ArticlePloS one2026
Pathogenic KRAS variants disrupt structure and dynamics: Insights from integrated computational analyses.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- The Role of KRAS in Non-Small Cell Lung Cancer: From Molecular Background to Precision Medicine.International journal of molecular sciences · 2026Review
- Editorial Note: Pathogenic KRAS variants disrupt structure and dynamics: Insights from integrated computational analyses.PloS one · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKRAS is among the most frequently mutated oncogenes in pancreatic, colorectal, and lung cancers, yet the structural and dynamic mechanisms by which specific coding variants alter its function remain poorly understood. This study employs an extensive in-silico protocol to identify the most detrimental non-synonymous single nucleotide polymorphisms (nsSNPs) within the KRAS gene.
objectiveTo identify and describe pathogenic non-synonymous single nucleotide polymorphisms (nsSNPs) in KRAS and elucidate their atomistic effects on structure, stability, and potential oncogenic initiation.
methodsA total of 173 nsSNPs were screened operating an integrated computational workflow combining pathogenicity prediction, evolutionary conservation assay, high-resolution structural modeling, molecular docking, atomistic molecular dynamics simulations, post-translational modification mapping, and protein-protein interaction assessment.
resultsFour high-impact variants (L79P, A130P, G138E, and F141L) were determined as the most deleterious. Simulations revealed distinct perturbations in conformational stability (RMSD), residue flexibility (RMSF), hydrogen bonding patterns, and binding energetics compared with the wild type, signifying mutation-induced destabilization and potential impairment of KRAS regulatory function. Notably, these variants are primarily associated with colorectal, pancreatic, and lung cancers, underscoring their clinical significance.
conclusionThis integrative examination provides mechanistic insightinto how specific KRAS variations may prompt oncogenic activation. The identified alterations represent high-priority targets for experimental confirmation, illuminating the power of computational techniquesin linking sequence variationand functional consequence in cancer biology.
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