Overview

  • Product name

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

    Rabbit polyclonal to C11B2/CYP11B2
  • Host species

    Rabbit
  • Tested applications

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

    Reacts with: Human
  • Immunogen

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

    FLYSLGRNAALFPRPERYNPQRWLDIRGSGRNFHHVPFGFGMRQCL

  • Positive control

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

     This product was previously labelled as C11B2

     

Properties

Applications

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.

Target

  • 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

Images

  • 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

References

ab151052 has not yet been referenced specifically in any publications.

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