|Application ||WB, IHC-P, FC, E|
|Calculated MW||44127 Da|
|Antigen Region||277-306 aa|
|Other Names||Corticosteroid 11-beta-dehydrogenase isozyme 2, 111-, 11-beta-hydroxysteroid dehydrogenase type 2, 11-DH2, 11-beta-HSD2, 11-beta-hydroxysteroid dehydrogenase type II, -HSD11 type II, NAD-dependent 11-beta-hydroxysteroid dehydrogenase, 11-beta-HSD, HSD11B2, HSD11K|
|Target/Specificity||This HSD11B2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 277-306 amino acids from the Central region of human HSD11B2.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||HSD11B2 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Catalyzes the conversion of cortisol to the inactive metabolite cortisone. Modulates intracellular glucocorticoid levels, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids.|
|Cellular Location||Microsome. Endoplasmic reticulum|
|Tissue Location||Found in placenta, kidney, pancreas, prostate, ovary, small intestine and colon|
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Provided below are standard protocols that you may find useful for product applications.
There 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.
Li, J., et al. Breast Cancer Res. 12 (2), R19 (2010)
Ni, X.T., et al. Placenta 30(12):1023-1028(2009)
Mericq, V., et al. Eur. J. Endocrinol. 161(3):419-425(2009)
Stark, M.J., et al. Am. J. Physiol. Regul. Integr. Comp. Physiol. 297 (2), R510-R514 (2009)
Lepenies, J., et al. Clin. Exp. Hypertens. 31(4):376-379(2009)
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