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Mouse Anti-CYP11B2 Recombinant Antibody (CBCNC-547) (CBMAB-C3283-CN)

This product is a Mouse antibody that recognizes CYP11B2. The antibody CBCNC-547 can be used for immunoassay techniques such as: ELISA, ICC, IHC-P, WB.
See all CYP11B2 antibodies

Summary

Host Animal
Mouse
Specificity
Rat
Clone
CBCNC-547
Antibody Isotype
IgG1, κ
Application
ELISA, ICC, IHC-P, WB

Basic Information

Specificity
Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Buffer
PBS, 50% glycerol
Preservative
0.09% Sodium azide

Target

Full Name
Cytochrome P450 Family 11 Subfamily B Member 2
Introduction
CYP11B2 (Cytochrome P450 Family 11 Subfamily B Member 2) is a Protein Coding gene. Diseases associated with CYP11B2 include Corticosterone Methyloxidase Type I Deficiency and Corticosterone Methyloxidase Type Ii Deficiency. Among its related pathways are superpathway of steroid hormone biosynthesis and Metabolism. Gene Ontology (GO) annotations related to this gene include iron ion binding and oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen. An important paralog of this gene is CYP11B1.
Entrez Gene ID
24294
UniProt ID
P30100
Alternative Names
Cytochrome P450 Family 11 Subfamily B Member 2; Cytochrome P450, Subfamily XIB (Steroid 11-Beta-Hydroxylase), Polypeptide 2; Cytochrome P450, Family 11, Subfamily B, Polypeptide 2; Aldosterone-Synthesizing Enzyme; Steroid 11-Beta-Monooxygenase; Aldosterone Synthase; Cytochrome P-450Aldo; Cytochrome P-450C18; EC 1.14.15.4; CYPXIB2; ALDOS; Mitochondrial Cytochrome P450, Family 11, Subfamily B, Polypeptide 2; Steroid 18-Hydroxylase, Aldosterone Synthase, P450C18, P450aldo;
Function
A cytochrome P450 monooxygenase that catalyzes the biosynthesis of adrenal mineralocorticoid aldosterone (PubMed:11856349, PubMed:23322723, PubMed:1594605, PubMed:9814506).

Catalyzes three sequential oxidative reactions of 11-deoxycorticosterone/21-hydroxyprogesterone, namely 11-beta hydroxylation followed with two successive oxidations at C18 to yield 18-hydroxy and then 18-aldehyde derivatives, resulting in the formation of aldosterone (PubMed:11856349, PubMed:23322723, PubMed:1594605, PubMed:9814506).

Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate and reducing the second into a water molecule. Two electrons are provided by NADPH via a two-protein mitochondrial transfer system comprising flavoprotein FDXR (adrenodoxin/ferredoxin reductase) and nonheme iron-sulfur protein FDX1 or FDX2 (adrenodoxin/ferredoxin) (PubMed:11856349, PubMed:23322723, PubMed:1594605, PubMed:9814506).
Biological Process
Aldosterone biosynthetic process Source: UniProtKB
C21-steroid hormone biosynthetic process Source: BHF-UCL
Cellular response to hormone stimulus Source: UniProtKB
Cellular response to peptide hormone stimulus Source: GO_Central
Cellular response to potassium ion Source: UniProtKB
Cholesterol metabolic process Source: GO_Central
Cortisol biosynthetic process Source: UniProtKB
Cortisol metabolic process Source: GO_Central
Glucocorticoid biosynthetic process Source: GO_Central
Mineralocorticoid biosynthetic process Source: Reactome
Potassium ion homeostasis Source: BHF-UCL
Regulation of blood volume by renal aldosterone Source: BHF-UCL
Renal water homeostasis Source: BHF-UCL
Sodium ion homeostasis Source: BHF-UCL
Sterol metabolic process Source: Reactome
Cellular Location
Mitochondrion inner membrane
Involvement in disease
Corticosterone methyloxidase 1 deficiency (CMO-1 deficiency):
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.
Corticosterone methyloxidase 2 deficiency (CMO-2 deficiency):
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.
Hyperaldosteronism, familial, 1 (HALD1):
The disease is caused by variants affecting the gene represented in this entry. The molecular defect causing hyperaldosteronism familial 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.
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.
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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