Assessing the efficacy of protein farnesyltransferase inhibitors in mouse models of progeria
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Endocrinology,Biochemistry
Reference21 articles.
1. Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome;Eriksson;Nature.,2003
2. Lamin A truncation in Hutchinson–Gilford progeria;de Sandre-Giovannoli;Science.,2003
3. Prelamin A, Zmpste24, misshapen cell nuclei, and progeria—new evidence suggesting that protein farnesylation could be important for disease pathogenesis;Young;J. Lipid Res.,2005
4. Alterations in mitosis and cell cycle progression caused by a mutant lamin A known to accelerate human aging;Dechat;Proc. Natl. Acad. Sci. USA.,2007
5. Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome;Goldman;Proc. Natl. Acad. Sci. USA.,2004
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