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Article

Activating the synthesis of progerin, the mutant prelamin A in Hutchinson-Gilford progeria syndrome, with antisense oligonucleotides.

Human molecular genetics - 1 Jul 2009

Fong Loren G, Vickers Timothy A, Farber Emily A, Choi Christine, Yun Ui Jeong, Hu Yan, Yang Shao H, Coffinier Catherine, Lee Roger, Yin Liya, Davies Brandon S J, Andres Douglas A, Spielmann H Peter, Bennett C Frank, Young Stephen G

Abstract excerpt

Hutchinson-Gilford progeria syndrome (HGPS) is caused by point mutations that increase utilization of an alternate splice donor site in exon 11 of LMNA (the gene encoding lamin C and prelamin A). The alternate splicing reduces transcripts for wild-type prelamin A and increases transcripts for a truncated prelamin A (progerin). Here, we show that antisense oligonucleotides (ASOs) against exon 11 sequences...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Open in PubMed Open full text

Identifiers

PMID: 19376814
DOI: 10.1093/hmg/ddp184
PMCID: PMC2694694

Genes

LMNA

Provenance

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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