Mouse Anti-HSD11B2 Recombinant Antibody (CBFYH-1994) (CBMAB-H3005-FY)

Hydroxysteroid 11-Beta Dehydrogenase 2

There are at least two isozymes of the corticosteroid 11-beta-dehydrogenase, a microsomal enzyme complex responsible for the interconversion of cortisol and cortisone. The type I isozyme has both 11-beta-dehydrogenase (cortisol to cortisone) and 11-oxoreductase (cortisone to cortisol) activities. The type II isozyme, encoded by this gene, has only 11-beta-dehydrogenase activity. In aldosterone-selective epithelial tissues such as the kidney, the type II isozyme catalyzes the glucocorticoid cortisol to the inactive metabolite cortisone, thus preventing illicit activation of the mineralocorticoid receptor. In tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, it protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development. Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension.

Hydroxysteroid 11-Beta Dehydrogenase 2; Short Chain Dehydrogenase/Reductase Family 9C Member 3; NAD-Dependent 11-Beta-Hydroxysteroid Dehydrogenase; 11-Beta-Hydroxysteroid Dehydrogenase Type II; 11-Beta-Hydroxysteroid Dehydrogenase Type 2; 11-Beta-HSD Type II; 11-HSD Type II; 11-Beta-HSD2; 11-DH2; HSD11K; SDR9C3

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.