Associated Papers
Beneficial base substitutions in Escherichia coli fucO gene for enhancement of glycolic acid production.
Nemoto M et al.
Journal of Bioscience and Bioengineering, 2024
A liquid-to-solid phase transition of Cu/Zn superoxide dismutase 1 initiated by oxidation and disease mutation.
Gu S et al.
The Journal of Biological Chemistry, 2023
Mutations in Superoxide Dismutase 1 (Sod1) Linked to Familial Amyotrophic Lateral Sclerosis Can Disrupt High-Affinity Zinc-Binding Promoted by the Copper Chaperone for Sod1 (Ccs).
Boyd SD et al.
Molecules (basel, Switzerland), 2020
Tryptophan residue 32 in human Cu-Zn superoxide dismutase modulates prion-like propagation and strain selection.
Crown A et al.
Plos One, 2020
The UPR-PERK pathway is not a promising therapeutic target for mutant SOD1-induced ALS.
Dzhashiashvili Y et al.
Neurobiology of Disease, 2019
Experimental Mutations in Superoxide Dismutase 1 Provide Insight into Potential Mechanisms Involved in Aberrant Aggregation in Familial Amyotrophic Lateral Sclerosis.
Crown AM et al.
G3 (bethesda, Md.), 2019
Tryptophan 32-mediated SOD1 aggregation is attenuated by pyrimidine-like compounds in living cells.
Pokrishevsky E et al.
Scientific Reports, 2018
Loss of charge mutations in solvent exposed Lys residues of superoxide dismutase 1 do not induce inclusion formation in cultured cell models.
Crosby K et al.
Plos One, 2018
Early and gender-specific differences in spinal cord mitochondrial function and oxidative stress markers in a mouse model of ALS.
Cacabelos D et al.
Acta Neuropathologica Communications, 2016
In-cell NMR reveals potential precursor of toxic species from SOD1 fALS mutants.
Luchinat E et al.
Nature Communications, 2014
Redox properties of the disulfide bond of human Cu,Zn superoxide dismutase and the effects of human glutaredoxin 1.
Bouldin SD et al.
The Biochemical Journal, 2012
Sorting of the yeast vacuolar-type, proton-translocating ATPase enzyme complex (V-ATPase): identification of a necessary and sufficient Golgi/endosomal retention signal in Stv1p.
Finnigan GC et al.
The Journal of Biological Chemistry, 2012
Nuclear localization of human SOD1 and mutant SOD1-specific disruption of survival motor neuron protein complex in transgenic amyotrophic lateral sclerosis mice.
Gertz B et al.
Journal of Neuropathology and Experimental Neurology, 2012
Variation in aggregation propensities among ALS-associated variants of SOD1: correlation to human disease.
Prudencio M et al.
Human Molecular Genetics, 2009
Proteomic characterization of lipid raft proteins in amyotrophic lateral sclerosis mouse spinal cord.
Zhai J et al.
The Febs Journal, 2009
Different regulation of wild-type and mutant Cu,Zn superoxide dismutase localization in mammalian mitochondria.
Kawamata H et al.
Human Molecular Genetics, 2008
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
Informatics-assisted protein profiling in a transgenic mouse model of amyotrophic lateral sclerosis.
Lukas TJ et al.
Molecular & Cellular Proteomics : Mcp, 2006
Calorimetric analysis of thermodynamic stability and aggregation for apo and holo amyotrophic lateral sclerosis-associated Gly-93 mutants of superoxide dismutase.
Stathopulos PB 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
Mechanism and thermodynamics of guanidinium chloride-induced denaturation of ALS-associated mutant Cu,Zn superoxide dismutases.
Rumfeldt JA et al.
Journal of Molecular Biology, 2006
Amyotrophic lateral sclerosis mutations have the greatest destabilizing effect on the apo- and reduced form of SOD1, leading to unfolding and oxidative aggregation.
Furukawa Y et al.
The Journal of Biological Chemistry, 2005
Mitochondrial proteomic analysis of a cell line model of familial amyotrophic lateral sclerosis.
Fukada K et al.
Molecular & Cellular Proteomics : Mcp, 2004
Glycation proceeds faster in mutated Cu, Zn-superoxide dismutases related to familial amyotrophic lateral sclerosis.
Takamiya R et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 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
Residues of VP26 of herpes simplex virus type 1 that are required for its interaction with capsids.
Desai P et al.
Journal of Virology, 2003
Identification of functionally important residues of the epidermal growth factor-2 domain of factor IX by alanine-scanning mutagenesis. Residues Asn(89)-Gly(93) are critical for binding factor VIIIa.
Chang YJ et al.
The Journal of Biological Chemistry, 2002
Mitochondrial dysfunction in a cell culture model of familial amyotrophic lateral sclerosis.
Menzies FM et al.
Brain : a Journal of Neurology, 2002
Release of copper ions from the familial amyotrophic lateral sclerosis-associated Cu,Zn-superoxide dismutase mutants.
Eum WS et al.
Molecules and Cells, 1999
Neurofilaments and orthograde transport are reduced in ventral root axons of transgenic mice that express human SOD1 with a G93A mutation.
Zhang B et al.
The Journal of Cell Biology, 1997