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Article

Lamin A-linked progerias: is farnesylation the be all and end all?

Biochemical Society transactions - 1 Feb 2010

Smallwood Dawn T, Shackleton Sue

Abstract excerpt

HGPS (Hutchinson-Gilford progeria syndrome) is a severe childhood disorder that appears to mimic an accelerated aging process. The disease is most commonly caused by gene mutations that disrupt the normal post-translational processing of lamin A, a structural component of the nuclear envelope. Im...

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PMID: 20074075
DOI: 10.1042/BST0380281

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-20074075-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

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Lamin A-linked progerias: is farnesylation the be all and end all?PMID 20074075Read ↗

[A-type lamins and progeroïd syndromes : persistent farnesylation with dramatic effects].Semantic proximity Read ↗

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Incomplete processing of mutant lamin A in Hutchinson-Gilford progeria leads to nuclear abnormalities, which are reversed by farnesyltransferase inhibition.Semantic proximity Read ↗

Progerin, an Aberrant Spliced form of Lamin A, is a Potential Therapeutic Target for HGPSSemantic proximity Read ↗

Towards delineating the chain of events that cause premature senescence in the accelerated aging syndrome Hutchinson-Gilford progeria (HGPS).Semantic proximity Read ↗

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome.Semantic proximity Read ↗

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