Gone with the Wnt/Notch: stem cells in laminopathies, progeria, and aging.
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.
Meshorer
Eran
E
Department of Genetics, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel. meshorer@cc.huji.ac.il
Gruenbaum
Yosef
Y
D000375:Aging / Q000378:metabolism*; D000818:Animals; D034882:Lamins / Q000235:genetics / Q000378:metabolism*; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism; D008666:Metalloendopeptidases / Q000235:genetics / Q000378:metabolism; D051379:Mice; D011371:Progeria / Q000378:metabolism*; D051880:Receptors, Notch / Q000378:metabolism; D015398:Signal Transduction; D013234:Stem Cells / Q000378:metabolism*; D051153:Wnt Proteins / Q000378:metabolism
D034882:Lamins; D008565:Membrane Proteins; D051880:Receptors, Notch; D051153:Wnt Proteins; D008666:Metalloendopeptidases