catalog number :
MBS2031421
products type :
Recombinant Protein
products full name :
Recombinant 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2)
products short name :
[11-Beta-Hydroxysteroid Dehydrogenase Type 2]
other names :
[11-beta-hydroxysteroid dehydrogenase type 2; Corticosteroid 11-beta-dehydrogenase isozyme 2; corticosteroid 11-beta-dehydrogenase isozyme 2; hydroxysteroid (11-beta) dehydrogenase 2; 11-beta-hydroxysteroid dehydrogenase type 2; 11-DH2; 11-beta-HSD2; 11-beta-hydroxysteroid dehydrogenase type II; 11-HSD type II; 11-beta-HSD type II; NAD-dependent 11-beta-hydroxysteroid dehydrogenase; 11-beta-HSD; Short chain dehydrogenase/reductase family 9C member 3]
products gene name :
[HSD11b2]
other gene names :
[HSD11B2; HSD11B2; AME; AME1; HSD2; HSD11K; SDR9C3; ; 11-DH2; 11-beta-HSD2; 11-HSD type II; 11-beta-HSD type II; 11-beta-HSD]
uniprot entry name :
DHI2_HUMAN
concentration :
Original Concentration: 200 ug/mL
storage stability :
Storage: Avoid repeated freeze/thaw cycles. Store at 2-8ºC for one month. Aliquot and store at -80ºC for 12 months. Stability Test: The thermal stability is described by the loss rate. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37°C for 48h, and no obvious degradation and precipitation were observed. The loss rate is less than 5% within the expiration date under appropriate storage condition
tested application :
Positive Control; Immunogen; SDS-PAGE; WB. (May be suitable for use in other assays to be determined by the end user.)
image1 heading :
Sequence Information
image2 heading :
SDS-Page
other info1 :
Organism Species: Rattus norvegicus (Rat). Source: Prokaryotic expression. Residues: Leu58~Pro393. Tags: N-terminal His Tag. Subcellular Location: Endoplasmic reticulum lumen. Traits: Freeze-dried powder. Buffer: 20mM Tris, 150mM NaCl, pH8.0, containing 0.01% SKL, 5% Trehalose
other info2 :
Predicted isoelectric point: 9.2. Predicted Molecular Mass: 40.5kDa. Accurate Molecular Mass: 41kDa as determined by SDS-PAGE reducing conditions. Usage: Reconstitute in 20mM Tris, 150mM NaCl (pH8.0) to a concentration of 0.1-1.0 mg/mL. Do notEe
vortex.
ncbi acc num :
AAC50356.1
ncbi pathways :
Aldosterone-regulated Sodium Reabsorption Pathway (130626); Aldosterone-regulated Sodium Reabsorption Pathway (130590); C21-Steroid Hormone Biosynthesis, Progesterone = Cortisol/cortisone Pathway (413395); C21-Steroid Hormone Biosynthesis, Progesterone = Cortisol/cortisone Pathway (468370); Glucocorticoid Mineralcorticoid Metabolism Pathway (198902); Glucocorticoid Biosynthesis Pathway (1270048); Metabolism Pathway (1269956); Metabolism Of Lipids And Lipoproteins Pathway (1270001); Metabolism Of Steroid Hormones And Vitamin D Pathway (1270046); Prostaglandin Synthesis And Regulation Pathway (198912)
ncbi summary :
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 summary :
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 drug; response to food; 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