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

Superoxide dismutase 1 mutation in a cellular model of amyotrophic lateral sclerosis shifts energy generation from oxidative phosphorylation to glycolysis.

Neurobiology of aging - 1 Jun 2014

Allen Scott P, Rajan Sandeep, Duffy Lynn, Mortiboys Heather, Higginbottom Adrian, Grierson Andrew J, Shaw Pamela J

Abstract excerpt

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder involving the progressive degeneration of motor neurons in the brain and spinal cord. Mitochondrial dysfunction plays a key role in ALS disease progression and has been observed in several ALS cellular and animal models. Here, we show that fibroblasts isolated from ALS cases with a Cu/Zn superoxide dismutase (SOD1) I113T mutation...

Read the complete abstract on PubMed

Topics

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

Share to Adenosine Triphosphate
Share to Amyotrophic Lateral Sclerosis

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Energy Metabolism

Share to Glycolysis

Share to Oxidative Phosphorylation

Share to Superoxide Dismutase

Share to Superoxide Dismutase-1

Source

Identifiers

PMID: 24439480
DOI: 10.1016/j.neurobiolaging.2013.11.025

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

Superoxide dismutase 1 mutation in a cellular model of amyotrophic lateral sclerosis shifts energy generation from oxidative phosphorylation to glycolysis.PMID 24439480Read ↗

Altered MAM function shifts mitochondrial metabolism in SOD1-mutant models of ALSSemantic proximity Read ↗

The effect of SOD1 mutation on cellular bioenergetic profile and viability in response to oxidative stress and influence of mutation-type.Semantic proximity Read ↗

Mitochondrial and energy metabolism dysfunctions are hallmarks of TDP-43G376D fibroblasts from members of an Amyotrophic Lateral Sclerosis familySemantic proximity Read ↗

Integrative Profiling of Amyotrophic Lateral Sclerosis Lymphoblasts Identifies Unique Metabolic and Mitochondrial Disease Fingerprints.Semantic proximity Read ↗

Altered MAM function shifts mitochondrial metabolism in SOD1-mutant models of ALSSemantic proximity Read ↗

Glucose clearance and uptake is increased in the SOD1 <sub>G93A</sub> mouse model of amyotrophic lateral sclerosis through an insulin-independent mechanismSemantic proximity Read ↗

Abnormal energy metabolism in ALS: a key player?Semantic proximity Read ↗

Metabolic Changes Associated With Muscle Expression of SOD1G93ASemantic proximity Read ↗

Integrative Profiling of Amyotrophic Lateral Sclerosis Lymphoblasts Identifies Unique Metabolic and Mitochondrial Disease FingerprintsSemantic proximity Read ↗

New links between SOD1 and metabolic dysfunction from a yeast model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Metabolic signatures of amyotrophic lateral sclerosis reveal insights into disease pathogenesis.Semantic proximity Read ↗

The familial amyotrophic lateral sclerosis-associated A4V SOD1 mutant is not able to regulate aerobic glycolysis.Semantic proximity Read ↗

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