PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24918438-1 2014 Patients with IgA nephropathy (IgAN) have elevated circulating levels of IgA1 with some O-glycans consisting of galactose (Gal)-deficient N-acetylgalactosamine (GalNAc) with or without N-acetylneuraminic acid (NeuAc). N-Acetylneuraminic Acid 185-208 IGAN1 Homo sapiens 31-35 24918438-5 2014 Distribution of NeuAc in IgA1 O-glycans may play an important role in the pathogenesis of IgAN. N-Acetylneuraminic Acid 16-21 IGAN1 Homo sapiens 90-94 24918438-1 2014 Patients with IgA nephropathy (IgAN) have elevated circulating levels of IgA1 with some O-glycans consisting of galactose (Gal)-deficient N-acetylgalactosamine (GalNAc) with or without N-acetylneuraminic acid (NeuAc). N-Acetylneuraminic Acid 210-215 IGAN1 Homo sapiens 31-35 18046671-11 2007 With regards to the individual residues, we found that IgAN sera contained less sugar and galactose and sialic acid moieties than sera from control subjects, was reduced in IgAN sera, while terminal N-acetylgalactosamine levels were higher when compared with normal serum. N-Acetylneuraminic Acid 104-115 IGAN1 Homo sapiens 55-59 22802576-4 2012 In patients with IgAN, circulating IgA1 molecules have an aberrant structure of O-glycans in the hinge region, which is characterized by abbreviated glycans composed of N-acetylgalactosamine, with or without sialic acid. N-Acetylneuraminic Acid 208-219 IGAN1 Homo sapiens 17-21 17913589-8 2007 Alpha 2, 6 SA level in patients with IgAN was lower than that in healthy controls (0.92+/-0.14 vs. 0.98+/-0.12, P=0.001) and non-IgAN glomerulonephritis (0.92+/-0.14 vs. 1.00+/-0.18, n=53, P=0.001). N-Acetylneuraminic Acid 11-13 IGAN1 Homo sapiens 37-41 23398317-6 2013 A significant increase in N-acetylgalactosamine (GalNAc) in terminal position (p = 0.02) observed in some of the IgAN patients, became more pronounced when sialic acid was removed from IgA1, indicating enhanced expression of alpha-2,6-sialyltransferase in patients compared with controls (p < 0.0001). N-Acetylneuraminic Acid 156-167 IGAN1 Homo sapiens 113-117 23098908-1 2012 Aberrant O-glycosylation in the hinge region of serum IgA is suggested to be involved in the pathogenesis of IgA nephropathy (IgAN), because the hypoglycosylation including N-acetylneuraminic acid or galactose has been reported in the mucin-type O-glycan of the hinge portion (HP) of IgA deposited in the IgAN patients" kidney. N-Acetylneuraminic Acid 173-196 IGAN1 Homo sapiens 126-130 17480010-2 2007 Increasing evidence has implicated that aberrant glycosylation of IgA1 molecules, including alpha2,6 sialic acid defects, are involved in the pathogenesis of IgAN. N-Acetylneuraminic Acid 101-112 IGAN1 Homo sapiens 158-162 17480010-10 2007 Furthermore, the ADG haplotype was associated with the deficient degrees of alpha2,6 sialic acid of IgA1 molecules in IgAN patients (r=0.408, p=0.0035). N-Acetylneuraminic Acid 85-96 IGAN1 Homo sapiens 118-122 11835525-14 2002 The negative charge from sialic acid may also favor mesangial deposition of macromolecular lambda-IgA1 in IgAN. N-Acetylneuraminic Acid 25-36 IGAN1 Homo sapiens 106-110 15086888-1 2004 Immunoglobulin A nephropathy (IgAN) patients exhibit circulating IgA1 with reduced galactose (Gal) and/or sialic acid (Neu5Ac) and increased exposure of N-acetylgalactosamine (GalNAc). N-Acetylneuraminic Acid 106-117 IGAN1 Homo sapiens 30-34 15086888-1 2004 Immunoglobulin A nephropathy (IgAN) patients exhibit circulating IgA1 with reduced galactose (Gal) and/or sialic acid (Neu5Ac) and increased exposure of N-acetylgalactosamine (GalNAc). N-Acetylneuraminic Acid 119-125 IGAN1 Homo sapiens 30-34 11835525-13 2002 This unusual glycosylation and sialylation pattern of the lambda-IgA1 may have important implications for the pathogenesis of IgAN, as both the masking effect of sialic acid on galactose and the reduced galactosylation will hinder the clearance of macromolecular lambda-IgA1 by asialoglycoprotein receptor of hepatocytes. N-Acetylneuraminic Acid 162-173 IGAN1 Homo sapiens 126-130 11518779-8 2001 Patients with IgAN displayed increased levels of IgA glycoforms exposing sialic acid in alpha2,6 linkage with N-acetylgalactosamine (Neu5Acalpha2,6GalNAc) (P < 0.02) and GalNAc (P < 0.05), indicating truncation of O-linked glycans of IgA1. N-Acetylneuraminic Acid 73-84 IGAN1 Homo sapiens 14-18 10777713-5 2000 The results obtained clearly showed a decrease of GalNAc, Gal, and sialic acid in IgAN compared with non-IgAN and normal controls, and those strongly suggested the possibility that the decreased galactosylation and sialylation of the IgA1 hinge result in its glomerular deposition in IgAN. N-Acetylneuraminic Acid 67-78 IGAN1 Homo sapiens 82-86 9989767-10 1999 This abnormality of IgA1 could bear considerable implication on the pathogenesis of IgAN, because the masking effect of sialic acid may hinder the clearance of polymeric IgA1 by the asialoglycoprotein receptor (ASGP-R) of the liver cells. N-Acetylneuraminic Acid 120-131 IGAN1 Homo sapiens 84-88