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Statements

Subject Item
n2:RIV%2F61989592%3A15110%2F07%3A00004340%21RIV10-MSM-15110___
rdf:type
skos:Concept n17:Vysledek
dcterms:description
IgA1 in the circulation and glomerular deposits of patients with IgA nephropathy (IgAN) is aberrantly glycosylated; the hinge-region O-linked glycans are galactose-deficient. The circulating IgA1 of patients with Henoch-Schoenlein purpura nephritis (HSPN) has a similar defect. This aberrancy exposes N-acetylgalactosamine-containing neoepitopes recognized by naturally occurring IgG or IgA1 antibodies resulting in formation of immune complexes. IgA1 contains up to six O-glycosylation sites per heavy chain; it is not known whether the glycosylation defect occurs randomly or preferentially at specific sites. We sought to define the aberrant glycosylation of a galactose-deficient IgA1 myeloma protein and analyze the formation of the immune complexes and their biological activities. Supplementation of serum or cord-blood serum with this IgA1 protein resulted in formation of new IgA1 complexes. These complexes stimulated proliferation of cultured human mesangial cells, as did the naturally-occurring IgA1-con IgA1 in the circulation and glomerular deposits of patients with IgA nephropathy (IgAN) is aberrantly glycosylated; the hinge-region O-linked glycans are galactose-deficient. The circulating IgA1 of patients with Henoch-Schoenlein purpura nephritis (HSPN) has a similar defect. This aberrancy exposes N-acetylgalactosamine-containing neoepitopes recognized by naturally occurring IgG or IgA1 antibodies resulting in formation of immune complexes. IgA1 contains up to six O-glycosylation sites per heavy chain; it is not known whether the glycosylation defect occurs randomly or preferentially at specific sites. We sought to define the aberrant glycosylation of a galactose-deficient IgA1 myeloma protein and analyze the formation of the immune complexes and their biological activities. Supplementation of serum or cord-blood serum with this IgA1 protein resulted in formation of new IgA1 complexes. These complexes stimulated proliferation of cultured human mesangial cells, as did the naturally-occurring IgA1-con
dcterms:title
IgA Nephropathy and Henoch-Schoenlein Purpura Nephritis: Aberrant Glycosylation of IgA1, Formation of IgA1-Containing Immune Complexes, and Activation of Mesangial Cells IgA Nephropathy and Henoch-Schoenlein Purpura Nephritis: Aberrant Glycosylation of IgA1, Formation of IgA1-Containing Immune Complexes, and Activation of Mesangial Cells
skos:prefLabel
IgA Nephropathy and Henoch-Schoenlein Purpura Nephritis: Aberrant Glycosylation of IgA1, Formation of IgA1-Containing Immune Complexes, and Activation of Mesangial Cells IgA Nephropathy and Henoch-Schoenlein Purpura Nephritis: Aberrant Glycosylation of IgA1, Formation of IgA1-Containing Immune Complexes, and Activation of Mesangial Cells
skos:notation
RIV/61989592:15110/07:00004340!RIV10-MSM-15110___
n3:aktivita
n8:S
n3:aktivity
S
n3:dodaniDat
n10:2010
n3:domaciTvurceVysledku
n18:1587307
n3:druhVysledku
n7:D
n3:duvernostUdaju
n15:S
n3:entitaPredkladatele
n4:predkladatel
n3:idSjednocenehoVysledku
425420
n3:idVysledku
RIV/61989592:15110/07:00004340
n3:jazykVysledku
n5:eng
n3:klicovaSlova
IgA nephropathy; abberant glucosylation; immune complex
n3:klicoveSlovo
n11:abberant%20glucosylation n11:IgA%20nephropathy n11:immune%20complex
n3:kontrolniKodProRIV
[E40ACA452AC1]
n3:mistoVydani
Basel
n3:nazevZdroje
IgA Nephropathy Today. Contrib Nephrol.
n3:obor
n19:EC
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
6
n3:rokUplatneniVysledku
n10:2007
n3:tvurceVysledku
Yanagihara, Takeshi Raška, Milan Novák, Jan Moldoveanu, Zina Suzuki, Hitoshi Renfrow, Matthew
s:numberOfPages
256
n16:hasPublisher
Karger
n12:isbn
978-3-8055-8286-5
n14:organizacniJednotka
15110