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Disease Info Card
Mineralocorticoid Excess Syndrome, Apparent
Information about Mineralocorticoid Excess Syndrome, Apparent: 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 Mineralocorticoid Excess Syndrome, Apparent
Most recent studies have shown that Mineralocorticoid Excess Syndrome, Apparent shares some biological mechanisms with adrenal-hyperplasia, alkalosis, congenital-adrenal-hyperplasia, conn-syndrome, cortisol-11-beta-ketoreductase-deficiency, cushing-syndrome, essential-hypertension, hyperaldosteronism, hypernatremia, hyperplasia, hypertensive-disease, kidney-diseases, liddle-syndrome, metabolic-alkalosis, pseudohypoaldosteronism.
Among the many pathways, these few ones have gauged particular interests from scientists studying Mineralocorticoid Excess Syndrome, Apparent, and have been seen in publications frequently: Aging, Aldosterone Secretion, Catecholamine Secretion, Cell Death, Cortisol Secretion, Excretion, Ion Transport, Localization, Menstruation, Metaphase, Natriuresis, Organ Maturation, Pathogenesis, Programmed Cell Death, Protein Stabilization, Regulation Of Blood Pressure, Secretion, Transport, Vasoconstriction
Quite a number of genes have been found to play important roles in Mineralocorticoid Excess Syndrome, Apparent, such as A4GALT, AGT, CHST3, CYP11B1, CYP11B2, GSR, HSD11B1, HSD11B2, NR3C1, NR3C2, POMC, PRF1, PRM1, REN, RPLP1, S100A6, SCNN1B. 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.