Rabbit anti-Human HSD11B2 Polyclonal Antibody

Uniprot Id

P80365

Target Species

Human

Target Name

HSD11B2

Target Full Name

11-beta-hydroxysteroid dehydrogenase type 2

Target 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.

Target Involvement

Apparent mineralocorticoid excess (AME)

Target Subcellular Location

Microsome. Endoplasmic reticulum.

Target Protein Families

Short-chain dehydrogenases/reductases (SDR) family

Target Tissue Specificity

Expressed in kidney, pancreas, prostate, ovary, small intestine and colon. At midgestation, expressed at high levels in placenta and in fetal kidney and, at much lower levels, in fetal lung and testis.

Target Research Area

Cancer

Target Synonyms

11 beta HSD2; 11 beta hydroxysteroid dehydrogenase type 2; 11 DH2; 11-beta-HSD2; 11-beta-hydroxysteroid dehydrogenase type 2; 11-DH2; AME; AME1; Corticosteroid 11 beta dehydrogenase isozyme 2; Corticosteroid 11-beta-dehydrogenase isozyme 2; DHI2_HUMAN; HSD11B2; HSD11K; HSD2; Hydroxysteroid 11 beta dehydrogenase 2; Hydroxysteroid 11 beta dehydrogenase isoenzyme 2; NAD dependent 11 beta hydroxysteroid dehydrogenase ; NAD-dependent 11-beta-hydroxysteroid dehydrogenase; SDR9C3; Short chain dehydrogenase/reductase family 9C; member 3

Target Background

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.