• Product name

    Anti-C11B2/CYP11B2 antibody
    See all C11B2/CYP11B2 primary antibodies
  • Description

    Rabbit polyclonal to C11B2/CYP11B2
  • Host species

  • Tested applications

    Suitable for: IHC-P, WBmore details
  • Species reactivity

    Reacts with: Human
  • Immunogen

    Recombinant fragment corresponding to Human C11B2/CYP11B2 aa 406-451.


  • Positive control

    • Human adrenal gland tissue, RT-4, U-251 MG, Liver & Tonsil lysates
  • General notes

     This product was previously labelled as C11B2




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.

Application Abreviews Notes
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.


  • Function

    Preferentially catalyzes the conversion of 11-deoxycorticosterone to aldosterone via corticosterone and 18-hydroxycorticosterone.
  • Involvement in disease

    Defects 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 similarities

    Belongs to the cytochrome P450 family.
  • Cellular localization

    Mitochondrion membrane.
  • Information by UniProt
  • Database links

  • Alternative names

    • ALDOS antibody
    • Aldosterone synthase antibody
    • Aldosterone-synthesizing enzyme antibody
    • C11B2_HUMAN antibody
    • CYP11B2 antibody
    • CYPXIB2 antibody
    • Cytochrome P-450Aldo antibody
    • Cytochrome P-450C18 antibody
    • Cytochrome P450 11B2 antibody
    • Cytochrome P450 11B2, mitochondrial antibody
    • mitochondrial antibody
    • P-450Aldo antibody
    • P-450C18 antibody
    • Steroid 18-hydroxylase antibody
    see all


  • 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.

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