ArticleThe Journal of clinical investigation2011
Loss of intestinal core 1-derived O-glycans causes spontaneous colitis in mice.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 219 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
219 citing papers in PubMed, 357 citations in OpenAlex.
- Article
- MUC17 and the intestinal glycocalyx: structure, regulation, and barrier function in health and disease.Bioscience reports · 2026Review
- The anti-diarrheal role of iron in piglets: Regulation of colonic goblet cell function.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Gut mucosal barrier: the frontline of bidirectional regulation of the gut-X axis.Medical review (2021) · 2026Review
- Cancer-associated alterations in O-GalNAc glycosylation.Glycobiology · 2026Review
- Deciphering themSphere · 2026Article
- ST8Sia6-dependent glycosylation restrains gut inflammation and pathogenic TCell reports · 2026Article
- B3GNT7 regulates mucin glycosylation and protects against colitis and infection.bioRxiv : the preprint server for biology · 2026Article
- Mucosal glycans: key drivers of the development of inflammatory bowel disease and a potential new therapeutic target.Nature reviews. Gastroenterology & hepatology · 2026Review
- Deletion of Core 1 β3GalT-specific molecular chaperone (Cosmc) in murine intestinal epithelia leads to major alterations in glycocalyx and tumorigenesis.The Journal of biological chemistry · 2026Article
- Novel Perspectives on the Relationship Between the Gastrointestinal Mucus Barrier and Soybean Agglutinin.Cells · 2026Review
- Hemocyte-secreted papilin bearing mucin-typeiScience · 2026Article
- Intestinal Mucin Glycosylation: Structural Regulation, Homeostasis Maintenance and Disease Association.Biomolecules · 2025Review
- Akkermansia muciniphila-Derived N-Acetylspermidine Modulates the Localization of Intestinal α1,2-Fucosylated Proteins to Maintain Gut Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neuromuscular Defects in aBiomolecules · 2025Article
- Advances in Understanding Intestinal Homeostasis: Lessons from Inflammatory Bowel Disease and Monogenic Intestinal Disorder Pathogenesis.International journal of molecular sciences · 2025Review
- Understanding how foods and enteral feedings influence the gut microbiome.Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition · 2025Review
- Loss of GalNAc-T14 links O-glycosylation defects to alterations in B cell homing in IgA nephropathy.The Journal of clinical investigation · 2025Article
- Overexpression of Tn antigen induces chronic pancreatitis in mice.Scientific reports · 2025Article
- Gut Goo: Physiology, Diet, and Therapy of Intestinal Mucus and Biofilms in Gastrointestinal Health and Disease.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2025Review
159 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Mucin-type O-linked oligosaccharides (O-glycans) are primary components of the intestinal mucins that form the mucus gel layer overlying the gut epithelium. Impaired expression of intestinal O-glycans has been observed in patients with ulcerative colitis (UC), but its role in the etiology of this disease is unknown. Here, we report that mice with intestinal epithelial cell-specific deficiency of core 1-derived O-glycans, the predominant form of O-glycans, developed spontaneous colitis that resembled human UC, including massive myeloid infiltrates and crypt abscesses. The colitis manifested in these mice was also characterized by TNF-producing myeloid infiltrates in colon mucosa in the absence of lymphocytes, supporting an essential role for myeloid cells in colitis initiation. Furthermore, induced deletion of intestinal core 1-derived O-glycans caused spontaneous colitis in adult mice. These data indicate a causal role for the loss of core 1-derived O-glycans in colitis. Finally, we detected a biosynthetic intermediate typically exposed in the absence of core 1 O-glycan, Tn antigen, in the colon epithelium of a subset of UC patients. Somatic mutations in the X-linked gene that encodes core 1 β1,3-galactosyltransferase-specific chaperone 1 (C1GALT1C1, also known as Cosmc), which is essential for core 1 O-glycosylation, were found in Tn-positive epithelia. These data suggest what we believe to be a new molecular mechanism for the pathogenesis of UC.
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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.