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

Human superoxide dismutase 1 overexpression in motor neurons of Caenorhabditis elegans causes axon guidance defect and neurodegeneration.

Neurobiology of aging - 1 Apr 2014

Li Jia, Li Ting, Zhang Xiaojie, Tang Yu, Yang Juan, Le Weidong

Abstract excerpt

Strong evidence indicates that mutant Cu, Zn-superoxide dismutase 1 (SOD1) exerts toxic effect on motor neurons in amyotrophic lateral sclerosis (ALS). However, the nature of mutant SOD1-mediated motor neuron degeneration is poorly understood. To provide new insight into the mechanism by which mutant SOD1 induces motor neuron injury, we developed novel Caenorhabditis elegans models of ALS. Expression of human...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis
Share to Axons

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Caenorhabditis elegans

Share to Disease Models, Animal

Share to Motor Neurons

Share to Nerve Degeneration

Share to Superoxide Dismutase

Share to Superoxide Dismutase-1

Source

Identifiers

PMID: 24126158
DOI: 10.1016/j.neurobiolaging.2013.09.003

Genes

SOD1

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

Human superoxide dismutase 1 overexpression in motor neurons of Caenorhabditis elegans causes axon guidance defect and neurodegeneration.PMID 24126158Read ↗

An ALS-linked mutant SOD1 produces a locomotor defect associated with aggregation and synaptic dysfunction when expressed in neurons of Caenorhabditis elegans.Semantic proximity Read ↗

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

Caenorhabditis elegans Models CountSemantic proximity Read ↗

Single copy/knock-in models of ALS SOD1 in C. elegans suggest loss and gain of function have different contributions to cholinergic and glutamatergic neurodegenerationSemantic proximity Read ↗

Motor Neuron Abnormalities Correlate with Impaired Movement in Zebrafish that Express Mutant Superoxide Dismutase 1Semantic proximity Read ↗

Neuron-specific knock-down of SMN1 causes neuron degeneration and death through an apoptotic mechanism.Semantic proximity Read ↗

Amyotrophic Lateral Sclerosis Mechanism: Insights from the Caenorhabditis elegans ModelsSemantic proximity Read ↗

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

Neuromuscular effects of G93A-SOD1 expression in zebrafish.Semantic proximity Read ↗

Neurodegenerative disorders: insights from the nematode Caenorhabditis elegans.Semantic proximity Read ↗

Caenorhabditis elegans as a Model System to Study Human Neurodegenerative DisordersSemantic proximity Read ↗

Pan-neuronal expression of human mutant SOD1 in Drosophila impairs survival and motor performance, induces early neuroinflammation and chromosome aberrations.Semantic proximity Read ↗

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