Associated Papers
Dysbiosis and Neurodegeneration in ALS: Unraveling the Gut-Brain Axis.
Sharma VK
Neuromolecular Medicine, 2025
Ubiquitination and the proteasome rather than caspase-3-mediated C-terminal cleavage are involved in the EAAT2 degradation by staurosporine-induced cellular stress.
Voss TD et al.
Journal of Neurochemistry, 2021
Massive transcriptome sequencing of human spinal cord tissues provides new insights into motor neuron degeneration in ALS.
D'Erchia AM et al.
Scientific Reports, 2017
Are Astrocytes the Predominant Cell Type for Activation of Nrf2 in Aging and Neurodegeneration?
Liddell JR
Antioxidants (basel, Switzerland), 2017
Mutation of the caspase-3 cleavage site in the astroglial glutamate transporter EAAT2 delays disease progression and extends lifespan in the SOD1-G93A mouse model of ALS.
Rosenblum LT et al.
Experimental Neurology, 2017
Olfactory ensheathing cell neurorestorotherapy for amyotrophic lateral sclerosis patients: benefits from multiple transplantations.
Chen L et al.
Cell Transplantation, 2012
Role of excitatory amino acid transporter-2 (EAAT2) and glutamate in neurodegeneration: opportunities for developing novel therapeutics.
Kim K et al.
Journal of Cellular Physiology, 2011
Immature copper-zinc superoxide dismutase and familial amyotrophic lateral sclerosis.
Seetharaman SV et al.
Experimental Biology and Medicine (maywood, N.j.), 2009
Neuron-specific expression of mutant superoxide dismutase is sufficient to induce amyotrophic lateral sclerosis in transgenic mice.
Jaarsma D et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2008
Caspase-3 cleaves and inactivates the glutamate transporter EAAT2.
Boston-Howes W et al.
The Journal of Biological Chemistry, 2006
Molecular and synaptic changes in the hippocampus underlying superior spatial abilities in pre-symptomatic G93A+/+ mice overexpressing the human Cu/Zn superoxide dismutase (Gly93 --> ALA) mutation.
Spalloni A et al.
Experimental Neurology, 2006
Mitochondrial proteomic analysis of a cell line model of familial amyotrophic lateral sclerosis.
Fukada K et al.
Molecular & Cellular Proteomics : Mcp, 2004
Increased expression of the glial glutamate transporter EAAT2 modulates excitotoxicity and delays the onset but not the outcome of ALS in mice.
Guo H et al.
Human Molecular Genetics, 2003
Sixteen novel mutations in the Cu/Zn superoxide dismutase gene in amyotrophic lateral sclerosis: a decade of discoveries, defects and disputes.
Andersen PM et al.
Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders : Official Publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases, 2003
Neuron-specific expression of mutant superoxide dismutase 1 in transgenic mice does not lead to motor impairment.
Pramatarova A et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2001
Superoxide dismutase-1 mutation-related neurotoxicity in familial amyotrophic lateral sclerosis.
Shibata N et al.
Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders : Official Publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases, 2000
Oxidative stress and motor neurone disease.
Cookson MR et al.
Brain Pathology (zurich, Switzerland), 1999
Distinct expression and regulation of the glutamate transporter isoforms GLT-1a and GLT-1b in cultured astrocytes from a rat model of amyotrophic lateral sclerosis (hSOD1G93A).
Goursaud S et al.
Neurochemistry International, 0
Superoxide dismutase and neurofilament transgenic models of amyotrophic lateral sclerosis.
Morrison BM et al.
The Journal of Experimental Zoology, 0