Article
Gliotoxin reverses age-dependent nuclear morphology phenotypes, ameliorates motility, but fails to affect lifespan of adult Caenorhabditis elegans.
Cell motility and the cytoskeleton - 1 Oct 2009
Bar Daniel Z, Neufeld Ester, Feinstein Naomi, Gruenbaum Yosef
Abstract excerpt
Specific mutations in human LMNA or loss of ZMPSTE26 activity cause abnormal processing of lamin A and early aging diseases, including Hutchinson Gilford progeria syndrome (HGPS). HGPS fibroblasts in culture undergo age-dependent progressive changes in nuclear architecture. Treating these cells w...
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