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Article

A mutation in dynein rescues axonal transport defects and extends the life span of ALS mice.

The Journal of cell biology - 23 May 2005

Kieran Dairin, Hafezparast Majid, Bohnert Stephanie, Dick James R T, Martin Joanne, Schiavo Giampietro, Fisher Elizabeth M C, Greensmith Linda

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative condition characterized by motoneuron degeneration and muscle paralysis. Although the precise pathogenesis of ALS remains unclear, mutations in Cu/Zn superoxide dismutase (SOD1) account for approximately 20-25% of familial ALS cases, and transgenic mice overexpressing human mutant SOD1 develop an ALS-like phenotype. Evidence suggests that defects in...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 15911875
DOI: 10.1083/jcb.200501085
PMCID: PMC2171702

Genes

SOD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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