ArticleBiochemistry and biophysics reports2025
Comprehensive in silico characterization of nonsynonymous SNPs in the human ezrin (EZR) gene and their role in disease pathogenesis.
Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- A comprehensive in silico investigation into the deleterious nonsynonymous single nucleotide polymorphisms of the human transcription factor EB (TFEB) gene and their predicted association with cancer.Journal, genetic engineering & biotechnology · 2026Article
- Comprehensive analysis of the deleterious nonsynonymous, non-coding SNPs and cancer variants of human aldo-keto reductase type 1 (AKR1C1) protein and their probable association with disease risk and progression: a computational study.Biochemistry and biophysics reports · 2026Article
- Article
- Pulsed electromagnetic field stimulation subtly modulates doxorubicin sensitivity in a spheroid co-culture model of osteosarcoma.Scientific reports · 2025Article
- Regulatory role of ezrin in esophageal cancer progression via the PI3K-AKT signaling pathway.Hereditas · 2025Article
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Authors and funding
7 authors.
Funding
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Abstract
Ezrin (EZR) is a crucial linker between the actin cytoskeleton and the plasma membrane. It interacts with proteins involved in cancer-related signaling pathways. To assess the impact of nonsynonymous single nucleotide polymorphisms (nsSNPs) on EZR structure and function, we employed bioinformatics tools (SIFT, PolyPhen-2, PROVEAN, PhD-SNP, SNPs&GO, SuSPect, and FATHMM) and identified deleterious variants. Stability analyses using MUpro, mCSM, I-Mutant 2.0, and DynaMut2 revealed six destabilizing nsSNPs (F240S, H288D, I248T, L59Q, L125S, and L225P). Structural modeling using HOPE, MutPred2, AlphaFold, Swiss-Model, and protein-protein docking using HADDOCK 2.4 assessed the impact on the EZR-EBP50 complex. Binding free energy calculations, salt bridge analysis, and interface residue mapping further confirmed that the L225P, F240S, and I248T mutations significantly impaired EZR-EBP50 interaction, potentially disrupting key signaling pathways. Molecular dynamics simulations indicated that mutant EZR proteins exhibited reduced stability, flexibility, and hydrogen bonding. This first comprehensive in silico analysis of EZR highlights pathogenic nsSNPs that may contribute to disease progression. These findings provide a foundation for experimental validation and may inform targeted therapies for EZR-related pathologies.
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