Description
HSD11B2 Antibody | 23-384 | Gentaur UK, US & Europe Distribution
Host: Rabbit
Reactivity: Human, Rat
Homology: N/A
Immunogen: Recombinant fusion protein containing a sequence corresponding to amino acids 266-405 of human HSD11B2 (NP_000187.3) .
Research Area: Cancer, Cell Cycle, Growth Factors, Signal Transduction
Tested Application: WB, IHC
Application: WB: 1:200 - 1:1000
IHC: 1:50 - 1:100
Specificiy: N/A
Positive Control 1: HepG2
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: Observed: 44kDa
Validation: N/A
Isoform: N/A
Purification: Affinity purification
Clonality: Polyclonal
Clone: N/A
Isotype: IgG
Conjugate: Unconjugated
Physical State: Liquid
Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.
Concentration: N/A
Storage Condition: Store at -20˚C. Avoid freeze / thaw cycles.
Alternate Name: HSD11B2, AME, AME1, HSD11K, HSD2, SDR9C3
User Note: Optimal dilutions for each application to be determined by the researcher.
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.