ArticleFrontiers in molecular biosciences2016
Screening of Drugs Inhibiting In vitro Oligomerization of Cu/Zn-Superoxide Dismutase with a Mutation Causing Amyotrophic Lateral Sclerosis.
Article in Frontiers in molecular biosciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
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- Engineering of an Fc-specific monovalent protein G for the light-controlled affinity purification of antibodies.Scientific reports · 2025Article
- Protein aggregation and therapeutic strategies in SOD1- and TDP-43- linked ALS.Frontiers in molecular biosciences · 2024Review
- Small molecules targeting different cellular pathologies for the treatment of amyotrophic lateral sclerosis.Medicinal research reviews · 2023Review
- Protective Effects of Lovastatin in a Population-Based ALS Study and Mouse Model.Annals of neurology · 2023Article
- A chemogenomic approach is required for effective treatment of amyotrophic lateral sclerosis.Clinical and translational medicine · 2022Review
- Advances in Applying Computer-Aided Drug Design for Neurodegenerative Diseases.International journal of molecular sciences · 2021Review
- Examination of SOD1 aggregation modulators and their effect on SOD1 enzymatic activity as a proxy for potential toxicity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Amyotrophic Lateral Sclerosis: Proteins, Proteostasis, Prions, and Promises.Frontiers in cellular neuroscience · 2020Article
- Article
- Molecular and Clinical Aspects of Protein Aggregation Assays in Neurodegenerative Diseases.Molecular neurobiology · 2018Review
- Determining the Effect of Catechins on SOD1 Conformation and Aggregation by Ion Mobility Mass Spectrometry Combined with Optical Spectroscopy.Journal of the American Society for Mass Spectrometry · 2018Article
- Current Therapeutic Molecules and Targets in Neurodegenerative Diseases Based on in silico Drug Design.Current neuropharmacology · 2018Review
- How Do Gyrating Beads Accelerate Amyloid Fibrillization?Biophysical journal · 2017Article
- Measurement of amyloid formation by turbidity assay-seeing through the cloud.Biophysical reviews · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dominant mutations in Cu/Zn-superoxide dismutase (SOD1) gene have been shown to cause a familial form of amyotrophic lateral sclerosis (SOD1-ALS). A major pathological hallmark of this disease is abnormal accumulation of mutant SOD1 oligomers in the affected spinal motor neurons. While no effective therapeutics for SOD1-ALS is currently available, SOD1 oligomerization will be a good target for developing cures of this disease. Recently, we have reproduced the formation of SOD1 oligomers abnormally cross-linked via disulfide bonds in a test tube. Using our in vitro model of SOD1 oligomerization, therefore, we screened 640 FDA-approved drugs for inhibiting the oligomerization of SOD1 proteins, and three effective classes of chemical compounds were identified. Those hit compounds will provide valuable information on the chemical structures for developing a novel drug candidate suppressing the abnormal oligomerization of mutant SOD1 and possibly curing the disease.
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