ArticleThe Journal of biological chemistry2010
Sulfation of colonic mucins by N-acetylglucosamine 6-O-sulfotransferase-2 and its protective function in experimental colitis in mice.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 123 citations in OpenAlex.
- The Association of Gut Microbiota With TRPM7 Genotype, Colorectal Polyps, and Magnesium.The Journal of nutrition · 2025Trial
- Bacterial constipation: Mucin-degrading intestinal commensal bacteria cause constipation.Gut microbes · 2026Article
- Fluorogenic Coupled Assays Reveal Catalytic Properties, Inhibition Constants and Cellular Location of Mucin-Active Carbohydrate Sulfatases.Angewandte Chemie (International ed. in English) · 2026Article
- Dietary sulfur amino acids enhance anti-tumor immunity in colon cancer via an NKT cell-XCL1-cDC1 circuit.Immunity · 2026Article
- B3GNT7 regulates mucin glycosylation and protects against colitis and infection.bioRxiv : the preprint server for biology · 2026Article
- Intestinal Mucin Glycosylation: Structural Regulation, Homeostasis Maintenance and Disease Association.Biomolecules · 2025Review
- Taurine prevents mitochondrial dysfunction and protects mitochondria from reactive oxygen species and deuterium toxicity.Amino acids · 2025Review
- Eosinophils in inflammatory bowel disease pathogenesis: an ROS-centric view.Frontiers in allergy · 2025Article
- Review
- Article
- Sulfoconjugation of protein peptides and glycoproteins in physiology and diseases.Pharmacology & therapeutics · 2023Review
- A novel monoclonal antibody against 6-sulfo sialyl Lewis x glycans attenuates murine allergic rhinitis by suppressing Th2 immune responses.Scientific reports · 2023Article
- N-acetylglucosamine-6-O sulfation on intestinal mucins prevents obesity and intestinal inflammation by regulating gut microbiota.JCI insight · 2023Article
- Organoids transplantation as a new modality to design epithelial signature to create a membrane-protective sulfomucin-enriched segment.Journal of gastroenterology · 2023Article
- Mucin O-glycan-microbiota axis orchestrates gut homeostasis in a diarrheal pig model.Microbiome · 2022Article
- How microbial glycosyl hydrolase activity in the gut mucosa initiates microbial cross-feeding.Glycobiology · 2022Review
- Finding the sweet spot: glycosylation mediated regulation of intestinal inflammation.Mucosal immunology · 2022Review
- Article
- Highly sialylated mucin-type glycopeptide from porcine intestinal mucosa after heparin extraction: O-glycan profiling and immunological activity evaluation.Glycoconjugate journal · 2021Article
- Intestinal Sulfation Is Essential to Protect Against Colitis and Colonic Carcinogenesis.Gastroenterology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
N-Acetylglucosamine 6-O-sulfotransferase-2 (GlcNAc6ST-2) catalyzes the sulfation of mucin-like glycoproteins, which function as ligands for a lymphocyte homing receptor, L-selectin, in the lymph node high endothelial venules (HEVs). We previously showed that GlcNAc6ST-2 is expressed not only in lymph node HEVs but also in the colonic epithelial cells in mice. Here we investigated the regulatory mechanism and physiological significance of colonic expression of GlcNAc6ST-2 in mice. Treatment of a mouse colonic epithelial cell line with butyrate, a short-chain fatty acid produced by anaerobic bacteria, induced GlcNAc6ST-2 expression in the presence of epidermal growth factor. Administration of butyrate in the drinking water stimulated GlcNAc6ST-2 expression in the mouse intestine, indicating that butyrate could serve as a regulatory molecule for the GlcNAc6ST-2 expression in vivo. Immunohistochemical analysis indicated that the sulfation of colonic mucins was greatly diminished in GlcNAc6ST-2-deficient mice. Liquid chromatography coupled to electrospray ionization tandem mass spectrometry of the colonic-mucin O-glycans from wild-type and GlcNAc6ST-2-deficient mice showed that GlcNAc-6-O-sulfation was the predominant sulfate modification of these mucins, and it was exclusively mediated by GlcNAc6ST-2. After colitis induction by dextran sulfate sodium, significantly more leukocyte infiltration was observed in the colon of GlcNAc6ST-2-deficient mice than in that of wild-type mice, indicating that the sulfation of colonic mucins by GlcNAc6ST-2 has a protective function in experimental colitis. These findings indicate that GlcNAc6ST-2, whose expression is regulated by butyrate, is a major sulfotransferase in the biosynthesis of sulfomucins in the mouse colon, where they serve as a mucosal barrier against colonic inflammation.
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Registered trials
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