Der Kaninchen Polyklonal anti-HSD11B2 Antikörper wird verwendet zum Nachweis von HSD11B2 in Proben von Human, Maus und Ratte. Er wurde validiert für WB und ELISA.
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-2000,ELISA 1:5000-20000
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Konzentration
1 mg/mL
Buffer
PBS, 50 % glycerol, 0.05 % Proclin 300, 0.05 %BSA
Konservierungsmittel
ProClin
Vorsichtsmaßnahmen
This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
-20 °C
Informationen zur Lagerung
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Corticosteroid 11-beta-dehydrogenase isozyme 2, 11-beta-hydroxysteroid dehydrogenase type 2, 11-DH2, 11-beta-HSD2, 11-beta-hydroxysteroid dehydrogenase type II, 11-HSD type II, 11-beta-HSD type II, NAD-dependent 11-beta-hydroxysteroid dehydrogenase, 11-beta-HSD, Short chain dehydrogenase/reductase family 9C member 3There 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.