Background:  HSD11B2 catalyzes the conversion of cortisol to the inactive metabolite cortisone. The protein modulates intracellular glucocorticoid levels, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids.Defects in HSD11B2 are the cause of apparent mineralocorticoid excess (AME). AME is a potentially fatal disease characterized by severe juvenile low-renin hypertension, sodium retention, hypokalemia and low levels of aldosterone. It often leads to nephrocalcinosis.

Description: Rabbit polyclonal to HSD11B2

Immunogen: KLH conjugated synthetic peptide derived from HSD11B2

Specificity:  ·Reacts with Human, Mouse and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 44 kDa;

·Immunohistochemistry (Frozen/paraffin tissue section): 1/200-500;

·Immunocytochemistry: 1/100-500;

·ELISA: 1/1000;

·Optimal working dilutions must be determined by the end user.