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

Absence of p53: no effect in a transgenic mouse model of familial amyotrophic lateral sclerosis.

Experimental neurology - 1 Sept 2000

Kuntz C, Kinoshita Y, Beal M F, Donehower L A, Morrison R S

Abstract excerpt

Familial amyotrophic lateral sclerosis (ALS) has been linked in some families to dominantly inherited mutations in the gene encoding copper-zinc superoxide dismutase 1 (Cu-Zn SOD1). Transgenic mice expressing a mutant human Cu-Zn SOD1 (G93A) develop a dominantly inherited adult-onset paralytic disorder that replicates many of the clinical and pathological features of familial ALS. Increased p53 immunoreactivity...

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 Cell Count
Share to Forelimb

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Motor Activity

Share to Motor Neurons

Share to Spinal Cord

Share to Superoxide Dismutase

Share to Tumor Suppressor Protein p53

Source

Identifiers

PMID: 10964497
DOI: 10.1006/exnr.2000.7464

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.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Absence of p53: no effect in a transgenic mouse model of familial amyotrophic lateral sclerosis.PMID 10964497Read ↗

Reduction of Purkinje cell pathology in SCA1 transgenic mice by p53 deletion.Semantic proximity Read ↗

Neuron-specific expression of mutant superoxide dismutase 1 in transgenic mice does not lead to motor impairment.Semantic proximity Read ↗

Transgenic mice with human mutant genes causing Parkinson's disease and amyotrophic lateral sclerosis provide common insight into mechanisms of motor neuron selective vulnerability to degeneration.Semantic proximity Read ↗

Lack of involvement of neuronal nitric oxide synthase in the pathogenesis of a transgenic mouse model of familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

A comprehensive assessment of the SOD1G93A low-copy transgenic mouse, which models human amyotrophic lateral sclerosisSemantic proximity Read ↗

Phenotype of transgenic mice carrying a very low copy number of the mutant human G93A superoxide dismutase-1 gene associated with amyotrophic lateral sclerosis.Semantic proximity Read ↗

Characterization of a Novel SOD-1(G93A) Transgenic Mouse Line with Very Decelerated Disease DevelopmentSemantic proximity Read ↗

Activation of the stress-activated MAP kinase, p38, but not JNK in cortical motor neurons during early presymptomatic stages of amyotrophic lateral sclerosis in transgenic mice.Semantic proximity Read ↗

A low expressor line of transgenic mice carrying a mutant human Cu,Zn superoxide dismutase (SOD1) gene develops pathological changes that most closely resemble those in human amyotrophic lateral sclerosis.Semantic proximity Read ↗

Effect of ubiquitin expression on neuropathogenesis in a mouse model of familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

Transgenic mice expressing an altered murine superoxide dismutase gene provide an animal model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Neuropathological changes in two lines of mice carrying a transgene for mutant human Cu,Zn SOD, and in mice overexpressing wild type human SOD: a model of familial amyotrophic lateral sclerosis (FALS).Semantic proximity Read ↗

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