ArticleThe Biochemical journal2002
Intestinal mucins from cystic fibrosis mice show increased fucosylation due to an induced Fucalpha1-2 glycosyltransferase.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Cystic fibrosis and inflammatory bowel disease: parallels in gut physiology and microbiota.Journal of bacteriology · 2025Review
- Goblet cells: guardians of gut immunity and their role in gastrointestinal diseases.eGastroenterology · 2024Article
- Targeting protein glycosylation to regulate inflammation in the respiratory tract: novel diagnostic and therapeutic candidates for chronic respiratory diseases.Frontiers in immunology · 2023Review
- Disease-associated dysbiosis and potential therapeutic role of Akkermansia muciniphila, a mucus degrading bacteria of gut microbiome.Folia microbiologica · 2022Review
- Exploring the impact of intestinal ion transport on the gut microbiota.Computational and structural biotechnology journal · 2021Review
- Impaired Intestinal Farnesoid X Receptor Signaling in Cystic Fibrosis Mice.Cellular and molecular gastroenterology and hepatology · 2020Article
- Intestinal Muc2 mucin O-glycosylation is affected by microbiota and regulated by differential expression of glycosyltranferases.Glycobiology · 2017Article
- Normalization of Host Intestinal Mucus Layers Requires Long-Term Microbial Colonization.Cell host & microbe · 2015Article
- Intestinal fucose as a mediator of host-microbe symbiosis.Journal of immunology (Baltimore, Md. : 1950) · 2015Review
- Rapid fucosylation of intestinal epithelium sustains host-commensal symbiosis in sickness.Nature · 2014Article
- Serum amyloid A is a retinol binding protein that transports retinol during bacterial infection.eLife · 2014Article
- γδ T-cell-deficient mice show alterations in mucin expression, glycosylation, and goblet cells but maintain an intact mucus layer.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Ion mobility mass spectrometry analysis of isomeric disaccharide precursor, product and cluster ions.Rapid communications in mass spectrometry : RCM · 2013Article
- Loss of NHE3 alters gut microbiota composition and influences Bacteroides thetaiotaomicron growth.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- A refined palate: bacterial consumption of host glycans in the gut.Glycobiology · 2013Review
- Studies of mucus in mouse stomach, small intestine, and colon. III. Gastrointestinal Muc5ac and Muc2 mucin O-glycan patterns reveal a regiospecific distribution.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Carbohydrate structure characterization by tandem ion mobility mass spectrometry (IMMS)2.Analytical chemistry · 2013Article
- Detailed O-glycomics of the Muc2 mucin from colon of wild-type, core 1- and core 3-transferase-deficient mice highlights differences compared with human MUC2.Glycobiology · 2012Article
- Bicarbonate and functional CFTR channel are required for proper mucin secretion and link cystic fibrosis with its mucus phenotype.The Journal of experimental medicine · 2012Article
- Bacteroides in the infant gut consume milk oligosaccharides via mucus-utilization pathways.Cell host & microbe · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
In gene-targeted mouse models for cystic fibrosis (CF), the disease is mainly manifested by mucus obstruction in the intestine. To explore the mucus composition, mucins insoluble and soluble in 6 M guanidinium chloride were purified by three rounds of isopycnic ultracentrifugation from the small and large intestines of CF mice (Cftr(m1UNC)/Cftr(m1UNC)) and compared with wild-type mice. The amino acid composition was typical of that for mucins and showed increased amounts of the insoluble (2.5-fold increase) and soluble (7-fold increase) mucins in the small intestine of the CF mice compared with wild-type mice. Mucins from the large intestine of both wild-type and CF mice showed a high but constant level of fucosylation. In contrast, the insoluble and soluble mucins of the small intestine in CF mice revealed a large increase in fucose, whereas those of wild-type mice contained only small amounts of fucose. This increased fucosylation was analysed by releasing the O-linked oligosaccharides followed by GC-MS. NMR spectroscopy revealed that the increased fucosylation was due to an increased expression of blood group H epitopes (Fucalpha1-2Gal-). Northern-blot analysis, using a probe for the murine Fucalpha1-2 fucosyltransferase (Fut2), showed an up-regulation of this mRNA in the small intestine of the CF mice, suggesting that this enzyme is responsible for the observed increase in blood group H-type glycosylation. The reason for this up-regulation could be a direct or indirect effect of a non-functional CF transmembrane conductance regulator (CFTR) caused by the absence of CFTR channel.
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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.