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HSD11B2 Antibody (Center) Blocking PeptideSynthetic peptide

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United States
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Ordering Information
Catalog # Size Availability Price  
BP9764c 0.1 mg 400 ul In Stock $ 45.00 Add to cart
  • Specification
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HSD11B2 Antibody (Center) Blocking Peptide - Product info

Primary AccessionP80365
Calculated MW44127 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

AP9764c: HSD11B2 Antibody (Center)

BP9764c: HSD11B2 Antibody (Center) Blocking Peptide

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Provided below are standard protocols that you may find useful for product applications.

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)