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

The human G93A-SOD1 mutation in a pre-symptomatic rat model of amyotrophic lateral sclerosis increases the vulnerability to a mild spinal cord compression.

BMC genomics - 15 Nov 2010

Jokic Natasa, Yip Ping K, Michael-Titus Adina, Priestley John V, Malaspina Andrea

Abstract excerpt

BACKGROUND: Traumatic injuries can undermine neurological functions and act as risk factors for the development of irreversible and fatal neurodegenerative disorders like amyotrophic lateral sclerosis (ALS). In this study, we have investigated how a mutation of the superoxide dismutase 1 (SOD1) g...

Read the complete abstract on PubMed

Topics

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

Share to Locomotion
Share to Motor Neurons
Share to Neurofilament Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Organ Size

Share to Recovery of Function

Share to Spinal Cord Injuries

Share to Superoxide Dismutase-1

Share to Synaptophysin

Source

Open in PubMed Open full text

Identifiers

PMID: 21078175
DOI: 10.1186/1471-2164-11-633
PMCID: PMC3020590

Genes

SOD1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-21078175-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The human G93A-SOD1 mutation in a pre-symptomatic rat model of amyotrophic lateral sclerosis increases the vulnerability to a mild spinal cord compression.PMID 21078175Read ↗

Comparative analysis of the time-dependent functional and molecular changes in spinal cord degeneration induced by the G93A SOD1 gene mutation and by mechanical compression.Semantic proximity Read ↗

Mutant SOD1 alters the motor neuronal transcriptome: implications for familial ALS.Semantic proximity Read ↗

Transcriptional profiling in the lumbar spinal cord of a mouse model of amyotrophic lateral sclerosis: a role for wild-type superoxide dismutase 1 in sporadic disease?Semantic proximity Read ↗

Molecular insights of the injured lesions of rat spinal cords: Inflammation, apoptosis, and cell survivalSemantic proximity Read ↗

Microarray Analysis of the Cellular Pathways Involved in the Adaptation to and Progression of Motor Neuron Injury in the SOD1 G93A Mouse Model of Familial ALSSemantic proximity Read ↗

State of the field: An informatics-based systematic review of the SOD1-G93A amyotrophic lateral sclerosis transgenic mouse model.Semantic proximity Read ↗

Transgenics, toxicity and therapeutics in rodent models of mutant SOD1-mediated familial ALS.Semantic proximity Read ↗

Highlight Commentary on "Redox proteomics analysis of oxidatively modified proteins in G93A-SOD1 transgenic mice--a model of familial amyotrophic lateral sclerosis".Semantic proximity Read ↗

The effect of peripheral nerve injury on disease progression in the SOD1(G93A) mouse model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Early gene expression changes in spinal cord from SOD1G93A Amyotrophic Lateral Sclerosis animal modelSemantic proximity Read ↗

Rats expressing human cytosolic copper-zinc superoxide dismutase transgenes with amyotrophic lateral sclerosis: associated mutations develop motor neuron disease.Semantic proximity Read ↗

Human neural stem cell replacement therapy for amyotrophic lateral sclerosis by spinal transplantation.Semantic proximity Read ↗

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