Mouse models of laminopathies
Author:
Affiliation:
1. Department of Cell Biology and Molecular Genetics; University of Maryland; College Park; MD 20742; USA
Publisher
Wiley
Subject
Cell Biology,Ageing
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/acel.12021/fullpdf
Reference55 articles.
1. Mouse model carrying H222P-Lmna mutation develops muscular dystrophy and dilated cardiomyopathy similar to human striated muscle laminopathies;Arimura;Hum. Mol. Genet.,2005
2. Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect;Bergo;Proc. Natl Acad. Sci. USA,2002
3. Differential temporal and spatial progerin expression during closure of the ductus arteriosus in neonates;Bokenkamp;PLoS ONE,2011
4. A lamin A protein isoform overexpressed in Hutchinson-Gilford progeria syndrome interferes with mitosis in progeria and normal cells;Cao;Proc. Natl Acad. Sci. USA,2007
5. Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts;Cao;J. Clin. Invest.,2011a
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