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Sökning: WFRF:(Bakoush Omran) > (2010-2014) > Galectin-8 in IgA N...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00006149naa a2200541 4500
001oai:DiVA.org:liu-77098
003SwePub
008120504s2012 | |||||||||||000 ||eng|
009oai:lup.lub.lu.se:860108c0-08ba-4a73-a570-43118c1c03f5
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-770982 URI
0247 a https://doi.org/10.1007/s10875-011-9618-32 DOI
0247 a https://lup.lub.lu.se/record/22739742 URI
040 a (SwePub)liud (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Carlsson, Michaelu Lund University,Lunds universitet,Avdelningen för mikrobiologi, immunologi och glykobiologi - MIG,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Microbiology, Immunology and Glycobiology - MIG,Department of Laboratory Medicine,Faculty of Medicine4 aut0 (Swepub:lu)med-mcc
2451 0a Galectin-8 in IgA Nephritis: Decreased Binding of IgA by Galectin-8 Affinity Chromatography and Associated Increased Binding in Non-IgA Serum Glycoproteins
264 c 2011-12-16
264 1b Springer Verlag (Germany),c 2012
338 a electronic2 rdacarrier
500 a Funding Agencies|Swedish Research Council (Vetenskapsradet)|2008-3356|Swedish Foundation for Swedish Research|FFL4|Swedish Healthcare System (ALF)||Region Skane||
520 a Background Immunoglobulin A nephritis (IgAN) is the most common primary glomerulonephritis worldwide. It is caused by accumulation of IgA1-containing immune complexes in the kidney resulting in renal failure, which is thought to be due to altered glycosylation of IgA with a decrease of 2-3-sialylated galactosides (NeuAc alpha 2-3Gal). less thanbrgreater than less thanbrgreater thanPurpose The purpose of this study was to analyze whether altered glycosylation of IgA would lead to an altered binding to galectin-8, an endogenous lectin with strong affinity for 2-3-sialylated galactosides. Galectins are a family of beta-galactoside-binding proteins; by binding various glycoproteins, they play important roles in the regulation of cellular functions in inflammation and immunity. Hence, an altered binding of IgA to galectin-8 could lead to pathologic immune functions, such as glomerulonephritis. less thanbrgreater than less thanbrgreater thanMethods Affinity chromatography of serum glycoproteins on the human sialogalactoside-binding lectin galectin-8N permitted quantitation of bound and unbound fractions, including IgA. less thanbrgreater than less thanbrgreater thanResults Analysis of similar to 100 IgA nephritis sera showed that the galectin-8N unbound fraction of IgA increased compared to similar to 100 controls, consistent with the known loss of galactosylation. A subgroup of similar to 15% of the IgAN patients had a ratio of galectin-8 bound/unbound IgA andlt;0.09, not found for any of the controls. Unexpectedly, the galectin-8N-binding fraction of serum glycoproteins other than IgA increased in the sera of IgAN patients but not in controls, suggesting a previously unrecognized change in this disease. less thanbrgreater than less thanbrgreater thanConclusion This is the first study that relates a galectin, an endogenous lectin family, to IgA nephritis and thus should stimulate new avenues of research into the pathophysiology of the disease.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Immunologi inom det medicinska området0 (SwePub)301102 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Immunology in the medical area0 (SwePub)301102 hsv//eng
653 a IgA nephropathy
653 a galectin-8
653 a affinity chromatography
653 a NeuAc alpha 2-3Gal
653 a MEDICINE
653 a MEDICIN
7001 a Bakoush, Omranu Lund University,Lunds universitet,Njurmedicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Nephrology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,University of Lund Hospital4 aut0 (Swepub:lu)njur-oba
7001 a Tengroth, Lottau Lund University4 aut
7001 a Kilsgard, Olau Lund University4 aut
7001 a Malmstrom, Johanu Lund University4 aut
7001 a Hellmark, Thomasu Lund University,Lunds universitet,Njurmedicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Autoimmunitet och njursjukdomar,Forskargrupper vid Lunds universitet,Nephrology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Autoimmunity and kidney diseases,Lund University Research Groups,University of Lund Hospital4 aut0 (Swepub:lu)njur-the
7001 a Segelmark, Mårtenu Lund University,Lunds universitet,Linköpings universitet,Farmakologi,Hälsouniversitetet,Njurmedicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Nephrology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)njur-mse
7001 a Leffler, Hakonu Lund University,Lunds universitet,Avdelningen för mikrobiologi, immunologi och glykobiologi - MIG,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Microbiology, Immunology and Glycobiology - MIG,Department of Laboratory Medicine,Faculty of Medicine4 aut0 (Swepub:lu)mmb-hle
7102 a Avdelningen för mikrobiologi, immunologi och glykobiologi - MIGb Institutionen för laboratoriemedicin4 org
7730 t Journal of Clinical Immunologyd : Springer Verlag (Germany)g 32:2, s. 246-255q 32:2<246-255x 0271-9142x 1573-2592
8564 u https://liu.diva-portal.org/smash/get/diva2:524946/FULLTEXT01.pdfx primaryx Raw objecty fulltext:postprint
8564 u https://link.springer.com/content/pdf/10.1007%2Fs10875-011-9618-3.pdf
8564 u http://www.ncbi.nlm.nih.gov/pubmed/22173878?dopt=Abstracty FULLTEXT
8564 u http://dx.doi.org/10.1007/s10875-011-9618-3y FULLTEXT
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-77098
8564 8u https://doi.org/10.1007/s10875-011-9618-3
8564 8u https://lup.lub.lu.se/record/2273974

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