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HSD11B2 Antibody (Center) Blocking PeptideSynthetic peptide
| Country | United States
Ordering Information
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|---|---|---|---|---|
| Catalog # | Size | Availability | Price | |
| BP9764c | 0.1 mg 400 ul | In Stock | $ 45.00 | DISCONTINED INQUIRE CLICK INQUIRE Add to cart |
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- Citiations : 0
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HSD11B2 Antibody (Center) Blocking Peptide - Product info | |
| Primary Accession | P80365 |
| Calculated MW | 44127 Da |
HSD11B2 Antibody (Center) Blocking Peptide - Additional info | |
| Gene ID 3291 | |
| 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. | |
HSD11B2 Antibody (Center) Blocking Peptide - Protein Information | |
| Name HSD11B2 | |
| Synonyms HSD11K | |
| 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 | |
HSD11B2 Antibody (Center) Blocking Peptide - Related products
HSD11B2 Antibody (Center) Blocking Peptide - Research Areas
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BACKGROUND
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.
REFERENCES
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)