DHI2 rabbit pAb

DHI2 rabbit pAb

AO-06-ES9568-100

DHI2 rabbit pAb 100μL

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Antibody Product Overview

ELK.NoES9568
Product nameDHI2 rabbit pAb
ReactivityHuman;Rat;Mouse;
ApplicationsWB;ELISA
Other name
Size100μL
Unit price ($)248
Human gene ID3291
Human Swiss-ProtP80365
SourceRabbit
IsotypeIgG
TargetDHI2
Fields>>Steroid hormone biosynthesis;>>Metabolic pathways;>>Aldosterone-regulated sodium reabsorption
Gene nameHSD11B2 HSD11K
Protein nameCorticosteroid 11-beta-dehydrogenase isozyme 2 (EC 1.1.1.-) (11-beta-hydroxysteroid dehydrogenase type 2) (11-DH2) (11-beta-HSD2) (11-beta-hydroxysteroid dehydrogenase type II) (-HSD11 type II) (NAD-d
Human gene link
Human Swiss linkView Human Swiss-Prot
Mouse gene ID
Mouse gene link
Mouse Swiss-ProtP51661
Mouse Swiss linkView Mouse Swiss-Prot
Rat gene ID
Rat gene link
Rat Swiss-ProtP50233
Rat Swiss linkView Rat Swiss-Prot
ImmunogenSynthesized peptide derived from part region of human protein
SpecificityDHI2 Polyclonal Antibody detects endogenous levels of protein.
FormulationLiquid in PBS containing 50% glycerol, and 0.02% sodium azide.
ClonalityPolyclonal
DilutionWB 1:500-2000 ELISA 1:5000-20000
PurificationThe antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration1 mg/ml
Storage stability-20°C/1 year
Molecular Weight (Da)
Observed band (KD)44kD
Backgroundhydroxysteroid 11-beta dehydrogenase 2(HSD11B2) Homo sapiens 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 mine
Functioncatalytic activity:An 11-beta-hydroxysteroid + NAD(+) = an 11-oxosteroid + NADH.,disease:Defects in HSD11B2 are the cause of apparent mineralocorticoid excess (AME) [MIM:218030]. AME is a potentially fatal disease characterized by severe juvenile low-renin hypertension, sodium retention, hypokalemia and low levels of aldosterone. It often leads to nephrocalcinosis.,enzyme regulation:Inhibited by glycyrrhetinic acid (derived from liquorice), carbenoloxone and 11-alpha-OH-progesterone.,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.,miscellaneous:Consumption of large amounts of liquorice can lead to apparent mineralocorticoid excess and hypertension.,similarity:Belongs to the short-chain dehydrogenases/reductases
Subcellular locationMicrosome . Endoplasmic reticulum .
ExpressionExpressed in kidney, placenta, pancreas, prostate, ovary, small intestine and colon, and in lower levels in the spleen and testis (PubMed:7859916). At midgestation, expressed at high levels in placenta and in fetal kidney and, at much lower levels, in fetal lung and testis (PubMed:8530071).

Additional Images

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Western blot analysis of lysates from PC12 cells, primary antibody was diluted at 1:1000, 4°over night
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: AO-06-ES9568-100
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