NP_000187.3
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NCBI GenBank Nucleotide #
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UniProt Secondary Accession #
UniProt Related Accession #
Molecular Weight
44,127 Da
NCBI Official Full Name
corticosteroid 11-beta-dehydrogenase isozyme 2
NCBI Official Synonym Full Names
hydroxysteroid (11-beta) dehydrogenase 2
NCBI Official Synonym Symbols
AME; AME1; HSD2; HSD11K; SDR9C3 [Similar Products]
NCBI Protein Information
corticosteroid 11-beta-dehydrogenase isozyme 2; 11-DH2; 11-beta-HSD2; -HSD11 type II; 11-beta-hydroxysteroid dehydrogenase type 2; 11-beta-hydroxysteroid dehydrogenase type II; NAD-dependent 11-beta-hydroxysteroid dehydrogenase; short chain dehydrogenase/reductase family 9C member 3
UniProt Protein Name
Corticosteroid 11-beta-dehydrogenase isozyme 2
UniProt Synonym Protein Names
11-beta-hydroxysteroid dehydrogenase type 2; 11-DH2; 11-beta-HSD2; 11-beta-hydroxysteroid dehydrogenase type II; -HSD11 type II; NAD-dependent 11-beta-hydroxysteroid dehydrogenase; 11-beta-HSD
UniProt Synonym Gene Names
UniProt Entry Name
DHI2_HUMAN
NCBI Summary for HSD11B2
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. [provided by RefSeq, Feb 2010]
UniProt Comments for HSD11B2
HSD11B2: Catalyzes the conversion of cortisol to the inactive metabolite cortisone. Modulates intracellular glucocorticoid levels, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids. Defects in HSD11B2 are the cause of 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. Belongs to the short-chain dehydrogenases/reductases (SDR) family.
Protein type: Oxidoreductase; Lipid Metabolism - C21-steroid hormone; Lipid Metabolism - androgen and estrogen; EC 1.1.1.-
Chromosomal Location of Human Ortholog: 16q22
Cellular Component: endoplasmic reticulum
Molecular Function: 11-beta-hydroxysteroid dehydrogenase activity; NAD binding; steroid binding
Biological Process: response to food; response to drug; response to glucocorticoid stimulus; response to hypoxia; aldosterone mediated regulation of blood volume; female pregnancy; glucocorticoid biosynthetic process; response to insulin stimulus
Disease: Apparent Mineralocorticoid Excess
Research Articles on HSD11B2
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Pathways associated with HSD11B2 elisa kit
Diseases associated with HSD11B2 elisa kit
Organs/Tissues associated with HSD11B2 elisa kit
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