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Intestinal mucins f...
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Thomsson, Kristina A,1969Gothenburg University,Göteborgs universitet,Institutionen för medicinsk och fysiologisk kemi,Institute of Medical Biochemistry
(författare)
Intestinal mucins from cystic fibrosis mice show increased fucosylation due to an induced Fucalpha1-2 glycosyltransferase.
- Artikel/kapitelEngelska2002
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LIBRIS-ID:oai:gup.ub.gu.se/106583
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https://gup.ub.gu.se/publication/106583URI
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https://doi.org/10.1042/BJ20020371DOI
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
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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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Hinojosa-Kurtzberg, Marina
(författare)
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Axelsson, Karin AGothenburg University,Göteborgs universitet,Institutionen för medicinsk och fysiologisk kemi,Institute of Medical Biochemistry
(författare)
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Domino, Steven E
(författare)
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Lowe, John B
(författare)
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Gendler, Sandra J
(författare)
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Hansson, Gunnar C.,1951Gothenburg University,Göteborgs universitet,Institutionen för medicinsk och fysiologisk kemi,Institute of Medical Biochemistry(Swepub:gu)xhagun
(författare)
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Göteborgs universitetInstitutionen för medicinsk och fysiologisk kemi
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:The Biochemical journal367:Pt 3, s. 609-160264-6021
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