ArticleScientific reports2017
Computing disease-linked SOD1 mutations: deciphering protein stability and patient-phenotype relations.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- Article
- The structure, redox chemistry and motor neuron toxicity of heterodimeric zinc-deficient SOD1-implications for the toxic gain of function observed in ALS.Neurobiology of disease · 2025Article
- The structure, redox chemistry and motor neuron toxicity of heterodimeric zinc-deficient SOD1-Implications for the toxic gain of function observed in ALS.bioRxiv : the preprint server for biology · 2025Article
- Structural insights into SOD1: from in silico and molecular dynamics to experimental analyses of ALS-associated E49K and R115G mutants.Frontiers in molecular biosciences · 2025Article
- Understanding large scale sequencing datasets through changes to protein folding.Briefings in functional genomics · 2024Review
- Development ofIranian journal of biotechnology · 2022Article
- Frustration analysis of TBK1 missense mutations reported in ALS/FTD and cancer patients.3 Biotech · 2022Article
- Characterization of the p.L145F and p.S135N Mutations in SOD1: Impact on the Metabolism of Fibroblasts Derived from Amyotrophic Lateral Sclerosis Patients.Antioxidants (Basel, Switzerland) · 2022Article
- Delineating the Aggregation-Prone Hotspot Regions (Peptides) in the Human Cu/Zn Superoxide Dismutase 1.ACS omega · 2021Article
- Proteostasis in the Male and Female Germline: A New Outlook on the Maintenance of Reproductive Health.Frontiers in cell and developmental biology · 2021Review
- Article
- PremPS: Predicting the impact of missense mutations on protein stability.PLoS computational biology · 2020Article
- Excavating the functionally crucial active-site residues of the DXS protein of Bacillus subtilis by exploring its closest homologues.Journal, genetic engineering & biotechnology · 2020Article
- Folliculin variants linked to Birt-Hogg-Dubé syndrome are targeted for proteasomal degradation.PLoS genetics · 2020Article
- Insights into the Conserved Regulatory Mechanisms of Human and Yeast Aging.Biomolecules · 2020Review
- Expedition into Taurine Biology: Structural Insights and Therapeutic Perspective of Taurine in Neurodegenerative Diseases.Biomolecules · 2020Review
- Computational Approaches to Prioritize Cancer Driver Missense Mutations.International journal of molecular sciences · 2018Review
- Review
- FoldX as Protein Engineering Tool: Better Than Random Based Approaches?Computational and structural biotechnology journal · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein stability is a requisite in the field of biotechnology, cell biology and drug design. To understand effects of amino acid substitutions, computational models are preferred to save time and expenses. As a systemically important, highly abundant, stable protein, the knowledge of Cu/Zn Superoxide dismutase1 (SOD1) is important, making it a suitable test case for genotype-phenotype correlation in understanding ALS. Here, we report performance of eight protein stability calculators (PoPMuSiC 3.1, I-Mutant 2.0, I-Mutant 3.0, CUPSAT, FoldX, mCSM, BeatMusic and ENCoM) against 54 experimental stability changes due to mutations of SOD1. Four different high-resolution structures were used to test structure sensitivity that may affect protein calculations. Bland-Altman plot was also used to assess agreement between stability analyses. Overall, PoPMuSiC and FoldX emerge as the best methods in this benchmark. The relative performance of all the eight methods was very much structure independent, and also displayed less structural sensitivity. We also analyzed patient's data in relation to experimental and computed protein stabilities for mutations of human SOD1. Correlation between disease phenotypes and stability changes suggest that the changes in SOD1 stability correlate with ALS patient survival times. Thus, the results clearly demonstrate the importance of protein stability in SOD1 pathogenicity.
Indexed as
Identifiers
What OpenQuestion holds
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.