catalytic activity:An 11-beta-hydroxysteroid + NAD(+) = an 11-oxosteroid + NADH.,disease:Defects in HSD11B2 are the cause of apparent mineralocorticoid excess (AME) [MIM:218030]. AME is a potentially fatal disease characterized by severe juvenile low-renin hypertension, sodium retention, hypokalemia and low levels of aldosterone. It often leads to nephrocalcinosis.,enzyme regulation:Inhibited by glycyrrhetinic acid (derived from liquorice), carbenoloxone and 11-alpha-OH-progesterone.,function:Catalyzes the conversion of cortisol to the inactive metabolite cortisone. Modulates intracellular glucocorticoid levels, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids.,miscellaneous:Consumption of large amounts of liquorice can lead to apparent mineralocorticoid excess and hypertension.,similarity:Belongs to the short-chain dehydrogenases/reductases (SDR) family.,subunit:Interacts with ligand-free cytoplasmic NR3C2.,tissue specificity:Found in placenta, kidney, pancreas, prostate, ovary, small intestine and colon.,
Microsome . Endoplasmic reticulum .
Expressed in kidney, placenta, pancreas, prostate, ovary, small intestine and colon, and in lower levels in the spleen and testis (PubMed:7859916). At midgestation, expressed at high levels in placenta and in fetal kidney and, at much lower levels, in fetal lung and testis (PubMed:8530071).