Gone with the Wnt/Notch: stem cells in laminopathies, progeria, and aging

J Cell Biol. 2008 Apr 7;181(1):9-13. doi: 10.1083/jcb.200802155. Epub 2008 Mar 31.

Abstract

Specific mutations in the human gene encoding lamin A or in the lamin A-processing enzyme, Zmpste24, cause premature aging. New data on mice and humans suggest that these mutations affect adult stem cells by interfering with the Notch and Wnt signaling pathways.

Publication types

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

MeSH terms

  • Aging / metabolism*
  • Animals
  • Lamins / genetics
  • Lamins / metabolism*
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism
  • Metalloendopeptidases / genetics
  • Metalloendopeptidases / metabolism
  • Mice
  • Progeria / metabolism*
  • Receptors, Notch / metabolism
  • Signal Transduction*
  • Stem Cells / metabolism*
  • Wnt Proteins / metabolism

Substances

  • Lamins
  • Membrane Proteins
  • Receptors, Notch
  • Wnt Proteins
  • Metalloendopeptidases