antibody

Hydroxysteroid Dehydrogenase, 11-beta Type II (HSD)

MBS617493

0.1 mg

745 USD

polyclonal

rabbit

nonconjugated

western blot, ELISA, enzyme immunoassay

Antibody

Hydroxysteroid Dehydrogenase, 11-beta Type II (HSD)

[Hydroxysteroid Dehydrogenase, 11-beta Type II]

[Anti -Hydroxysteroid Dehydrogenase, 11-beta Type II (HSD)]

Polyclonal

IgG

Rabbit

Mouse

Recognizes mouse Hydroxysteroid Dehydrogenase, 11-beta Type II (HSD).

Affinity Purified. Purified by immunoaffinity chromatography.

Supplied as a liquid in PBS, 0.1% BSA.

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.

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.

Immunogen: Synthetic peptide corresponding to 16aa near the C-terminus of mouse Hydroxysteroid Dehydrogenase, 11-beta Type II conjugated to KLH (P51661). Epitope: ~Mid-region

Antibodies; Abs to Enzymes, Dehydrogenase

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.

0.1 mg

745 USD