Associated Papers
Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells.
Pokrishevsky E et al.
Scientific Reports, 2018
30349065 (PubMed )
Supplement: 41598_2018_32835_MOESM4_ESM.docx
Sigma 1 receptor activation modifies intracellular calcium exchange in the G93AhSOD1 ALS model.
Tadić V et al.
Neuroscience, 2017
Are Astrocytes the Predominant Cell Type for Activation of Nrf2 in Aging and Neurodegeneration?
Liddell JR
Antioxidants (basel, Switzerland), 2017
Improved proteostasis in the secretory pathway rescues Alzheimer's disease in the mouse.
Peng Y et al.
Brain : a Journal of Neurology, 2016
Proteomic analysis of mitochondrial dysfunction in neurodegenerative diseases.
Rodolfo C et al.
Expert Review of Proteomics, 2010
Variation in aggregation propensities among ALS-associated variants of SOD1: correlation to human disease.
Prudencio M et al.
Human Molecular Genetics, 2009
Destabilizing protein polymorphisms in the genetic background direct phenotypic expression of mutant SOD1 toxicity.
Gidalevitz T et al.
Plos Genetics, 2009
How do ALS-associated mutations in superoxide dismutase 1 promote aggregation of the protein?
Shaw BF et al.
Trends in Biochemical Sciences, 2007
Structural properties and neuronal toxicity of amyotrophic lateral sclerosis-associated Cu/Zn superoxide dismutase 1 aggregates.
Matsumoto G et al.
The Journal of Cell Biology, 2005
Effect of ubiquitin expression on neuropathogenesis in a mouse model of familial amyotrophic lateral sclerosis.
Gilchrist CA et al.
Neuropathology and Applied Neurobiology, 2005
Depletion of wild-type huntingtin in mouse models of neurologic diseases.
Zhang Y et al.
Journal of Neurochemistry, 2003
Analysis of the cytosolic proteome in a cell culture model of familial amyotrophic lateral sclerosis reveals alterations to the proteasome, antioxidant defenses, and nitric oxide synthetic pathways.
Allen S et al.
The Journal of Biological Chemistry, 2003
Health implications of creatine: can oral creatine supplementation protect against neurological and atherosclerotic disease?
Wyss M et al.
Neuroscience, 2002
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