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

Regulation of system x(c)- in the SOD1-G93A mouse model of ALS.

Experimental neurology - 1 Dec 2013

Albano Rebecca, Liu XiaoQian, Lobner Doug

Abstract excerpt

The cystine/glutamate antiporter (system xc-) is critical for the generation of the antioxidant glutathione by transporting cystine into the cell. At the same time, system xc- also releases glutamate, which can potentially lead to excitotoxicity. The dual actions of system xc- make it of great interest in any disease, like amyotrophic lateral sclerosis (ALS), in which there is evidence of the involvement of both...

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 Disease Models, Animal
Share to Excitatory Amino Acid Transporter 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to SOD1 gene

Share to Genotype

Share to Mice, Transgenic

Share to Spinal Cord

Source

Identifiers

PMID: 24041987
DOI: 10.1016/j.expneurol.2013.09.008

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

Regulation of system x(c)- in the SOD1-G93A mouse model of ALS.PMID 24041987Read ↗

Loss of system x(c)- does not induce oxidative stress but decreases extracellular glutamate in hippocampus and influences spatial working memory and limbic seizure susceptibility.Semantic proximity Read ↗

System xC- is a mediator of microglial function and its deletion slows symptoms in amyotrophic lateral sclerosis mice.Semantic proximity Read ↗

Dysregulation of system xc(-) expression induced by mutant huntingtin in a striatal neuronal cell line and in R6/2 mice.Semantic proximity Read ↗

Neuronal glutathione deficiency and age-dependent neurodegeneration in the EAAC1 deficient mouse.Semantic proximity Read ↗

Implication of system xc- in neuroinflammation during the onset and maintenance of neuropathic pain.Semantic proximity Read ↗

Paradoxical roles of serine racemase and D-serine in the G93A mSOD1 mouse model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Activation of a glycine transporter on spinal cord neurons causes enhanced glutamate release in a mouse model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Absence of system xc- in mice decreases anxiety and depressive-like behavior without affecting sensorimotor function or spatial vision.Semantic proximity Read ↗

Human cystine/glutamate transporter: cDNA cloning and upregulation by oxidative stress in glioma cells.Semantic proximity Read ↗

Impairment of glutamate transport and increased vulnerability to oxidative stress in neuroblastoma SH-SY5Y cells expressing a Cu,Zn superoxide dismutase typical of familial amyotrophic lateral sclerosis.Semantic proximity Read ↗

Impaired long-term potentiation and long-term memory deficits in xCT-deficient sut mice.Semantic proximity Read ↗

Deficiency of the cystine-transporter gene, xCT, does not exacerbate the deleterious phenotypic consequences of SOD1 knockout in mice.Semantic proximity Read ↗

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