For Research Use Only. Not for use in diagnostic procedures.

E.coli

> 90%

Original Concentration: 200 ug/mL (lot specific)

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

Manufactured in an ISO 9001:2008 and ISO 13485:2003 Certified Laboratory.

Manufactured in a lab with traceable raw materials. Bulk orders can typically be prepared to the customera??s specifications, please inquire.

Small volumes of HSD11b2 recombinant protein vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Positive Control; Immunogen; SDS-PAGE; WB.

(May be suitable for use in other assays to be determined by the end user.)

hydroxysteroid (11-beta) dehydrogenase 2

corticosteroid 11-beta-dehydrogenase isozyme 2

Corticosteroid 11-beta-dehydrogenase isozyme 2

; 11-DH2; 11-beta-HSD2; 11-HSD type II; 11-beta-HSD type II; 11-beta-HSD??[Similar Products]

DHI2_HUMAN

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: 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

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