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 mitochondrial permeability transition pore in motor neurons: involvement in the pathobiology of ALS mice.

Experimental neurology - 1 Aug 2009

Martin Lee J, Gertz Barry, Pan Yan, Price Ann C, Molkentin Jeffery D, Chang Qing

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of motor neurons (MNs) that causes paralysis. Some forms of ALS are inherited, caused by mutations in the superoxide dismutase-1 (SOD1) gene. The mechanisms of human mutant SOD1 (mSOD1) toxicity to MNs are unresolved. Mitochondria in MNs might be key sites for ALS pathogenesis, but cause-effect relationships between mSOD1 and...

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 Cyclophilins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Microscopy, Electron

Share to Mitochondria

Share to Mitochondrial Membrane Transport Proteins

Share to Motor Neurons

Share to Superoxide Dismutase

Share to Superoxide Dismutase-1

Source

Open in PubMed Open full text

Identifiers

PMID: 19272377
DOI: 10.1016/j.expneurol.2009.02.015
PMCID: PMC2710399

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

The mitochondrial permeability transition pore in motor neurons: involvement in the pathobiology of ALS mice.PMID 19272377Read ↗

Mitochondrial dysfunction and its role in motor neuron degeneration in ALS.Semantic proximity Read ↗

Mutant SOD1 in neuronal mitochondria causes toxicity and mitochondrial dynamics abnormalities.Semantic proximity Read ↗

In vivo pathogenic role of mutant SOD1 localized in the mitochondrial intermembrane space.Semantic proximity Read ↗

Mitochondrial dysfunction and amyotrophic lateral sclerosis.Semantic proximity Read ↗

Mutant Cu, Zn superoxide dismutase that causes motoneuron degeneration is present in mitochondria in the CNS.Semantic proximity Read ↗

Mitochondria, a Key Target in Amyotrophic Lateral Sclerosis PathogenesisSemantic proximity Read ↗

Skeletal Muscle-Restricted Expression of Human SOD1 in Transgenic Mice Causes a Fatal ALS-Like SyndromeSemantic proximity Read ↗

Mitochondrial pathobiology in Parkinson's disease and amyotrophic lateral sclerosis.Semantic proximity Read ↗

Mitochondrial dysfunction in amyotrophic lateral sclerosis.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 ↗

Mitochondrial Function, Morphology, and Axonal Transport in Amyotrophic Lateral SclerosisSemantic proximity Read ↗

Enhancing mitochondrial calcium buffering capacity reduces aggregation of misfolded SOD1 and motor neuron cell death without extending survival in mouse models of inherited amyotrophic lateral sclerosis.Semantic proximity Read ↗

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