Key features and details
- Rabbit polyclonal to C11B2/CYP11B2
- Suitable for: IHC-P
- Reacts with: Mouse, Rat, Human
- Isotype: IgG
Product nameAnti-C11B2/CYP11B2 antibody
See all C11B2/CYP11B2 primary antibodies
DescriptionRabbit polyclonal to C11B2/CYP11B2
Tested applicationsSuitable for: IHC-Pmore details
Species reactivityReacts with: Mouse, Rat, Human
This product was previously labelled as C11B2
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.09% Sodium azide
Constituents: 0.01% BSA, 50% Glycerol
Concentration information loading...
PurityProtein A purified
Our Abpromise guarantee covers the use of ab203069 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/100 - 1/500.
When using a fluorescent probe the recommended dilution is 1/50 – 1/200.
FunctionPreferentially catalyzes the conversion of 11-deoxycorticosterone to aldosterone via corticosterone and 18-hydroxycorticosterone.
Involvement in diseaseDefects in CYP11B2 are the cause of corticosterone methyloxidase type 1 deficiency (CMO-1 deficiency) [MIM:203400]; also known as aldosterone deficiency due to defect in 18-hydroxylase or aldosterone deficiency I. CMO-1 deficiency is an autosomal recessive disorder of aldosterone biosynthesis. There are two biochemically different forms of selective aldosterone deficiency be termed corticosterone methyloxidase (CMO) deficiency type 1 and type 2. In CMO-1 deficiency, aldosterone is undetectable in plasma, while its immediate precursor, 18-hydroxycorticosterone, is low or normal.
Defects in CYP11B2 are the cause of corticosterone methyloxidase type 2 deficiency (CMO-2 deficiency) [MIM:610600]. CMO-2 is an autosomal recessive disorder of aldosterone biosynthesis. In CMO-2 deficiency, aldosterone can be low or normal, but at the expense of increased secretion of 18-hydroxycorticosterone. Consequently, patients have a greatly increased ratio of 18-hydroxycorticosterone to aldosterone and a low ratio of corticosterone to 18-hydroxycorticosterone in serum.
Defects in CYP11B2 are a cause of familial hyperaldosteronism type 1 (FH1) [MIM:103900]. It is a disorder characterized by hypertension, variable hyperaldosteronism, and abnormal adrenal steroid production, including 18-oxocortisol and 18-hydroxycortisol. There is significant phenotypic heterogeneity, and some individuals never develop hypertension. Note=The molecular defect causing hyperaldosteronism familial type 1 is an anti-Lepore-type fusion of the CYP11B1 and CYP11B2 genes. The hybrid gene has the promoting part of CYP11B1, ACTH-sensitive, and the coding part of CYP11B2.
Sequence similaritiesBelongs to the cytochrome P450 family.
Cellular localizationMitochondrion membrane.
- Information by UniProt
- ALDOS antibody
- Aldosterone synthase antibody
- Aldosterone-synthesizing enzyme antibody
Immunohistochemical analysis of formalin fixed and paraffin embedded mouse embryo tissue labeling C11B2/CYP11B2 using ab203069 at 1/200 dilution. DAB staining.
Immunohistochemical analysis of formalin fixed and paraffin embedded human colon carcinoma labeling C11B2/CYP11B2 using ab203069 at 1/200 dilution. DAB staining.
ab203069 has not yet been referenced specifically in any publications.