anti-Human Hydroxysteroid Dehydrogenase, 11-beta Type II Polyclonal Antibody

Rabbit Anti-Hydroxysteroid Dehydrogenase, 11-beta Type II

Cat. Num. AAA614847

• Reactivity: Human
• Applications: ELISA, Western Blot
• Purity: Serum
• Synonyms: Hydroxysteroid Dehydrogenase; 11-beta Type II; Polyclonal Antibody; Rabbit Anti-Hydroxysteroid Dehydrogenase; 11-beta Type II (11b-HSD2); anti-Hydroxysteroid Dehydrogenase; 11-beta Type II antibody

• Host: Host: Rabbit; Source: Human
• Reactivity: Human
• Clonality: Polyclonal
• Isotype: IgG
• Specificity: Recognizes 11b-HSD2. No significant sequence homology of is seen with 11b-HSD1 or other proteins. Species crossreactivity: Human. Does not crossreact with Rat or mouse. For rat corresponding products, refer to Cat# MBS610911, MBS618532. For mouse corresponding products, refer to Cat# MBS617493, MBS617368,
• Purity/Purification: Serum
• Form/Format: Supplied as a liquid, neat serum, 40% glycerol.

• Applicable Applications for anti-Hydroxysteroid Dehydrogenase, 11-beta Type II antibody: ELISA, Western Blot
• Application Notes: Western Blot: 1:1000-1:5000 using ECL. ELISA: 1:10,000-1:100,000 using 50-100ng control peptide/well.
• Immunogen: A 19-aa synthetic peptide, mapping near the C-terminus of human 11beta-HSD2 (1), coupled to KLH.
• Preparation and Storage: May be stored at 4 degree C for short-term only. For long-term storage, store at -20 degree C. Aliquots are stable for at least 12 months at -20 degree C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.

Related Product Information for anti-Hydroxysteroid Dehydrogenase, 11-beta Type II antibody

11-b-hydroxysteroid dehydrogenase (11b-HSD) is a microsomal short chain dehydrogenase/reductase (SDR) which catalyzes the inter-conversion of biologically active glucocorticoid (cortisol in human and 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 which is manifested by hypertension, hypokalemia, low plasma renin activity, and responsiveness to spironolactone. 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. 11bHSD-2 (rat 400-aa, mouse 396-aa, human 405-aa) 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. In mouse, the over-all aa seq of 11b-HSD2 is >80% identical to that of 11b-HSD2.

Product Categories/Family for anti-Hydroxysteroid Dehydrogenase, 11-beta Type II antibody

Abs to Enzymes

References

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