Progeria syndromes, which are caused in part by methylation of prelamin A, result in a premature ageing phenotype. This study showed that a mouse model of progeria that had reduced genetic expression of isoprenylcysteine carboxylmethyltransferase (ICMT) had increased body weight, fewer bone fractures and a lower death rate. Moreover, the premature senescence of fibroblasts from these mice was abolished. Inhibition of ICMT by a short hairpin RNA delayed senescence in human progeria fibroblasts, which suggests that inhibiting ICMT might be beneficial for treating progeroid disorders.
References
Ibrahim, M. X. et al. Targeting isoprenylcysteine methylation ameliorates disease in a mouse model of progeria. Science 16 May 2013 (10.1126/science.1238880)
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Charlotte, H. A new target for treating progeria. Nat Rev Drug Discov 12, 506 (2013). https://doi.org/10.1038/nrd4059
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DOI: https://doi.org/10.1038/nrd4059