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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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| 主要な著者: | , , , , , , , |
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| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
Oxford University Press
2011
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| 主題: | |
| オンライン・アクセス: | 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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