L’anticorps anti-HSD11B2 Polyclonal Lapin est utilisé pour la détection de HSD11B2 dans des échantillons de Humain, Souris et Rat. Il a été validé pour WB et 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
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
PBS, 50 % glycerol, 0.05 % Proclin 300, 0.05 %BSA
Agent conservateur
ProClin
Précaution d'utilisation
This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
-20 °C
Stockage commentaire
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.