The premature aging disorders Hutchinson-Gilford progeria syndrome (HGPS) and Mandibuloacral Dysplasia Type B (MADB) share a defective lamin A maturation and exhibit farnesylated lamin A isoforms. A central aim is to analyze the distribution of endogenous lamin A and its isoforms progerin and prelamin A during the cell cycle in relation to interacting proteins and provide a better understanding of the similarities and dissimilarities of progerin, prelamin A and mature lamin A. In conclusion, the causes for some morphological and functional changes in HGPS and MADB are identified.
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The premature aging disorders Hutchinson-Gilford progeria syndrome (HGPS) and Mandibuloacral Dysplasia Type B (MADB) share a defective lamin A maturation and exhibit farnesylated lamin A isoforms. A central aim is to analyze the distribution of endogenous lamin A and its isoforms progerin and prelamin A during the cell cycle in relation to interacting proteins and provide a better understanding of the similarities and dissimilarities of progerin, prelamin A and mature lamin A. In conclusion, the...
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