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Article

Restoration of SMN to Emx-1 expressing cortical neurons is not sufficient to provide benefit to a severe mouse model of Spinal Muscular Atrophy.

Transgenic research - 1 Oct 2013

Taylor Alexander S, Glascock Jacqueline J, Rose Ferrill F, Lutz Cathleen, Lorson Christian L

Abstract excerpt

Spinal Muscular Atrophy (SMA), an autosomal recessive neuromuscular disorder, is a leading genetic cause of infant mortality. SMA is caused by the homozygous loss of Survival Motor Neuron-1 (SMN1). However, low, but essential, levels of SMN protein are produced by a nearly identical copy gene called SMN2. Detailed analysis of neuromuscular junctions in SMA mice has revealed a selective vulnerability in a subset...

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Source

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Identifiers

PMID: 23512182
DOI: 10.1007/s11248-013-9702-y
PMCID: PMC3745810

Genes

SMN1
SMN2

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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Restoration of SMN to Emx-1 expressing cortical neurons is not sufficient to provide benefit to a severe mouse model of Spinal Muscular Atrophy.PMID 23512182Read ↗

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