To the top

Page Manager: Webmaster
Last update: 9/11/2012 3:13 PM

Tell a friend about this page
Print version

Intestinal mucins from cy… - University of Gothenburg, Sweden Till startsida
To content Read more about how we use cookies on

Intestinal mucins from cystic fibrosis mice show increased fucosylation due to an induced Fucalpha1-2 glycosyltransferase.

Journal article
Authors Kristina A Thomsson
Marina Hinojosa-Kurtzberg
Karin A Axelsson
Steven E Domino
John B Lowe
Sandra J Gendler
Gunnar C. Hansson
Published in The Biochemical journal
Volume 367
Issue Pt 3
Pages 609-16
ISSN 0264-6021
Publication year 2002
Published at Institute of Medical Biochemistry
Pages 609-16
Language en
Keywords Animals, Blotting, Northern, Chromatography, Gas, Cystic Fibrosis, metabolism, Fucose, metabolism, Glycosyltransferases, metabolism, Intestines, metabolism, Mice, Mucins, chemistry, isolation & purification, metabolism, Nuclear Magnetic Resonance, Biomolecular
Subject categories Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)


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.

Page Manager: Webmaster|Last update: 9/11/2012

The University of Gothenburg uses cookies to provide you with the best possible user experience. By continuing on this website, you approve of our use of cookies.  What are cookies?

Denna text är utskriven från följande webbsida:
Utskriftsdatum: 2020-08-07