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Mouse Anti-Cyp11b1 Recombinant Antibody (CBYC-A947) (CBMAB-A4360-YC)

Provided herein is a Mouse monoclonal antibody against Mouse Cytochrome P450 Family 11 Subfamily B Member 1. The antibody can be used for immunoassay techniques, such as ELISA.
See all Cyp11b1 antibodies

Summary

Host Animal
Mouse
Specificity
Mouse
Clone
CBYC-A947
Antibody Isotype
IgG1
Application
ELISA

Basic Information

Specificity
Mouse
Antibody Isotype
IgG1
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!]

Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Cytochrome P450 Family 11 Subfamily B Member 1
Introduction
CYP11B1 (Cytochrome P450 Family 11 Subfamily B Member 1) is a protein coding gene. Diseases associated with CYP11B1 include Adrenal Hyperplasia, Congenital, Due To Steroid 11-Beta-Hydroxylase Deficiency and Hyperaldosteronism, Familial, Type I. Among its
Entrez Gene ID
110115
UniProt ID
Q3UQH5
Alternative Names
Cpn2; Cyp11b; Cyp11b-2
Function
A cytochrome P450 monooxygenase involved in the biosynthesis of adrenal corticoids (PubMed:18215163).

Catalyzes the hydroxylation of carbon hydrogen bond at 11-beta position of 11-deoxycortisol and 11-deoxycorticosterone/21-hydroxyprogesterone yielding cortisol or corticosterone, respectively (PubMed:18215163).

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:18215163).
Biological Process
Aldosterone biosynthetic process Source: BHF-UCL
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: BHF-UCL
Cortisol metabolic process Source: GO_Central
Glucocorticoid biosynthetic process Source: GO_Central
Glucose homeostasis Source: BHF-UCL
Immune response Source: BHF-UCL
Regulation of blood pressure Source: BHF-UCL
Sterol metabolic process Source: Reactome
Cellular Location
Mitochondrion inner membrane
Involvement in disease
Adrenal hyperplasia 4 (AH4):
A form of congenital adrenal hyperplasia, a common recessive disease due to defective synthesis of cortisol. Congenital adrenal hyperplasia is characterized by androgen excess leading to ambiguous genitalia in affected females, rapid somatic growth during childhood in both sexes with premature closure of the epiphyses and short adult stature. Four clinical types: 'salt wasting' (SW, the most severe type), 'simple virilizing' (SV, less severely affected patients), with normal aldosterone biosynthesis, 'non-classic form' or late-onset (NC or LOAH) and 'cryptic' (asymptomatic).
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.

Fylaktou, I., Smyrnaki, P., Sertedaki, A., Dracopoulou, M., & Kanaka-Gantenbein, C. (2021). Congenital adrenal hyperplasia caused by compound heterozygosity of two novel CYP11B1 gene variants. Hormones, 1-7.

Nakano, Y., Iwata, N., Ogura-Ochi, K., Hasegawa, K., Hirasawa, A., & Otsuka, F. (2021). Preclinical diagnosis and identification of the chimeric CYP11B1/CYP11B2 gene in two pediatric cases of a Japanese family with glucocorticoid-remediable aldosteronism. Hypertension Research, 44(7), 891-893.

Grgic, O., Gazzara, M. R., Chesi, A., Medina-Gomez, C., Cousminer, D. L., Mitchell, J. A., ... & Rivadeneira, F. (2021). CYP11B1 variants influence skeletal maturation via alternative splicing. Communications biology, 4(1), 1-10.

Bongarzone, S., Basagni, F., Sementa, T., Singh, N., Gakpetor, C., Faugeras, V., ... & Gee, A. D. (2019). Development of [18F] FAMTO: A novel fluorine-18 labelled positron emission tomography (PET) radiotracer for imaging CYP11B1 and CYP11B2 enzymes in adrenal glands. Nuclear medicine and biology, 68, 14-21.

Baş, F., Toksoy, G., Ergun-Longmire, B., Uyguner, Z. O., Abalı, Z. Y., Poyrazoğlu, Ş., ... & Darendeliler, F. (2018). Prevalence, clinical characteristics and long-term outcomes of classical 11 β-hydroxylase deficiency (11BOHD) in Turkish population and novel mutations in CYP11B1 gene. The Journal of steroid biochemistry and molecular biology, 181, 88-97.

MacKenzie, S. M., Davies, E., & Alvarez-Madrazo, S. (2017). Analysis of the aldosterone synthase (CYP11B2) and 11β-hydroxylase (CYP11B1) genes. Hypertension, 139-150.

Kometani, M., Yoneda, T., Demura, M., Koide, H., Nishimoto, K., Mukai, K., ... & Takeda, Y. (2017). Cortisol overproduction results from DNA methylation of CYP11B1 in hypercortisolemia. Scientific reports, 7(1), 1-9.

Emmerich, J., van Koppen, C. J., Burkhart, J. L., Hu, Q., Siebenbürger, L., Boerger, C., ... & Hartmann, R. W. (2017). Lead optimization generates CYP11B1 inhibitors of pyridylmethyl isoxazole type with improved pharmacological profile for the treatment of Cushing’s disease. Journal of Medicinal Chemistry, 60(12), 5086-5098.

Kandemir, N., Yilmaz, D. Y., Gonc, E. N., Ozon, A., Alikasifoglu, A., Dursun, A., & Ozgul, R. K. (2017). Novel and prevalent CYP11B1 gene mutations in Turkish patients with 11-β hydroxylase deficiency. The Journal of Steroid Biochemistry and Molecular Biology, 165, 57-63.

Hawton, K., Walton-Betancourth, S., Rumsby, G., Raine, J., & Dattani, M. (2017). Growth hormone with aromatase inhibitor may improve height in CYP11B1 congenital adrenal hyperplasia. Pediatrics, 139(2).

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For research use only. Not intended for any clinical use.

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