ArticleProceedings of the National Academy of Sciences of the United States of America2019
Characterization of the activity, aggregation, and toxicity of heterodimers of WT and ALS-associated mutant Sod1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Pathology of general proprioception in a canine disease model of amyotrophic lateral sclerosis.Journal of the neurological sciences · 2026Article
- Decoupling metabolic defense: Mutational and recombinational chaos in Sod1-deficient cells.PLoS genetics · 2026Article
- The effect of aging on post-translational modifications of wild-type human SOD1 and the A5V ALS mutant.GeroScience · 2026Article
- Mitochondrial dysfunction in neurodegenerative disorders: mechanisms and therapeutic advances.Molecular biomedicine · 2026Review
- Impact of Orchiectomy on Oxidative Stress-Induced Neurodegeneration in the Male Rat Retina: A Proteomic Analysis.Antioxidants (Basel, Switzerland) · 2026Article
- Molecular Modulation of the Crosstalk Between TDP-43 and SOD1.International journal of molecular sciences · 2026Article
- Stabilized real-time Brillouin microscopy reveals fractal organization of protein condensates in living cells.Nature communications · 2026Article
- From Yeast to Therapeutics: Modeling Neurodegenerative Diseases in Saccharomyces cerevisiae.Yeast (Chichester, England) · 2025Review
- Proteome Signature of Alzheimer-Like Phenotypes in Frontal Cortices From Young and Old Individuals With Down Syndrome.Molecular neurobiology · 2025Article
- Exposure to an environmentally relevant mixture of polychlorinated biphenyls affects mitochondrial bioenergetics and plasticity.Redox biology · 2025Article
- SOD1, A Crucial Protein for Neural Biochemistry: Dysfunction and Risk of Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2025Review
- Landscapes of missense variant impact for human superoxide dismutase 1.American journal of human genetics · 2025Article
- Exploring Protein Misfolding in Amyotrophic Lateral Sclerosis: Structural and Functional Insights.Biomedicines · 2025Review
- A role for mitochondria-ER crosstalk in amyotrophic lateral sclerosis 8 pathogenesis.Life science alliance · 2025Article
- Chemical composition and toxicity studies onRSC advances · 2024Article
- Trehalose Protects against Superoxide Dismutase 1 Proteinopathy in an Amyotrophic Lateral Sclerosis Model.Antioxidants (Basel, Switzerland) · 2024Article
- Seeding activity of human superoxide dismutase 1 aggregates in familial and sporadic amyotrophic lateral sclerosis postmortem neural tissues by real-time quaking-induced conversion.Acta neuropathologica · 2024Article
- Ebselen analogues delay disease onset and its course in fALS by on-target SOD-1 engagement.Scientific reports · 2024Article
- Vcp overexpression and leucine supplementation extend lifespan and ameliorate neuromuscular junction phenotypes of a SOD1G93A-ALS mouse model.Human molecular genetics · 2024Article
- An Increase in Peroxiredoxin 6 Expression Induces Neurotoxic A1 Astrocytes in the Lumbar Spinal Cord of Amyotrophic Lateral Sclerosis Mice Model.Neurochemical research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in Cu/Zn superoxide dismutase (Sod1) have been reported in both familial and sporadic amyotrophic lateral sclerosis (ALS). In this study, we investigated the behavior of heteromeric combinations of wild-type (WT) and mutant Sod1 proteins A4V, L38V, G93A, and G93C in human cells. We showed that both WT and mutant Sod1 formed dimers and oligomers, but only mutant Sod1 accumulated in intracellular inclusions. Coexpression of WT and hSod1 mutants resulted in the formation of a larger number of intracellular inclusions per cell than that observed in cells coexpressing WT or mutant hSod1. The number of inclusions was greater in cells expressing A4V hSod1. To eliminate the contribution of endogenous Sod1, and better evaluate the effect of ALS-associated mutant Sod1 expression, we expressed human Sod1 WT and mutants in human cells knocked down for endogenous Sod1 (Sod1-KD), and in
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