Targeting Isoprenylcysteine Methylation Ameliorates Disease in a Mouse Model of Progeria
Copyright policy )Targeting Isoprenylcysteine Methylation Ameliorates Disease in a Mouse Model of Progeria
Methylation and Methuselah? Hutchinson-Gilford progeria syndrome (HGPS) and other prelamin A–associated progeroid disorders arise when farnesylated and methylated forms of prelamin A accumulate at the nuclear envelope. Ibrahim et al. (p. 1330 , published online 16 May; see the Perspective by Johnson ) show that reducing the activity of the isoprenylcysteine carboxyl methyltransferase (ICMT) mislocalizes prelamin A, triggers prelamin A–dependent AKT-mTOR signaling, and eliminates disease phenotypes in 30-week-old progeria model mice. Reduced ICMT expression increased the proliferation and delayed the premature senescence of progeria model mouse fibroblasts and cells from children with HGPS.
- University of Gothenburg Sweden
- University of California, Los Angeles United States
Cell Nucleus, Hand Strength, TOR Serine-Threonine Kinases, Membrane Proteins, Metalloendopeptidases, Nuclear Proteins, Fibroblasts, Lamin Type A, Weight Gain, Methylation, Mice, Mutant Strains, Disease Models, Animal, Gene Knockout Techniques, Mice, Progeria, Animals, Humans, Protein Methyltransferases, Protein Precursors, Cellular Senescence
Cell Nucleus, Hand Strength, TOR Serine-Threonine Kinases, Membrane Proteins, Metalloendopeptidases, Nuclear Proteins, Fibroblasts, Lamin Type A, Weight Gain, Methylation, Mice, Mutant Strains, Disease Models, Animal, Gene Knockout Techniques, Mice, Progeria, Animals, Humans, Protein Methyltransferases, Protein Precursors, Cellular Senescence
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