ArticleBiomedical engineering online2021
Dysregulation of alternative splicing is associated with the pathogenesis of ulcerative colitis.
Article in Biomedical engineering online, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- New Approach for Studying of Isoforms and High-Homology Proteins in Mammalian Cells.International journal of molecular sciences · 2023Article
- The regulatory role of alternative splicing in inflammatory bowel disease.Frontiers in immunology · 2023Review
- Cell Type-Specific Induction of Inflammation-Associated Genes in Crohn's Disease and Colorectal Cancer.International journal of molecular sciences · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough numerous risk loci for ulcerative colitis (UC) have been identified in the human genome, the pathogenesis of UC remains unclear. Recently, multiple transcriptomic analyses have shown that aberrant gene expression in the colon tissues of UC patients is associated with disease progression. A pioneering study also demonstrated that altered post-transcriptional regulation is involved in the progression of UC. Here, we provide a genome-wide analysis of alternative splicing (AS) signatures in UC patients. We analyzed three datasets containing 74 tissue samples from UC patients and identified over 2000 significant AS events.
resultsSkipped exon and alternative first exon were the two most significantly altered AS events in UC patients. The immune response-related pathways were remarkably enriched in the UC-related AS events. Genes with significant AS events were more likely to be dysregulated at the expression level.
conclusionsWe present a genomic landscape of AS events in UC patients based on a combined analysis of two cohorts. Our results indicate that dysregulation of AS may have a pivotal role in determining the pathogenesis of UC. In addition, our study uncovers genes with potential therapeutic implications for UC treatment.
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