SOD1 in neurotoxicity and its controversial roles in SOD1 mutation-negative ALS.
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Summary
The toxic mechanisms of mutant SOD1 (SOD1(mut)) and misfolded S OD1(WT) in the context of ALS as well as the potential implication of these mechanisms in SOD 1 mutation-negative ALS are discussed.
- Type
- review
- Published
- 2016-01-01
- Cited by
- 130
- References
- 109
- OpenAlex
- https://openalex.org/W1921779421
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:30177763
Keywords
SOD1, Amyotrophic lateral sclerosis, Excitotoxicity, Neurotoxicity, Mutation
References
- ITPR2 as a susceptibility gene in sporadic amyotrophic lateral sclerosis: a genome-wide association study.
- Dynamical roles of metal ions and the disulfide bond in Cu, Zn superoxide dismutase folding and aggregation
- A role for motoneuron subtype–selective ER stress in disease manifestations of FALS mice
- Intercellular propagated misfolding of wild-type Cu/Zn superoxide dismutase occurs via exosome-dependent and -independent mechanisms
- Abnormal exocytotic release of glutamate in a mouse model of amyotrophic lateral sclerosis
- An α2-Na/K ATPase/α-adducin complex in astrocytes triggers non–cell autonomous neurodegeneration
- Familial amyotrophic lateral sclerosis
- TDP-43 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis
- Neural mitochondrial Ca2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn‐superoxide dismutase mutant mice
- Wild‐type superoxide dismutase acquires binding and toxic properties of ALS‐linked mutant forms through oxidation
- Deficits in axonal transport precede ALS symptoms in vivo
- Decreased glutamate transport by the brain and spinal cord in amyotrophic lateral sclerosis.
- Histological evidence of protein aggregation in mutant SOD1 transgenic mice and in amyotrophic lateral sclerosis neural tissues.
- Evidence of Increased Oxidative Damage in Both Sporadic and Familial Amyotrophic Lateral Sclerosis
- Toxic mutants in Charcot's sclerosis
- Astrocyte-derived TGF-β1 accelerates disease progression in ALS mice by interfering with the neuroprotective functions of microglia and T cells.
- Experimental transmissibility of mutant SOD1 motor neuron disease
- GLT1 overexpression in SOD1(G93A) mouse cervical spinal cord does not preserve diaphragm function or extend disease.
- Wild-type human TDP-43 expression causes TDP-43 phosphorylation, mitochondrial aggregation, motor deficits and early mortality in transgenic mice
- Exposure of Hydrophobic Surfaces Initiates Aggregation of Diverse ALS-Causing Superoxide Dismutase-1 Mutants
Cited by
- Redox Imbalance and Viral Infections in Neurodegenerative Diseases
- Endogenous Cu in the central nervous system fails to satiate the elevated requirement for Cu in a mutant SOD1 mouse model of ALS.
- Reactive Oxygen Species: Physiological and Physiopathological Effects on Synaptic Plasticity
- Management and therapeutic perspectives in amyotrophic lateral sclerosis
- Mutant PFN1 causes ALS phenotypes and progressive motor neuron degeneration in mice by a gain of toxicity
- Intrinsic disorder in proteins involved in amyotrophic lateral sclerosis
- The Identification and Targeting of Partially-Folded Conformations on the Folding Free-Energy Landscapes of ALS-Linked Proteins for Therapeutic Intervention: A Dissertation
- A Boronic Acid Conjugate of Angiogenin that Shows ROS-Responsive Neuroprotective Activity
- Evaluating a Gene-Environment Interaction in Amyotrophic Lateral Sclerosis: Methylmercury Exposure and Mutated SOD1
- Nuclear export of misfolded SOD1 mediated by a normally buried NES-like sequence reduces proteotoxicity in the nucleus
- Determining Protein-Protein Interactions of ALS-Associated SOD1
- Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases.
- The regulatory and signaling mechanisms of the ASK family.
- Implications of white matter damage in amyotrophic lateral sclerosis
- TDP-43 and FUS in Amyotrophic Lateral Sclerosis: From Animal Models to Disease Mechanisms
- ASK1 in neurodegeneration.
- NLRP3 Inflammasome Activation in a Transgenic Amyotrophic Lateral Sclerosis Model
- Effects of berberine, curcumin, resveratrol alone and in combination with chemotherapeutic drugs and signal transduction inhibitors on cancer cells-Power of nutraceuticals.
- The roles of intrinsic disorder-based liquid-liquid phase transitions in the “Dr. Jekyll–Mr. Hyde” behavior of proteins involved in amyotrophic lateral sclerosis and frontotemporal lobar degeneration
- Therapeutic application of apoptosis signal-regulating kinase 1 inhibitors.
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