ArticleBiology2022
Predicting Deleterious Non-Synonymous Single Nucleotide Polymorphisms (nsSNPs) of
Article in Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Computational screening of oncogenic genetic variations in tumor suppressor proteins driving gastric cancer pathogenesis.PloS one · 2026Article
- Editorial Note: Pathogenic KRAS variants disrupt structure and dynamics: Insights from integrated computational analyses.PloS one · 2026Article
- Computational Identification and Functional Analysis of Potentially Pathogenic nsSNPs in the NLRP3 Gene Linked to Alzheimer's Disease.Cell biochemistry and biophysics · 2025Article
- Exploring the impact of deleterious missense nonsynonymous single nucleotide polymorphisms in the DRD4 gene using computational approaches.Scientific reports · 2025Article
- Comprehensive computational analysis of deleterious nsSNPs inMolecular biology research communications · 2025Article
- Exploring the Structural and Functional Consequences of Deleterious Missense Nonsynonymous SNPs in theJournal of personalized medicine · 2024Article
- Identification and analysis of oncogenic non-synonymous single nucleotide polymorphisms in the human NRAS gene: An exclusive in silico study.Journal, genetic engineering & biotechnology · 2024Article
- In-silico identification of deleterious non-synonymous SNPs of TBX1 gene: Functional and structural impact towards 22q11.2DS.PloS one · 2024Article
- Computational Exploration of Single-Nucleotide Polymorphisms in the Human hRAS Gene: Implications and Insights.Cureus · 2024Article
- Predicting the effects of rare genetic variants on oncogenic signaling pathways: A computational analysis of HRAS protein function.Frontiers in chemistry · 2023Article
Corrections and comments
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Authors and funding
9 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Harvey rat sarcoma (HRAS) proto-oncogene belongs to the RAS family and is one of the pathogenic genes that cause cancer. Deleterious nsSNPs might have adverse consequences at the protein level. This study aimed to investigate deleterious nsSNPs in the HRAS gene in predicting structural alterations associated with mutants that disrupt normal protein-protein interactions. Functional and structural analysis was employed in analyzing the HRAS nsSNPs. Putative post-translational modification sites and the changes in protein-protein interactions, which included a variety of signal cascades, were also investigated. Five different bioinformatics tools predicted 33 nsSNPs as "pathogenic" or "harmful". Stability analysis predicted rs1554885139, rs770492627, rs1589792804, rs730880460, rs104894227, rs104894227, and rs121917759 as unstable. Protein-protein interaction analysis revealed that HRAS has a hub connecting three clusters consisting of 11 proteins, and changes in HRAS might cause signal cascades to dissociate. Furthermore, Kaplan-Meier bioinformatics analyses indicated that the HRAS gene deregulation affected the overall survival rate of patients with breast cancer, leading to prognostic significance. Thus, based on these analyses, our study suggests that the reported nsSNPs of HRAS may serve as potential targets for different proteomic studies, diagnoses, and therapeutic interventions focusing on cancer.
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