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Article

Increasing the length of progerin's isoprenyl anchor does not worsen bone disease or survival in mice with Hutchinson-Gilford progeria syndrome.

Journal of lipid research - 1 Jan 2009

Davies Brandon S J, Yang Shao H, Farber Emily, Lee Roger, Buck Suzanne B, Andres Douglas A, Spielmann H Peter, Agnew Brian J, Tamanoi Fuyuhiko, Fong Loren G, Young Stephen G

Abstract excerpt

Hutchinson-Gilford progeria syndrome (HGPS) is caused by the synthesis of a truncated prelamin A, commonly called progerin, that contains a carboxyl-terminal farnesyl lipid anchor. The farnesyl lipid anchor helps to target progerin to membrane surfaces at the nuclear rim, where it disrupts the integrity of the nuclear lamina and causes misshapen nuclei. Several lines of evidence have suggested that progerin's...

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Identifiers

PMID: 18757838
DOI: 10.1194/jlr.M800424-JLR200
PMCID: PMC3837462

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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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Increasing the length of progerin's isoprenyl anchor does not worsen bone disease or survival in mice with Hutchinson-Gilford progeria syndrome.PMID 18757838Read ↗

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Blocking protein farnesylation improves nuclear shape abnormalities in keratinocytes of mice expressing the prelamin A variant in Hutchinson-Gilford progeria syndrome.Semantic proximity Read ↗

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