3.4.24.84	malfunction	defective prelamin A processing induces accelerated features of age-related bone loss including lower osteoblast and osteocyte numbers and higher levels of marrow adipogenesis	712629	
3.4.24.84	malfunction	enzyme mutations cause the premature aging disease Hutchinson-Gilford progeria syndrome, and the related progeroid disorders mandibuloacral dysplasia type B and restrictive dermopathy	753395	
3.4.24.84	metabolism	the enzyme is crucial for the final step in the biogenesis of the nuclear scaffold protein lamin A	753395	
3.4.24.84	physiological function	Zmpste24-null progeroid mice exhibit nuclear lamina defects and accumulate unprocessed prelamin A. Defective prelamin A processing induces accelerated features of age-related bone loss including lower osteoblast and osteocyte numbers and higher levels of marrow adipogenesis. There is a significant loss in trabecular and cortical bone between the Zmpste24 -/- mice compared with the wild-type controls. At 3 months of age, Zmpste24 -/- mice show a significant decrease in bone volume/tissue volume, trabecular thickness, and trabecular number compared with their wild-type littermates	712629