|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|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. 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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