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Article

Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome.

Proceedings of the National Academy of Sciences of the United States of America - 4 Oct 2005

Mallampalli Monica P, Huyer Gregory, Bendale Pravin, Gelb Michael H, Michaelis Susan

Abstract excerpt

Hutchinson-Gilford progeria syndrome (HGPS) is a devastating premature aging disease resulting from a mutation in the LMNA gene, which encodes nuclear lamins A and C. Lamin A is synthesized as a precursor (prelamin A) with a C-terminal CaaX motif that undergoes farnesylation, endoproteolytic cleavage, and carboxylmethylation. Prelamin A is subsequently internally cleaved by the zinc metalloprotease Ste24...

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Source

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Identifiers

PMID: 16186497
DOI: 10.1073/pnas.0503712102
PMCID: PMC1242289

Genes

LMNA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome.PMID 16186497Read ↗

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