Human HSD11B2 ELISA Kit (V2LY-0626-LY5460)

Hydroxysteroid 11-Beta Dehydrogenase 2

Catalyzes the conversion of biologically active 11beta-hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD+ (PubMed:7859916, PubMed:8538347, PubMed:10497248, PubMed:22796344, PubMed:27927697, PubMed:30902677, PubMed:33387577, PubMed:12788846, PubMed:17314322).

Functions as a dehydrogenase (oxidase), thereby decreasing the concentration of active glucocorticoids, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids (PubMed:7859916, PubMed:10497248, PubMed:33387577, PubMed:12788846, PubMed:17314322).

Plays an important role in maintaining glucocorticoids balance during preimplantation and protects the fetus from excessive maternal corticosterone exposure (By similarity).

Catalyzes the oxidation of 11beta-hydroxytestosterone (11beta,17beta-dihydroxyandrost-4-ene-3-one) to 11-ketotestosterone (17beta-hydroxyandrost-4-ene-3,11-dione), a major bioactive androgen (PubMed:22796344, PubMed:27927697).

Catalyzes the conversion of 11beta-hydroxyandrostenedione (11beta-hydroxyandrost-4-ene-3,17-dione) to 11-ketoandrostenedione (androst-4-ene-3,11,17-trione), which can be further metabolized to 11-ketotestosterone (PubMed:27927697).

Converts 7-beta-25-dihydroxycholesterol to 7-oxo-25-hydroxycholesterol in vitro (PubMed:30902677).

7-beta-25-dihydroxycholesterol (not 7-oxo-25-hydroxycholesterol) acts as ligand for the G-protein-coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2) and may thereby regulate immune cell migration (PubMed:30902677).

May protect ovulating oocytes and fertilizing spermatozoa from the adverse effects of cortisol (By similarity).

Cortisol metabolic process Source: UniProtKB
Female pregnancy Source: Ensembl
Regulation of blood volume by renal aldosterone Source: Ensembl
Response to food Source: Ensembl
Response to glucocorticoid Source: Ensembl
Response to hypoxia Source: Ensembl
Response to insulin Source: Ensembl
Response to xenobiotic stimulus Source: Ensembl

Microsome; Endoplasmic reticulum

Apparent mineralocorticoid excess (AME):
An autosomal recessive form of low-renin hypertension. It is usually diagnosed within the first years of life and is characterized by polyuria and polydipsia, failure to thrive, hypernatremia, severe hypertension with low renin and aldosterone levels, profound hypokalemia with metabolic alkalosis, and most often nephrocalcinosis.