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Article

A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation.

The Journal of clinical investigation - 1 Aug 2006

Yang Shao H, Meta Margarita, Qiao Xin, Frost David, Bauch Joy, Coffinier Catherine, Majumdar Sharmila, Bergo Martin O, Young Stephen G, Fong Loren G

Abstract excerpt

Hutchinson-Gilford progeria syndrome (HGPS) is caused by the production of a truncated prelamin A, called progerin, which is farnesylated at its carboxyl terminus. Progerin is targeted to the nuclear envelope and causes misshapen nuclei. Protein farnesyltransferase inhibitors (FTI) mislocalize progerin away from the nuclear envelope and reduce the frequency of misshapen nuclei. To determine whether an FTI would...

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Identifiers

PMID: 16862216
DOI: 10.1172/JCI28968
PMCID: PMC1513052

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation.PMID 16862216Read ↗

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Treatment with a farnesyltransferase inhibitor improves survival in mice with a Hutchinson-Gilford progeria syndrome mutation.Semantic proximity Read ↗

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