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Title: B cell O-galactosyltransferase activity, and expression of O-glycosylation genes in bone marrow in IgA nephropathy
Authors: Buck, Katharine S.
Smith, Alice C.
Molyneux, Karen
El-Barbary, Hany
Feehally, John
Barratt, Jonathan
First Published: May-2008
Publisher: Nature Publishing Group
Citation: Kidney International, 2008, 73 (10), pp. 1128-1136
Abstract: In IgA nephropathy pathogenic IgA1 is likely derived from bone marrow cells and exhibits reduced O-galactosylation. Defective O-galactosylation may arise from compromised expression or function of the enzyme β-galactosyltransferase and/or its molecular chaperone (Cosmc). We measured B cell O-galactosylation activity and the relative gene expression of β-galactosyltransferase and Cosmc in peripheral blood and bone marrow taken from patientswith IgA nephropathy and controls. O-galactosylation activity was measured in peripheral and bone marrow cells controls by the incorporation of radiolabelled galactose into an asialo-mucin acceptor. Gene expression of β-galactosyltransferase and Cosmc was measured by real time PCR and related to that of the enzyme GalNAc-T2, which synthesizes the core O-glycan. Neither the B cell O-galactosylation activity nor the gene expression of the enzyme or chaperone were different between patients and controls. However, the relationships between the O-glycosylation of serum IgA1, galactosylation activity and β-galactosyltransferase gene expression showed different patterns in IgA nephropathy and controls. In IgA nephropathy, O-galactosylation activity correlated with β-galactosyltransferase gene expression, but not with IgA1 O-glycosylation, suggesting that factors other than the availability of β-galactosyltransferase or Cosmc are responsible for altered IgA1 O-glycosylation.
DOI Link: 10.1038/
ISSN: 0085-2538
Type: Article
Rights: This is the author's final draft of the paper published as Kidney International, 2008, 73 (10), pp. 1128-1136. The final version is available from Doi: 10.1038/
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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