Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Neurofilament accumulation at the motor endplate and lack of axonal sprouting in a spinal muscular atrophy mouse model

1 Jun 2002

Abstract excerpt

Mutations of survival of the motor neuron gene (SMN1) are responsible for spinal muscular atrophy (SMA), a common genetic cause of death in childhood. The cellular mechanism by which mutations of SMN1 are responsible for the selective neuromuscular defect and motor neuron cell degeneration observed in SMA has not been described. We have previously generated mice carrying a homozygous deletion of Smn exon 7...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Neurogenetic and Muscular Disorders Research
Share to RNA modifications and cancer
Share to RNA Research and Splicing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 12023986
DOI: 10.1093/hmg/11.12.1439

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Neurofilament accumulation at the motor endplate and lack of axonal sprouting in a spinal muscular atrophy mouse modelPMID 12023986Read ↗

Selective vulnerability of motor neurons and dissociation of pre- and post-synaptic pathology at the neuromuscular junction in mouse models of spinal muscular atrophy.Semantic proximity Read ↗

Reduced SMN protein impairs maturation of the neuromuscular junctions in mouse models of spinal muscular atrophySemantic proximity Read ↗

The spinal muscular atrophy mouse model, SMAΔ7, displays altered axonal transport without global neurofilament alterations.Semantic proximity Read ↗

SMN deficiency induces an early non-atrophic myopathy with alterations in the contractile and excitatory coupling machinery of skeletal myofibers in the SMNΔ7 mouse model of spinal muscular atrophySemantic proximity Read ↗

Ciliary neurotrophic factor-induced sprouting preserves motor function in a mouse model of mild spinal muscular atrophySemantic proximity Read ↗

At the "junction" of spinal muscular atrophy pathogenesis: the role of neuromuscular junction dysfunction in SMA disease progression.Semantic proximity Read ↗

Smn deficiency causes neuritogenesis and neurogenesis defects in the retinal neurons of a mouse model of spinal muscular atrophySemantic proximity Read ↗

Distinct and overlapping alterations in motor and sensory neurons in a mouse model of spinal muscular atrophySemantic proximity Read ↗

Survival motor neuron protein in motor neurons determines synaptic integrity in spinal muscular atrophy.Semantic proximity Read ↗

Axonal-SMN (a-SMN), a protein isoform of the survival motor neuron gene, is specifically involved in axonogenesisSemantic proximity Read ↗

Axon outgrowth and neuronal differentiation defects after a-SMN and FL-SMN silencing in primary hippocampal cultures.Semantic proximity Read ↗

Pre-symptomatic development of lower motor neuron connectivity in a mouse model of severe spinal muscular atrophySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.