This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
, No Gclids
Disease Info Card
Tumoral Calcinosis
Information about Tumoral Calcinosis: 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 Tumoral Calcinosis
Most recent studies have shown that Tumoral Calcinosis shares some biological mechanisms with arthropathy, bone-diseases, bone-neoplasms, calcinosis, dermatologic-disorders, hypercalcemia, hyperparathyroidism-secondary, hyperphosphatemia, hypophosphatemia, kidney-diseases, kidney-failure, kidney-failure-chronic, metabolic-diseases, neoplasms, osteomalacia, pain, rickets, soft-tissue-neoplasms, uremia.
Among the many pathways, these few ones have gauged particular interests from scientists studying Tumoral Calcinosis, and have been seen in publications frequently: Aging, Bone Remodeling, Cell Migration, Endochondral Ossification, Excretion, Glomerular Filtration, Glycosylation, Hypersensitivity, Inflammatory Response, Intestinal Absorption, Localization, Ossification, Pathogenesis, Protein Secretion, Proteolysis, Renal Phosphate Excretion, Response To Vitamin, Response To Vitamin D, Secretion, Transport
Quite a number of genes have been found to play important roles in Tumoral Calcinosis, such as CALCA, CD55, DMP1, EGR1, FGF23, FGF7, FGFR2, GALNT3, HHIP, KL, PHEX, PTH, PTRH1, RAPGEF5, REG3A, RPL29, SAMD9, ST13, TCN2. 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.