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Disease Info Card
Nephrocalcinosis
Information about Nephrocalcinosis: 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 Nephrocalcinosis
Most recent studies have shown that Nephrocalcinosis shares some biological mechanisms with acidosis, bartter-disease, calcinosis, hypercalcemia, hypercalciuria, hyperoxaluria, hyperoxaluria-primary, hyperparathyroidism-primary, kidney-calculi, kidney-diseases, kidney-failure, kidney-failure-chronic, nephrolithiasis, proteinuria-of-undiagnosed-cause, renal-insufficiency, renal-tubular-acidosis, renal-tubular-acidosis-type-i, rickets, urolithiasis.
Among the many pathways, these few ones have gauged particular interests from scientists studying Nephrocalcinosis, and have been seen in publications frequently: Amelogenesis, Bone Mineralization, Bone Resorption, Chloride Transport, Diuresis, Endocytosis, Excretion, Glomerular Filtration, Hormone Secretion, Intestinal Absorption, Ion Homeostasis, Ion Transport, Lactation, Localization, Pathogenesis, Regeneration, Secretion, Translation, Transport, Vasoconstriction
Quite a number of genes have been found to play important roles in Nephrocalcinosis, such as AGT, AGXT, ALB, CALCA, CASR, CLCN5, CLCNKB, CLDN16, CLDN19, KCNJ1, PHEX, PTH, PTRH1, RAPGEF5, REN, SLC12A1, SLC12A3, SLC4A1, SPP1, UMOD. 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.