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Disease Info Card
Hyperoxaluria, Primary
Information about Hyperoxaluria, Primary: 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.
Overview of Hyperoxaluria, Primary
Most recent studies have shown that Hyperoxaluria, Primary shares some biological mechanisms with acute-kidney-injury, bone-diseases, hereditary-diseases, hyperoxaluria, inborn-errors-of-metabolism, kidney-calculi, kidney-diseases, kidney-failure, kidney-failure-chronic, liver-diseases, metabolic-diseases, nephrocalcinosis, nephrolithiasis, primary-hyperoxaluria-type-2, primary-hyperoxaluria-type-i, renal-insufficiency, urinary-tract-infection, urolithiasis.
Among the many pathways, these few ones have gauged particular interests from scientists studying Hyperoxaluria, Primary, and have been seen in publications frequently: Bone Resorption, Cell Proliferation, Coagulation, Diuresis, Donor Selection, Excretion, Glomerular Filtration, Gluconeogenesis, Intestinal Absorption, Localization, Organelle Localization, Oxalate Transport, Pathogenesis, Phagocytosis, Protein Import, Proteolysis, Secretion, Translation, Transport, Urea Cycle
Quite a number of genes have been found to play important roles in Hyperoxaluria, Primary, such as AGT, AGXT, CAT, CRAT, GRHPR, GSR, HAO1, HAO2, HOGA1, HTT, NR3C1, PAH, PDXP, PHC1, PHC2, PLP1, PRDX5, PTHLH, RAPGEF5, SMARCB1. 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.