Key features and details
- Rabbit polyclonal to C11B2/CYP11B2
- Suitable for: IHC-P, WB
- Reacts with: Human
- Isotype: IgG
Product nameAnti-C11B2/CYP11B2 antibody
See all C11B2/CYP11B2 primary antibodies
DescriptionRabbit polyclonal to C11B2/CYP11B2
Tested applicationsSuitable for: IHC-P, WBmore details
Species reactivityReacts with: Human
- Human adrenal gland tissue, RT-4, U-251 MG, Liver & Tonsil lysates
This product was previously labelled as C11B2
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term.
Storage bufferpH: 7.20
Preservative: 0.02% Sodium azide
Constituents: 59% PBS, 40% Glycerol
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab151052 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||1/200 - 1/500. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.|
|WB||1/200 - 1/500. Predicted molecular weight: 58 kDa.|
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
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human adrenal gland tissue labelling C11B2/CYP11B2 with ab151052. Staining shows strong cytoplasmic positivity in glandular cells.
All lanes : Anti-C11B2/CYP11B2 antibody (ab151052) at 1/250 dilution
Lane 1 : RT-4 lysate
Lane 2 : U-251 MG lysate
Lane 3 : Human Plasma lysate
Lane 4 : Liver lysate
Lane 5 : Tonsil lysate
Predicted band size: 58 kDa
ab151052 has not yet been referenced specifically in any publications.