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- Table of Contents
Information about Familial Hypophosphatemia: 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 Familial Hypophosphatemia shares some biological mechanisms with bone-diseases, congenital-abnormality, diabetes-mellitus, familial-hypophosphatemic-bone-disease, fanconi-syndrome, hypercalcemia, hypercalciuria, hyperparathyroidism-secondary, hypocalcemia, hypophosphatemia, hypophosphatemic-rickets, neoplasms, nephrocalcinosis, osteomalacia, pain, phosphate-diabetes, renal-tubular-acidosis, rickets, vitamin-d-deficiency.
Among the many pathways, these few ones have gauged particular interests from scientists studying Familial Hypophosphatemia, and have been seen in publications frequently: Bone Mineralization, Bone Resorption, Cell Differentiation, Dentinogenesis, Excretion, Glomerular Filtration, Gluconeogenesis, Hormone Secretion, Hypersensitivity, Intestinal Absorption, Localization, Ossification, Parathyroid Hormone Secretion, Pathogenesis, Reflex, Renal Phosphate Excretion, Secretion, Sodium-dependent Phosphate Transport, Translation, Transport
Quite a number of genes have been found to play important roles in Familial Hypophosphatemia, such as BGLAP, CALCA, CYP24A1, CYP27B1, FGF23, GGH, GH1, GSTP1, IGF1, PHEX, PTH, PTRH1, RAPGEF5, SERPINA1, SLC34A1, SLC34A3, VDR. 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.