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Rabbit anti-Mouse Hydroxysteroid Dehydrogenase, 11-beta Type II Polyclonal Antibody

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Catalog # MBS617493
Unit / Price
  0.1 mg  /  $745 +1 FREE 8GB USB
anti-Hydroxysteroid Dehydrogenase, 11-beta Type II antibody
Product Name

Hydroxysteroid Dehydrogenase, 11-beta Type II, Polyclonal Antibody

Popular Item
Also Known As

Hydroxysteroid Dehydrogenase, 11-beta Type II (HSD)

Product Synonym Names
Anti -Hydroxysteroid Dehydrogenase, 11-beta Type II (HSD)
Research Use Only
For Research Use Only. Not for use in diagnostic procedures.
Species Reactivity
Recognizes mouse Hydroxysteroid Dehydrogenase, 11-beta Type II (HSD).
Affinity Purified
Purified by immunoaffinity chromatography.
Supplied as a liquid in PBS, 0.1% BSA.
Synthetic peptide corresponding to 16aa near the C-terminus of mouse Hydroxysteroid Dehydrogenase, 11-beta Type II conjugated to KLH (P51661). Epitope: ~Mid-region
Preparation and Storage
May be stored at 4 degree C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degree C. Aliquots are stable for 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. 
Other Notes
Small volumes of anti-Hydroxysteroid Dehydrogenase, 11-beta Type II 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.
11-b-hydroxysteroid dehydrogenase (11b-HSD) is a microsomal short chain dehydrogenase/reductase which catalyzes the inter-conversion of biologically active glucocorticoid (cortisol in human, corticosterone in rats and mice) and inactive glucocorticoid (cortisone and 11-dehydrocorticosterone). Two tissue specific isoforms (11b-HSD1 and 11b-HSD2) of 11b-HSD with two different functions regarding glucocorticoid availability, have been identified. The decreased 11b-hydroxy oxidation of cortisol results in Apparent Mineralocorticoid Excess (AME) disorder. AME is principally a disorder of juveniles and children with this condition oxidize cortisol to cortisone poorly but carry out the reverse process unimpaired. AME arises from mutations in the 11b-HSD2 gene. The glucocorticoids can also be produced locally by 11b-HSD1 and increased visceral accumulation of glucocorticoids results in visceral obesity, insulin resistant diabetes, hyperlipidemia and hyperphagia. 11betaHSD-2 (rat 400aa, mouse 396aa, human 405aa) is a ~41kD glycosylated membrane-protein present in the endoplasmic reticulum (ER). The N-terminal and C-terminal (catalytic domain) of 11b-HSD2 are in the lumen and cytoplasm of ER, respectively. 11b-HSD2 irreversibly catalyzes the dehydrogenation of active 11b-hydroxycorticoids before they occupy mineralocorticoid receptors (MR) and thus confers aldosterone selectivity for inherently nonselective MR. The enzyme is expressed in a wide array of tissues, with highest level mineralocorticoid target cells such as the renal and outer medullary collecting ducts. In mouse, rat and human, the over-all aa seq of 11b-HSD2 is >80% identical.
ELISA (EL/EIA), Western Blot (WB)
Suitable for use in ELISA and Western Blot.
Dilution: Western Blot: 1-10ug/ml using ECL technique.
ELISA: 1:10,000-1:100,000 using 50-100ng of H9117-82 control peptide per well.
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While every efforts were made to ensure the accuracy of the information provided in this datasheet, MyBioSource will not be liable for any omissions or errors contained herein. MyBioSource reserves the right to make changes to this datasheet at any time without prior notice.

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