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Article

Defective Ca2+ channel clustering in axon terminals disturbs excitability in motoneurons in spinal muscular atrophy.

The Journal of cell biology - 8 Oct 2007

Jablonka Sibylle, Beck Marcus, Lechner Barbara Dorothea, Mayer Christine, Sendtner Michael

Abstract excerpt

Proximal spinal muscular atrophy (SMA) is a motoneuron disease for which there is currently no effective treatment. In animal models of SMA, spinal motoneurons exhibit reduced axon elongation and growth cone size. These defects correlate with reduced beta-actin messenger RNA and protein levels in distal axons. We show that survival motoneuron gene (Smn)-deficient motoneurons exhibit severe defects in clustering...

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Source

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Identifiers

PMID: 17923533
DOI: 10.1083/jcb.200703187
PMCID: PMC2064743

Genes

SMN2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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