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Absence of progeria-like disease phenotypes in knock-in mice expressing a non-farnesylated version of progerin

Hutchinson–Gilford progeria syndrome (HGPS) is caused by a mutant prelamin A, progerin, that terminates with a farnesylcysteine. HGPS knock-in mice (Lmna(HG/+)) develop severe progeria-like disease phenotypes. These phenotypes can be ameliorated with a protein farnesyltransferase inhibitor (FTI), su...

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Main Authors: Yang, Shao H., Chang, Sandy Y., Ren, Shuxun, Wang, Yibin, Andres, Douglas A., Spielmann, H. Peter, Fong, Loren G., Young, Stephen G.
格式: Artigo
語言:Inglês
出版: Oxford University Press 2011
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在線閱讀:https://ncbi.nlm.nih.gov/pmc/articles/PMC3016906/
https://ncbi.nlm.nih.gov/pubmed/21088111
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/hmg/ddq490
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