Download Mouse models of the nuclear envelopathies and related by Colin Stewart PDF
By Colin Stewart
Quantity 109 of Current subject matters in Developmental Biology covers mouse versions of the nuclear envelopathies and similar illnesses, with contributions from a world board of authors. The chapters offer a finished set of reports protecting such issues as mouse types neurodegenerative ailments together with Parkinson's and dystonia, muscle getting older and sarcopenia, cardiac failure and service, getting old and customers lifespan extension, lipodystrophy and the importance in fats legislation, additionally deciding on developmental mutations in mammals and nuclear envelope and LINC advanced in disease.
- Covers the realm of mouse types of developmental genetic disease
- International board of authors
- Provides a finished set of studies overlaying such subject matters as mouse types neurodegenerative illnesses together with Parkinson's, muscle getting older, lipodystrophy, and more
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Brown, W. , Gordon, L. , Glynn, M. , et al. (2003). Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome. Nature, 423, 293–298. Ershler, W. , & Longo, D. L. (2008). Hutchinson-Gilford progeria syndrome. New England Journal of Medicine, 358, 2409–2410, author reply 2410–2401. , Wolff, M. , et al. (1999). Missense mutations in the rod domain of the lamin A/C gene as causes of dilated cardiomyopathy and conduction-system disease. New England Journal of Medicine, 341, 1715–1724.
2008). , 2002). , 2005). , 2006). This result indicated that the accumulation of farnesylated prelamin A protein is the prime cause of the pathologies. Furthermore, it is probably the retention of the farnesyl group by prelamin A that underlies most of the pathologies, as mice engineered to solely express lamin A, so bypassing prelamin A processing, are seemingly normal and have a longer lifespan. , 2010). In HGPS, the progerin variant remains farnesylated, as the 50-amino acid deletion removes the second ZMSTE24 endoproteolytic site used to cleave the farnesylated and methylated cysteine.
Stewart Gordon, L. , Harten, I. , Patti, M. , & Lichtenstein, A. H. (2005). Reduced adiponectin and HDL cholesterol without elevated C-reactive protein: Clues to the biology of premature atherosclerosis in Hutchinson-Gilford Progeria Syndrome. Journal of Pediatrics, 146, 336–341. Gordon, L. , Kleinman, M. , Miller, D. , Neuberg, D. , et al. (2012). Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson-Gilford progeria syndrome. Proceedings of the National Academy of Sciences of the United States of America, 109, 16666–16671.