ArticlePloS one2022
In silico functional and pathway analysis of risk genes and SNPs for type 2 diabetes in Asian population.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Identification and characterization of 13 gene families encoding enzymes involved in flavonoid biosynthesis in barley and their roles under abiotic stress.Scientific reports · 2026Article
- In silico functional, structural, and pathogenicity assessment of single nucleotide polymorphisms in the human SOX9 gene.Scientific reports · 2025Article
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- Molecular mechanisms of how black barley accumulates higher anthocyanins than blue barley following transcriptomic evaluation and expression analysis of key genes in anthocyanins biosynthesis pathway.Frontiers in plant science · 2025Article
- In Silico Functional and Structural Analysis of Non-synonymous Single Nucleotide Polymorphisms (nsSNPs) in Human Paired Box 4 Gene.Biochemical genetics · 2024Article
- Prediction and assessment of deleterious and disease causing nonsynonymous single nucleotide polymorphisms (nsSNPs) in humanHeliyon · 2024Article
- In silico functional, structural and pathogenicity analysis of missense single nucleotide polymorphisms in human MCM6 gene.Scientific reports · 2024Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes (T2D) has earned widespread recognition as a primary cause of death, disability, and increasing healthcare costs. There is compelling evidence that hereditary factors contribute to the development of T2D. Clinical trials in T2D have mostly focused on genes and single nucleotide polymorphisms (SNPs) in protein-coding areas. Recently, it was revealed that SNPs located in noncoding areas also play a significant impact on disease vulnerability. It is required for cell type-specific gene expression. However, the precise mechanism by which T2D risk genes and SNPs work remains unknown. We integrated risk genes and SNPs from genome-wide association studies (GWASs) and performed comprehensive bioinformatics analyses to further investigate the functional significance of these genes and SNPs. We identified four intriguing transcription factors (TFs) associated with T2D. The analysis revealed that the SNPs are engaged in chromatin interaction regulation and/or may have an effect on TF binding affinity. The Gene Ontology (GO) study revealed high enrichment in a number of well-characterized signaling pathways and regulatory processes, including the STAT3 and JAK signaling pathways, which are both involved in T2D metabolism. Additionally, a detailed KEGG pathway analysis identified two major T2D genes and their prospective therapeutic targets. Our findings underscored the potential functional significance of T2D risk genes and SNPs, which may provide unique insights into the disease's pathophysiology.
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