HSD11B2, Polyclonal Antibody

Corticosteroid 11-beta-dehydrogenase isozyme 2; 111-; 11-beta-hydroxysteroid dehydrogenase type 2; 11-DH2; 11-beta-HSD2; 11-beta-hydroxysteroid dehydrogenase type II; -HSD11 type II; NAD-dependent 11-beta-hydroxysteroid dehydrogenase; 11-beta-HSD; HSD11B2; HSD11K

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

Polyclonal

Rabbit Ig

Rabbit

This HSD11B2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 277-306 amino acids from the Central region of human HSD11B2.

Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab)

Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.

Vial Concentration: 0.5 (lot specific)

Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C in small aliquots to prevent freeze-thaw cycles.

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.

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.

Cancer; Cardiovascular; Cell Biology; Metabolism; Signal Transduction

Western Blot (WB), ELISA (EIA), Immunohistochemistry (IHC), Flow Cytometry (FC/FACS)

WB~~1:1000

Western blot analysis of HSD11B2 Antibody (Center) in MCF-7 cell line lysates (35ug/lane). HSD11B2 (arrow) was detected using the purified Pab.

HSD11B2 Antibody (Center) IHC analysis in formalin fixed and paraffin embedded skeletal muscle followed by peroxidase conjugation of the secondary antibody and DAB staining. This data demonstrates the use of the HSD11B2 Antibody (Center) for immunohistochemistry. Clinical relevance has not been evaluated.

HSD11B2 Antibody (Center) flow cytometric analysis of MCF-7 cells (bottom histogram) compared to a negative control cell (top histogram).FITC-conjugated goat-anti-rabbit secondary antibodies were used for the analysis.

44127

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

Li, J., et al. Breast Cancer Res. 12 (2), R19 (2010)
Ni, X.T., et al. Placenta 30(12):1023-1028(2009)
Mericq, V., et al. Eur. J. Endocrinol. 161(3):419-425(2009)
Stark, M.J., et al. Am. J. Physiol. Regul. Integr. Comp. Physiol. 297 (2), R510-R514 (2009)
Lepenies, J., et al. Clin. Exp. Hypertens. 31(4):376-379(2009)

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