ArticleMedicine2022
Investigation of hub genes involved in Turner syndrome using biological informatics methods.
Article in Medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Integrative Bioinformatics Analyses Reveal X Chromosome Inactivation Escape Genes Dosage Dysregulation Is the Primary Contributor to Turner Syndrome.Iranian journal of biotechnology · 2026Article
- Review
- Identification of genetic factors underlying severe retinopathy of prematurity in preterm infants.Molecular vision · 2025Article
- Hyperglycemia in Turner syndrome: Impact, mechanisms, and areas for future research.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aimed to explore candidate genes and their potential interaction mechanism critical to the pathophysiology of Turner syndrome by using the Gene Expression Omnibus database.
methodsGSE58435 data set was obtained by querying the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were screened using R and subsequently annotated by Gene Ontology. Functional enrichment analysis was performed based on the Kyoto Encyclopedia of Genes and Genomes database for annotation, visualization, and integrated discovery. A protein-protein interaction network of different genes was constructed based on the STRING database, in which hub genes were explored through Cytoscape software. The expression of the hub genes was verified by analyzing the gene expression in the GSE46687 data set.
resultsA total of 733 differential genes were identified. These differentially expressed genes were significantly enriched in nucleoplasm and nucleus. Their molecular function was concentrated on DNA binding and transcription, coronary artery, and adipose tissue development. According to the annotation of Kyoto Encyclopedia of Genes and Genomes, the identified DEGs were mainly enriched in inflammatory mediator regulation of TRP channels, osteoclast differentiation. A total of 10 hub genes (HIST1H2BA, TRIM71, HIST1H2BB, HIST1H4D, TNF, TP53BP1, CDCA8, EGF, HMG20B, and BCL9) were identified from the constructed protein-protein interaction network. These genes were discovered to be highly expressed in osteoclasts, ovaries, digestive tract, blood, and lymphatic tissues through the online application of human protein atlas.
conclusionIn this study, 733 DEGs and 10 hub genes were identified. They would be new candidate targets in Turner syndrome.
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