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

Cultured glial cells are resistant to the effects of motor neurone disease-associated SOD1 mutations.

Neuroscience letters - 20 Apr 2001

Williams R E, Cookson M R, Fray A E, Manning P M, Menzies F M, Figlewicz D A, Shaw P J

Abstract excerpt

Free radical damage has been implicated in the pathophysiology of motor neurone disease (MND); mutations have been identified in the gene encoding Cu/Zn superoxide dismutase (SOD1). There is evidence that glial cell dysfunction may contribute to motor neurone injury, but the exact role of glial cells in MND has yet to be established. The aim of this study was to determine whether expression of mutant SOD1 affects...

Read the complete abstract on PubMed

Topics

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

Share to Astrocytes
Share to Central Nervous System

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Free Radicals

Share to Glioma

Share to Motor Neuron Disease

Share to Motor Neurons

Share to Superoxide Dismutase

Share to Superoxide Dismutase-1

Source

Identifiers

PMID: 11290408
DOI: 10.1016/s0304-3940(01)01686-x

Genes

SOD1

Variants

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.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cultured glial cells are resistant to the effects of motor neurone disease-associated SOD1 mutations.PMID 11290408Read ↗

Overexpression of metallothionein protects cultured motor neurons against oxidative stress, but not mutant Cu/Zn-superoxide dismutase toxicity.Semantic proximity Read ↗

Cu/Zn superoxide dismutase (SOD1) mutations associated with familial amyotrophic lateral sclerosis (ALS) affect cellular free radical release in the presence of oxidative stress.Semantic proximity Read ↗

Chronic infusion of SOD1G93A astrocyte-secreted factors induces spinal motoneuron degeneration and neuromuscular dysfunction in healthy rats.Semantic proximity Read ↗

Cuprizone-Induced Neurotoxicity in Human Neural Cell Lines Is Mediated by a Reversible Mitochondrial Dysfunction: Relevance for Demyelination ModelsSemantic proximity Read ↗

Urate mitigates oxidative stress and motor neuron toxicity of astrocytes derived from ALS-linked SOD1G93A mutant mice.Semantic proximity Read ↗

Non-cell-autonomous effect of human SOD1 G37R astrocytes on motor neurons derived from human embryonic stem cells.Semantic proximity Read ↗

The protective effect of growth hormone on Cu/Zn superoxide dismutase-mutant motor neurons.Semantic proximity Read ↗

Astrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neurons.Semantic proximity Read ↗

Loss of the Parkinson’s disease-associated protein DJ-1 impacts dopamine metabolism in astrocytesSemantic proximity Read ↗

Early nuclear phenotypes and reactive transformation in human iPSC-derived astrocytes from ALS patients with <i>SOD1</i> mutationsSemantic proximity Read ↗

Mitochondrial dysfunction in a cell culture model of familial amyotrophic lateral sclerosisSemantic proximity Read ↗

Expression of SOD1 G93A or wild-type SOD1 in primary cultures of astrocytes down-regulates the glutamate transporter GLT-1: lack of involvement of oxidative stress.Semantic proximity Read ↗

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