ArticleEMBO molecular medicine2018
Deficiency in intestinal epithelial O-GlcNAcylation predisposes to gut inflammation.
Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 62 citations in OpenAlex.
- O-GlcNAcylation regulates PPAR-driven metabolic programming in intestinal stem cells.bioRxiv : the preprint server for biology · 2026Article
- Functional shotgun metagenomic insights into gut microbial pathway and enzyme disruptions linking metabolism, affect, cognition, and suicidal ideation in major depressive disorder.Acta neuropsychiatrica · 2026Article
- Metabolic regulation of gut barrier integrity in IBD: protein, lipid, and carbohydrate pathways.Frontiers in nutrition · 2026Review
- Intestinal Mucin Glycosylation: Structural Regulation, Homeostasis Maintenance and Disease Association.Biomolecules · 2025Review
- FBXO31-mediated ubiquitination of OGT maintains O-GlcNAcylation homeostasis to restrain endometrial malignancy.Nature communications · 2025Article
- Biological characteristics, immune infiltration and drug prediction of PANoptosis related genes and possible regulatory mechanisms in inflammatory bowel disease.Scientific reports · 2025Article
- Targeted urinary metabolomics combined with machine learning to identify biomarkers related to central carbon metabolism for IBD.Frontiers in molecular biosciences · 2025Article
- Article
- B3GNT7 regulates mucin O-glycosylation to alleviate colonic inflammation.BMC gastroenterology · 2024Article
- Gut metabolic changes during pregnancy reveal the importance of gastrointestinal region in sample collection.Metabolomics : Official journal of the Metabolomic Society · 2024Article
- What we need to know about the germ-free animal models.AIMS microbiology · 2024Review
- Intestinal Barrier Function and Neurodegenerative Disease.CNS & neurological disorders drug targets · 2024Review
- Monogenic deficiency in murine intestinal Cdc42 leads to mucosal inflammation that induces crypt dysplasia.Genes & diseases · 2024Article
- Deletion of Smooth Muscle O-GlcNAc Transferase Prevents Development of Atherosclerosis in Western Diet-Fed Hyperglycemic ApoEInternational journal of molecular sciences · 2023Article
- Deglycosylation Differentially Regulates Weaned Porcine Gut Alkaline Phosphatase Isoform Functionality along the Longitudinal Axis.Pathogens (Basel, Switzerland) · 2023Article
- Role of glycolysis in inflammatory bowel disease and its associated colorectal cancer.Frontiers in endocrinology · 2023Review
- Genetic Ablation of the Nutrient Sensor Ogt in Endocrine Progenitors Is Dispensable for β-Cell Development but Essential for Maintenance of β-Cell Mass.Biomedicines · 2022Article
- Quercetin Alleviates Lipopolysaccharide-Induced Cell Damage and Inflammation via Regulation of the TLR4/NF-κB Pathway in Bovine Intestinal Epithelial Cells.Current issues in molecular biology · 2022Article
- Intestinal Epithelial STAT6 Activation Rescues the Defective Anti-Helminth Responses Caused byInternational journal of molecular sciences · 2022Article
- Protein O-GlcNAcylation and the regulation of energy homeostasis: lessons from knock-out mouse models.Journal of biomedical science · 2022Review
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
Post-translational modifications in intestinal epithelial cells (IECs) allow for precise control in intestinal homeostasis, the breakdown of which may precipitate the pathological damage and inflammation in inflammatory bowel disease. The O-linked β-N-acetylglucosamine (O-GlcNAc) modification on intracellular proteins controls diverse biological processes; however, its roles in intestinal homeostasis are still largely unexplored. Here, we found that levels of protein O-GlcNAcylation and the expression of O-GlcNAc transferase (OGT), the enzyme adding the O-GlcNAc moiety, were reduced in IECs in human IBD patients. Deletion of OGT specifically in IECs resulted in disrupted epithelial barrier, microbial dysbiosis, Paneth cell dysfunction, and intestinal inflammation in mice. Using fecal microbiota transplantation in mice, we demonstrated that microbial dysbiosis although was insufficient to induce spontaneous inflammation but exacerbated chemical-induced colitis. Paneth cell-specific deletion of OGT led to Paneth cell dysfunction, which might predispose mice to chemical-induced colitis. On the other hand, the augmentation of O-GlcNAc signaling by inhibiting O-GlcNAcase, the enzyme removing O-GlcNAcylation, alleviated chemical-induced colitis. Our data reveal that protein O-GlcNAcylation in IECs controls key regulatory mechanisms to maintain mucosal homeostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.