Abstract
Hutchinson-Gilford Progeria Syndrome (HGPS) is characterized by accelerated aging due toa de novo mutation in the LMNA gene (c.1824C>T, G608G). The mutated LaminA (progerin) is permanently farnesylated, localizing to and distorting the nuclear envelope. HGPS children suffer from growth failure, loss of body fat and hair, aged- skin and joint stiffness. Progressive vascular aging causes death from heart attack or stroke in the teen years. Previously, we have demonstrated that in vitro treatment with human telomerase (hTERT) RNA of fibroblasts from HGPS children increased telomere length and reversed many functional and transcriptional changes associated with senescence.
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