Farnesylated prelamin A is a processing intermediate produced in the lamin A matura-tion pathway. Accumulation of a truncated far-nesylated prelamin A form, called progerin, is a hallmark of the severe premature ageing syn-drome, Hutchinson-Gilford progeria. Progerin elicits toxic effects in cells, leading to chro-matin damage and cellular senescence and ultimately causes skin and endothelial defects, bone resorption, lipodystrophy and accelerated ageing. Knowledge of the mechanism underly-ing prelamin A turnover is critical for the development of clinically effective protein inhibitors that can avoid accumulation to toxi

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