ArticleJournal of applied genetics2026
Computational analysis of MYC gene variants: structural and functional impact of non-synonymous SNPs.
Article in Journal of applied genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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
1 citing paper in PubMed.
- Discovery of Macrocyclic Peptide Inhibitors Targeting MYC Oncoprotein via mRNA Display.Pharmaceuticals (Basel, Switzerland) · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
The MYC proto-oncogene encodes a basic helix-loop-helix leucine zipper (HLH-LZ) transcription factor, acting as a master regulator of genes involved in cellular proliferation, differentiation, and immune surveillance. Dysregulation of MYC is implicated in over 70% of human cancers, driving oncogenic processes through altered gene expression and disrupted cellular functions. Non-synonymous single nucleotide polymorphisms (nsSNPs) within coding regions can significantly impact protein structure and function, leading to abnormal cellular behaviours. This study employed 29 in silico tools to systematically evaluate the deleteriousness of nsSNPs within the MYC gene. These tools assessed the variants' effects on protein structure, disease association, functional domains, and post-translational modification sites. This study investigated if these variants may disrupt protein-protein interactions, critical for MYC's oncogenic roles and normal cellular functions. Our analysis identified 21 nsSNPs that were predicted to be deleterious and pathogenic. These variants correspond to residues D63H, D63Y, P74L, P75L, N375D, N375I, E378K, E378Q, E378A, E378G, E378V, R379P, R381K, R381T, R382W, L392P, R393C, R393H, R393P, L411H, and L411P. Stability assessments indicated that these variants could destabilise the MYC protein. None of the variants affected post-translational modifications. Protein-protein interaction and docking analysis revealed that variants within bHLH and LZ domains may disrupt MYC/MAX binding, potentially impacting MYC's oncogenic activity and transcriptional regulation. This computational assessment enhances our understanding of genetic variations within the MYC gene and prioritises candidate nsSNPs for experimental validation and therapeutic exploration.
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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.