ArticlePloS one2023
Impact of highly deleterious non-synonymous polymorphisms on GRIN2A protein's structure and function.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Computational analysis and validation of UGT1A1/4 missense variants impacting tecovirimat metabolism in monkeypox patients.Frontiers in systems biology · 2026Article
- Article
- Exploring the impact of deleterious missense nonsynonymous single nucleotide polymorphisms in the DRD4 gene using computational approaches.Scientific reports · 2025Article
- In-silico screening and analysis of missense SNPs in human CYP3A4/5 affecting drug-enzyme interactions of FDA-approved COVID-19 antiviral drugs.Scientific reports · 2025Article
- Review
- Unraveling the function and structure impact of deleterious missense SNPs in the human OX1R receptor by computational analysis.Scientific reports · 2024Article
- Investigation of pathogenic germline variants in gastric cancer and development of "GasCanBase" database.Cancer reports (Hoboken, N.J.) · 2023Article
- Computational analysis of the functional and structural impact of the most deleterious missense mutations in the human Protein C.PloS one · 2023Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GRIN2A is a gene that encodes NMDA receptors found in the central nervous system and plays a pivotal role in excitatory synaptic transmission, plasticity and excitotoxicity in the mammalian central nervous system. Changes in this gene have been associated with a spectrum of neurodevelopmental disorders such as epilepsy. Previous studies on GRIN2A suggest that non-synonymous single nucleotide polymorphisms (nsSNPs) can alter the protein's structure and function. To gain a better understanding of the impact of potentially deleterious variants of GRIN2A, a range of bioinformatics tools were employed in this study. Out of 1320 nsSNPs retrieved from the NCBI database, initially 16 were predicted as deleterious by 9 tools. Further assessment of their domain association, conservation profile, homology models, interatomic interaction, and Molecular Dynamic Simulation revealed that the variant I463S is likely to be the most deleterious for the structure and function of the protein. Despite the limitations of computational algorithms, our analyses have provided insights that can be a valuable resource for further in vitro and in vivo research on GRIN2A-associated diseases.
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