Effects of p21 deletion in mouse models of premature aging

Cell Cycle. 2009 Jul 1;8(13):2002-4. doi: 10.4161/cc.8.13.8997. Epub 2009 Jul 12.

Abstract

An approach to investigate the role of cellular senescence in organismal aging has been to abrogate signaling pathways known to induce cellular senescence and to assess the effects in mouse models of premature aging. Recently, we reported the effect of loss of function of p21, a gene implicated in p53-induced cellular senescence, in the background of the Ku80(-/-) premature aging mouse (Zhao et al., EMBO Rep 2009). Here, we provide an overview of the effects of p21 deletion in different models of premature aging.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Aging, Premature / genetics*
  • Animals
  • Antigens, Nuclear / genetics
  • Antigens, Nuclear / metabolism
  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins / metabolism
  • Cellular Senescence
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics*
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Gene Knockout Techniques
  • Ku Autoantigen
  • Mice
  • Mice, Knockout
  • Protein Serine-Threonine Kinases / metabolism
  • RNA / genetics
  • RNA / metabolism
  • Telomerase / genetics
  • Telomerase / metabolism
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Proteins / metabolism

Substances

  • Antigens, Nuclear
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • DNA-Binding Proteins
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • telomerase RNA
  • RNA
  • Ataxia Telangiectasia Mutated Proteins
  • Atm protein, mouse
  • Protein Serine-Threonine Kinases
  • Telomerase
  • Xrcc6 protein, mouse
  • Ku Autoantigen