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Article

Modulation of LMNA splicing as a strategy to treat prelamin A diseases.

The Journal of clinical investigation - 1 Apr 2016

Lee John M, Nobumori Chika, Tu Yiping, Choi Catherine, Yang Shao H, Jung Hea-Jin, Vickers Timothy A, Rigo Frank, Bennett C Frank, Young Stephen G, Fong Loren G

Abstract excerpt

The alternatively spliced products of LMNA, lamin C and prelamin A (the precursor to lamin A), are produced in similar amounts in most tissues and have largely redundant functions. This redundancy suggests that diseases, such as Hutchinson-Gilford progeria syndrome (HGPS), that are caused by prelamin A-specific mutations could be treated by shifting the output of LMNA more toward lamin C. Here, we investigated...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Oligodeoxyribonucleotides, Antisense

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Source

Open in PubMed Open full text

Identifiers

PMID: 26999604
DOI: 10.1172/JCI85908
PMCID: PMC4811112

Genes

LMNA
SRSF2

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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