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

Phenotypic effects of familial amyotrophic lateral sclerosis mutant Sod alleles in transgenic Drosophila.

Proceedings of the National Academy of Sciences of the United States of America - 7 Jan 2003

Mockett Robin J, Radyuk Svetlana N, Benes Judith J, Orr William C, Sohal Rajindar S

Abstract excerpt

A subset of patients suffering from familial amyotrophic lateral sclerosis (FALS) exhibit point mutations in the gene encoding Cu-Zn superoxide dismutase [superoxide:superoxide oxidoreductase, EC (SOD)]. The human wild-type and five FALS Sod mutant transgenes were introduced into the fruit fly, Drosophila melanogaster, in a Cu-Zn Sod null background. Sod null flies had dramatically decreased life span,...

Read the complete abstract on PubMed

Topics

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

Share to Aging
Share to Animals, Genetically Modified

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drosophila melanogaster

Share to Glutathione

Share to Life Expectancy

Share to Methionine

Share to Motor Neuron Disease

Share to Superoxide Dismutase

Source

Open in PubMed Open full text

Identifiers

PMID: 12502789
DOI: 10.1073/pnas.0136976100
PMCID: PMC140958

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.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Phenotypic effects of familial amyotrophic lateral sclerosis mutant Sod alleles in transgenic Drosophila.PMID 12502789Read ↗

Drosophila expressing human SOD1 successfully recapitulates mitochondrial phenotypic features of familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

Expression of human FALS SOD in motorneurons of Drosophila.Semantic proximity Read ↗

Human SOD1 ALS Mutations in a Drosophila Knock-In Model Cause Severe Phenotypes and Reveal Dosage-Sensitive Gain- and Loss-of-Function Components.Semantic proximity Read ↗

A Drosophila Model for Amyotrophic Lateral Sclerosis Reveals Motor Neuron Damage by Human SOD1Semantic proximity Read ↗

Transgenic models of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Oxidative stress causes abnormal accumulation of familial amyotrophic lateral sclerosis-related mutant SOD1 in transgenic Caenorhabditis elegans.Semantic proximity Read ↗

Pathogenic mechanisms in familial amyotrophic lateral sclerosis due to mutation of Cu, Zn superoxide dismutase.Semantic proximity Read ↗

Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation.Semantic proximity Read ↗

Familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

Extension of Drosophila lifespan by overexpression of human SOD1 in motorneurons.Semantic proximity Read ↗

Molecular genetic basis of familial ALS.Semantic proximity Read ↗

Expression of zinc-deficient human superoxide dismutase in Drosophila neurons produces a locomotor defect linked to mitochondrial dysfunction.Semantic proximity Read ↗

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