11-Beta-Hydroxysteroid Dehydrogenase Type 2 (HSD11b2), Polyclonal Antibody

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

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

Polyclonal

Rabbit

200ug/ml (lot specific)

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 customer’s specifications, please inquire.

Small volumes of anti-HSD11b2 antibody 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.

Western Blot (WB), Immunocytochemistry (ICC), Immunohistochemistry (IHC) Formalin/Paraffin, ELISA (ELISA)

44,127 Da

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]

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

Chromosomal Location of Human Ortholog: 16q22.1

Cellular Component: endoplasmic reticulum membrane

Molecular Function: 11-beta-hydroxysteroid dehydrogenase activity

Biological Process: glucocorticoid biosynthetic process

Disease: Apparent Mineralocorticoid Excess

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