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Article

Mice that express farnesylated versions of prelamin A in neurons develop achalasia.

Human molecular genetics - 15 May 2015

Yang Shao H, Procaccia Shiri, Jung Hea-Jin, Nobumori Chika, Tatar Angelica, Tu Yiping, Bayguinov Yulia R, Hwang Sung Jin, Tran Deanna, Ward Sean M, Fong Loren G, Young Stephen G

Abstract excerpt

Neurons in the brain produce lamin C but almost no lamin A, a consequence of the removal of prelamin A transcripts by miR-9, a brain-specific microRNA. We have proposed that miR-9-mediated regulation of prelamin A in the brain could explain the absence of primary neurological disease in Hutchinson-Gilford progeria syndrome, a genetic disease caused by the synthesis of an internally truncated form of...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 25652409
DOI: 10.1093/hmg/ddv043
PMCID: PMC4406294

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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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