ArticleBiophysical journal2016
Effect of Oxidative Damage on the Stability and Dimerization of Superoxide Dismutase 1.
Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- A Systematic and Comprehensive Review on Disease-Causing Genes in Amyotrophic Lateral Sclerosis.Journal of molecular neuroscience : MN · 2020Pooled it
- Tetrahedral framework nucleic acids: Nanokeys unlocking a new era of precision biomedicine.Journal of advanced research · 2026Review
- Salivary Oxidative Stress and Antioxidant Markers in Oral Leukoplakia: A Systematic Review and Meta-Analysis.Antioxidants (Basel, Switzerland) · 2026Review
- Principles ofbioRxiv : the preprint server for biology · 2026Article
- Parkinson-like wild-type superoxide dismutase 1 pathology induces nigral dopamine neuron degeneration in a novel murine model.Acta neuropathologica · 2025Article
- Modulatory Impact of Oxidative Stress on Action Potentials in Pathophysiological States: A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024Review
- Trehalose Protects against Superoxide Dismutase 1 Proteinopathy in an Amyotrophic Lateral Sclerosis Model.Antioxidants (Basel, Switzerland) · 2024Article
- Stability of Protein Pharmaceuticals: Recent Advances.Pharmaceutical research · 2024Review
- Using Human-Induced Pluripotent Stem Cell Derived Neurons on Microelectrode Arrays to Model Neurological Disease: A Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Oxidative Stress and Antioxidants in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2023Review
- Modulation of histone H3K4 dimethylation by spermidine ameliorates motor neuron survival and neuropathology in a mouse model of ALS.Journal of biomedical science · 2022Article
- SOD1 in ALS: Taking Stock in Pathogenic Mechanisms and the Role of Glial and Muscle Cells.Antioxidants (Basel, Switzerland) · 2022Review
- Antioxidant Therapy in Oxidative Stress-Induced Neurodegenerative Diseases: Role of Nanoparticle-Based Drug Delivery Systems in Clinical Translation.Antioxidants (Basel, Switzerland) · 2022Review
- Hydrogen Peroxide and Amyotrophic Lateral Sclerosis: From Biochemistry to Pathophysiology.Antioxidants (Basel, Switzerland) · 2021Review
- Towards an Understanding of Oxidative Damage in an α-L-Arabinofuranosidase of Trichoderma reesei: a Molecular Dynamics Approach.Applied biochemistry and biotechnology · 2021Article
- Perturbation Free-Energy Toolkit: An Automated Alchemical Topology Builder.Journal of chemical information and modeling · 2021Article
- Change in Cationic Amino Acid Transport System and Effect of Lysine Pretreatment on Inflammatory State in Amyotrophic Lateral Sclerosis Cell Model.Biomolecules & therapeutics · 2021Article
- A strategy for proline and glycine mutations to proteins with alchemical free energy calculations.Journal of computational chemistry · 2021Article
- Human Pluripotent Stem-Cell-Derived Models as a Missing Link in Drug Discovery and Development.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic.Angewandte Chemie (International ed. in English) · 2021Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
During their life cycle, proteins are subject to different modifications involving reactive oxygen species. Such oxidative damage to proteins may lead to the formation of insoluble aggregates and cytotoxicity and is associated with age-related disorders including neurodegenerative diseases, cancer, and diabetes. Superoxide dismutase 1 (SOD1), a key antioxidant enzyme in human cells, is particularly susceptible to such modifications. Moreover, this homodimeric metalloenzyme has been directly linked to both familial and sporadic amyotrophic lateral sclerosis (ALS), a devastating, late-onset motor neuronal disease, with more than 150 ALS-related mutations in the SOD1 gene. Importantly, oxidatively damaged SOD1 aggregates have been observed in both familial and sporadic forms of the disease. However, the molecular mechanisms as well as potential implications of oxidative stress in SOD1-induced cytotoxicity remain elusive. In this study, we examine the effects of oxidative modification on SOD1 monomer and homodimer stability, the key molecular properties related to SOD1 aggregation. We use molecular dynamics simulations in combination with thermodynamic integration to study microscopic-level site-specific effects of oxidative "mutations" at the dimer interface, including lysine, arginine, proline and threonine carbonylation, and cysteine oxidation. Our results show that oxidative damage of even single residues at the interface may drastically destabilize the SOD1 homodimer, with several modifications exhibiting a comparable effect to that of the most drastic ALS-causing mutations known. Additionally, we show that the SOD1 monomer stability decreases upon oxidative stress, which may lead to partial local unfolding and consequently to increased aggregation propensity. Importantly, these results suggest that oxidative stress may play a key role in development of ALS, with the mutations in the SOD1 gene being an additional factor.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.