DNA damage: cell-cycle checkpoints, apoptosis and the roles of p53 and ATM

Trends Biochem Sci. 1995 Oct;20(10):426-30. doi: 10.1016/s0968-0004(00)89093-3.

Abstract

'Checkpoint' controls arrest the cell cycle after DNA damage, allowing repair to take place before mutations can be perpetuated. In multicellular organisms, DNA damage can also induce apoptotic cell death, protecting the organism at the expense of the individual cell. How does a cell 'choose' between cycle arrest and death? Analysis of two human tumour suppressor proteins, p53 and the ATM (ataxia-telangiectasia mutated) gene product, may provide some answers.

Publication types

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

MeSH terms

  • Apoptosis / genetics*
  • Ataxia Telangiectasia / genetics
  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins
  • Cell Cycle*
  • DNA Damage*
  • DNA-Binding Proteins
  • G2 Phase
  • Genes, p53*
  • Humans
  • Models, Genetic
  • Phosphatidylinositol 3-Kinases
  • Phosphotransferases (Alcohol Group Acceptor) / genetics
  • Protein-Serine-Threonine Kinases*
  • Proteins / genetics*
  • Tumor Suppressor Proteins

Substances

  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Proteins
  • Tumor Suppressor Proteins
  • Phosphatidylinositol 3-Kinases
  • Phosphotransferases (Alcohol Group Acceptor)
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein-Serine-Threonine Kinases