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- Table of Contents
Information about Idiopathic Membranous Glomerulonephritis: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Most recent studies have shown that Idiopathic Membranous Glomerulonephritis shares some biological mechanisms with decreased-immunologic-activity-[pe], fibrosis, focal-glomerulosclerosis, glomerulonephritis, glomerulonephritis-membranoproliferative, glomerulosclerosis-(disorder), hypertensive-disease, iga-glomerulonephritis, kidney-diseases, kidney-failure, kidney-failure-chronic, lipoid-nephrosis, lupus-erythematosus-systemic, membranous-glomerulonephritis, nephritis, nephrotic-syndrome, proteinuria-of-undiagnosed-cause, renal-glomerular-disease, renal-insufficiency, segmental-glomerulosclerosis.
Among the many pathways, these few ones have gauged particular interests from scientists studying Idiopathic Membranous Glomerulonephritis, and have been seen in publications frequently: Adaptive Immune Response, Angiogenesis, Cell Activation, Cell Adhesion, Cell Proliferation, Chemotaxis, Coagulation, Complement Activation, Endothelial Cell Proliferation, Excretion, Glomerular Filtration, Hypersensitivity, Immune Complex Formation, Immune Response, Intestinal Absorption, Localization, Monocyte Chemotaxis, Pathogenesis, Platelet Aggregation, Secretion
Quite a number of genes have been found to play important roles in Idiopathic Membranous Glomerulonephritis, such as ACE, ACTN4, AGT, ALB, C3, CA9, CFB, GNL3, GYPA, HLA-DQA1, KRAS, KRT20, MS4A1, PLA2G1B, PLA2R1, PLB1, POMC, RAPGEF5, YWHAZ. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.