Bmi1, stem cells, and senescence regulation

J Clin Invest. 2004 Jan;113(2):175-9. doi: 10.1172/JCI20800.

Abstract

Stem cells generate the differentiated cell types within many organs throughout the lifespan of an organism and are thus ultimately responsible for the longevity of multicellular organisms. Therefore, senescence of stem cells must be prevented. Bmi1 is required for the maintenance of adult stem cells in some tissues partly because it represses genes that induce cellular senescence and cell death.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Line
  • Cellular Senescence*
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • Gene Expression Regulation
  • Humans
  • Mice
  • Models, Biological
  • Mutation
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism
  • Nuclear Proteins / physiology*
  • Polycomb Repressive Complex 1
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins / physiology*
  • Repressor Proteins*
  • Stem Cells / metabolism*
  • Tumor Suppressor Protein p14ARF / metabolism

Substances

  • BMI1 protein, human
  • Bmi1 protein, mouse
  • Cdkn2a protein, mouse
  • Cyclin-Dependent Kinase Inhibitor p16
  • Nuclear Proteins
  • Proto-Oncogene Proteins
  • Repressor Proteins
  • Tumor Suppressor Protein p14ARF
  • Polycomb Repressive Complex 1