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Disease Info Card
Primary Hyperoxaluria, Type I
Information about Primary Hyperoxaluria, Type I: 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 Primary Hyperoxaluria, Type I
Most recent studies have shown that Primary Hyperoxaluria, Type I shares some biological mechanisms with bone-diseases, decreased-immunologic-activity-[pe], fibrosis, hereditary-diseases, hyperoxaluria, hyperoxaluria-primary, inborn-errors-of-metabolism, kidney-calculi, kidney-diseases, kidney-failure, kidney-failure-chronic, metabolic-diseases, nephrocalcinosis, nephrolithiasis, primary-hyperoxaluria-type-2, renal-insufficiency, urolithiasis.
Among the many pathways, these few ones have gauged particular interests from scientists studying Primary Hyperoxaluria, Type I, and have been seen in publications frequently: Antiport, Bone Maturation, Bone Mineralization, Bone Resorption, Cell Proliferation, Diuresis, Excretion, Glomerular Filtration, Gluconeogenesis, Intracellular Transport, Localization, Organelle Localization, Pathogenesis, Protein Folding, Protein Import, Proteolysis, Secretion, Translation, Transport, Urea Cycle
Quite a number of genes have been found to play important roles in Primary Hyperoxaluria, Type I, such as AGT, AGXT, CAT, GGT2, GRHPR, HAO1, HAO2, HDAC4, HTT, LTA, PAH, PDXP, PHC1, PHC2, PLP1, PRDX5, PTHLH, QPCT, RAPGEF5, TIMM8A. 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.