Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Our results give novel additional information on the abnormal O-glycosylation process of IgA1 in IgAN patients. 25744272 2015
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Analyses of serum IgA1 from IgAN patients revealed abnormal galactosylation of the O-linked carbohydrate moieties of IgA that may result from altered activity in the core of 1 b1,3-galactosyltransferase (C1GalT1). 26125729 2015
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Inhibition of miR-374b increased PTEN and Cosmc expression, and prevented cell proliferation and aberrant glycosylation of IgA1, thus representing a new therapeutic approach for IgAN. 26545495 2015
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Moreover, serum levels of the pathogenic galactose-deficient glycoform of IgA1 were also associated with the degree of mesangial C3 deposition in patients with IgAN. 25205734 2015
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 AlteredExpression disease BEFREE In conclusion, the activation of innate immunity via TLRs and ubiquitin-proteasome pathways and the pro-oxidative milieu were not affected by tonsillectomy, even though the levels of aberrantly galactosylated IgA1 were lower in patients with IgAN who had tonsillectomy. 24756968 2015
CUI: C1318233
Disease: immunoglobulin G index
immunoglobulin G index
0.100 GeneticVariation phenotype GWASCAT Genetic variants are major determinants of CSF antibody levels in multiple sclerosis. 25616667 2015
CUI: C1446147
Disease: IgG Index (procedure)
IgG Index (procedure)
0.100 GeneticVariation phenotype GWASCAT Genetic variants are major determinants of CSF antibody levels in multiple sclerosis. 25616667 2015
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 GeneticVariation disease BEFREE Deficient glycosylation of O-linked glycans in the IgA1 hinge region is associated with IgA nephropathy in humans, but the pathogenic contribution of the underlying structural aberrations remains incompletely understood. 24511137 2014
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 AlteredExpression disease BEFREE AMI can up-regulate Cosmc expression of peripheral B lymphocytes and reverse IgA1 aberrant O-glycosylation level, which might be the underlying mechanism of AMI therapy in treating IgAN. 24942185 2014
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Specifically, overexpression of miR-148b might explain the aberrant glycosylation of IgA1, which has a central pathogenetic role in the early phase of IgA nephropathy. 24709842 2014
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE In conclusion, we demonstrated that Hp infection, at least via CagA, may participate in the pathogenesis of IgAN by influencing the production and glycosylation of IgA1 in B cells. 24462875 2014
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 AlteredExpression disease BEFREE Genetic studies have revealed that an elevated level of Gd-IgA1 in the circulation of IgAN patients is a hereditable trait. 25152896 2014
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 AlteredExpression disease BEFREE In the absence and presence of capsaicin, the BAFF expression and IgA1 secretion were higher in IgAN patients than that in non-IgAN patients, meanwhile, the gene expression of C1GALT1 and Cosmc and IgA1 O-glycosylation level were significantly lower. 25167771 2014
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Patients with IgAN develop characteristic IgA1-containing immune complexes that deposit in the glomerular mesangium, producing progressive kidney injury. 24892706 2014
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE It remains unclear why there is an increase in poorly galactosylated IgA1 molecules in the serum in IgAN. 22318424 2012
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Abnormal expression of miR-148b may explain the aberrant glycosylation of IgA1, providing a potential pharmacologic target for IgA nephropathy. 22362909 2012
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 AlteredExpression disease BEFREE Patients with IgA nephropathy often have a genetically determined increase in circulating levels of IgA1 with galactose-deficient O-glycans in the hinge-region (Hit 1). 21949093 2011
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE This review will summarize the works on the genetics, the mucosal and systemic IgA immune response, mechanism of underglycosylation of IgA1, and the pathological effect of mesangial IgA deposition in IgAN. 21188648 2011
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 AlteredExpression disease BEFREE Thus, serum galactose-deficient IgA1 levels are highly inherited in pediatric patients with IgAN and HSPN, providing support for another shared pathogenic link between these disorders. 21326171 2011
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE New data from Kiryluk et al. show the importance of genetic factors in determining the profile of serum IgA1 O-glycoforms in IgA nephropathy and Henoch-Schönlein purpura nephritis. 21673733 2011
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 GeneticVariation disease BEFREE Furthermore, we investigated the influence of IgA1-containing CIC from sera of children with IgAN with clinically active disease (i.e., abnormal urinalysis and/or serum creatinine concentration) or inactive disease (i.e., normal urinalysis and serum creatinine concentration) on the expression of IL-6 and IL-8 genes by mesangial cells. 21828345 2011
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 AlteredExpression disease BEFREE The aim of this study was to investigate IgA and IgA1 levels in the supernatant of tonsillar mononuclear cells (TMCs) and the expression of Iα-Cα germline transcript and AID in TMCs stimulated with lipopolysaccharide or hemolytic streptococcus in IgAN patients and chronic tonsillitis patients. 21614556 2011
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Our findings suggest that compared with SpIgAN patients, macromolecular IgA1 taken from MpIgAN patients is more pathogenic to cultured PTEC through a glomerulotubular interaction. 20484297 2010
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 Biomarker disease BEFREE Recent data indicates that these IgA1 glycosylation defects are inherited and constitute a heritable risk factor for IgAN. 20386929 2010
CUI: C0017661
Disease: IGA Glomerulonephritis
IGA Glomerulonephritis
0.100 GeneticVariation disease BEFREE Thus, aberrant IgA1 glycosylation is a heritable risk factor for IgAN in African Americans. 20634323 2010