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Article

A dynein mutation attenuates motor neuron degeneration in SOD1(G93A) mice.

Experimental neurology - 1 Mar 2006

Teuchert M, Fischer D, Schwalenstoecker B, Habisch H-J, Böckers T M, Ludolph A C

Abstract excerpt

Cu/Zn SOD1(G93A) transgenic mice develop phenotypical hallmarks of ALS and serve therefore as an established model to study the molecular mechanisms underlying this disease. Recent reports demonstrate that mutations in the motor protein dynein in Legs at odd angles (Loa) and Cramping (Cra1) mice lead to similar but milder phenotypes. Surprisingly, double transgenic mice (Loa/SOD1(G93A)) have been recently shown...

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Source

Identifiers

PMID: 16427626
DOI: 10.1016/j.expneurol.2005.12.005

Genes

SOD1

Variants

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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A dynein mutation attenuates motor neuron degeneration in SOD1(G93A) mice.PMID 16427626Read ↗

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The legs at odd angles (Loa) mutation in cytoplasmic dynein ameliorates mitochondrial function in SOD1G93A mouse model for motor neuron disease.Semantic proximity Read ↗

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Mutant dynein (Loa) triggers proprioceptive axon loss that extends survival only in the SOD1 ALS model with highest motor neuron death.Semantic proximity Read ↗

Severe dynein dysfunction in cholinergic neurons exacerbates ALS-like phenotypes in a new mouse model.Semantic proximity Read ↗

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Defective axonal transport in motor neuron disease.Semantic proximity Read ↗

UNRAVELING THE MECHANISMS INVOLVED IN MOTOR NEURON DEGENERATION IN ALSSemantic proximity Read ↗

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