ELISA/assay

11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2) ELISA Kit

MBS2019764

48-Strip-Wells

605 USD

ELISA Kit

11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2) ELISA Kit

11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2)

AME; AME1; HSD11K; HSD2; SDR9C3; Short Chain Dehydrogenase/Reductase Family 9C,Member 3; NAD-dependent 11-beta-hydroxysteroid dehydrogenase

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

HSD11b2

HSD11B2; HSD11B2; AME; AME1; HSD2; HSD11K; SDR9C3; ; 11-DH2; 11-beta-HSD2; 11-HSD type II; 11-beta-HSD type II; 11-beta-HSD

DHI2_HUMAN

Rat

405

This assay has high sensitivity and excellent specificity for detection of 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2). No significant cross-reactivity or interference between 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2) and analogues was observed.

For unopened kit: All the reagents should be kept according to the labels on vials. The Standard, Detection Reagent A, Detection Reagent B and the 96-well strip plate should be stored at -20 degree C upon receipt while the others should be at 4 degree C. For opened kit: When the kit is opened, the remaining reagents still need to be stored according to the above storage condition. Besides, please return the unused wells to the foil pouch containing the desiccant pack, and reseal along entire edge of zip-seal. The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. To minimize extra influence on the performance, operation procedures and lab conditions, especially room temperature, air humidity, incubator temperature should be strictly controlled. It is also strongly suggested that the whole assay is performed by the same operator from the beginning to the end.

Samples: Tissue homogenates, Cell lysates and other biological fluids. Assay Type: Sandwich. Detection Range: 0.781-50ng/mL. Sensitivity: Typically less than 0.30ng/mL.

Precision: Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2) were tested 20 times on one plate, respectively. Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2) were tested on 3 different plates, 8 replicates in each plate. CV(%) = SD/meanX100 . Intra-Assay: CV<10% . Inter-Assay: CV<12% . Assay Procedure Summary: 1. Prepare all reagents, samples and standards;. 2. Add 100uL standard or sample to each well. Incubate 2 hours at 37 degree C;. 3. Aspirate and add 100uL prepared Detection Reagent A. Incubate 1 hour at 37 degree C;. 4. Aspirate and wash 3 times;. 5. Add 100uL prepared Detection Reagent B. Incubate 30 minutes at 37 degree C;. 6. Aspirate and wash 5 times;. 7. Add 90uL Substrate Solution. Incubate 15-25 minutes at 37 degree C;. 8. Add 50uL Stop Solution. Read at 450nm immediately.

Principle of the Assay: The test principle applied in this kit is Sandwich enzyme immunoassay. The microtiter plate provided in this kit has been pre-coated with an antibody specific to 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2). Standards or samples are then added to the appropriate microtiter plate wells with a biotin-conjugated antibody specific to 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2). Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2), biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm 10nm. The concentration of 11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2) in the samples is then determined by comparing the O.D. of the samples to the standard curve.

1173512

AAC50356.1

P80365

44,127 Da

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); Prostaglandin Synthesis And Regulation Pathway (198912); Steroid Hormone Biosynthesis Pathway (82940); Steroid Hormone Biosynthesis Pathway (301)

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]

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: Lipid Metabolism - C21-steroid hormone; Lipid Metabolism - androgen and estrogen; EC 1.1.1.-; Oxidoreductase. 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

48-Strip-Wells

605 USD

96-Strip-Wells

820

5x96-Strip-Wells

3220

10x96-Strip-Wells

5795