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Rabbit Anti-CYP24A1 Recombinant Antibody (EG888) (CBMAB-EN1059-LY)

The product is antibody recognizes CYP24A1. The antibody EG888 immunoassay techniques such as: WB: 1:500~1:1000 ELISA: 1:10000.
See all CYP24A1 antibodies

Summary

Host Animal
Rabbit
Specificity
Human
Clone
EG888
Antibody Isotype
IgG
Application
WB: 1:500~1:1000 ELISA: 1:10000

Basic Information

Immunogen
The antibody was produced against synthesized peptide derived from internal of human Cytochrome P450 24A1.
Specificity
Human
Antibody Isotype
IgG
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!]

Format
Liquid
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Cytochrome P450 Family 24 Subfamily A Member 1
Introduction
CYP24A1 (Cytochrome P450 Family 24 Subfamily A Member 1) is a Protein Coding gene. Diseases associated with CYP24A1 include Hypercalcemia, Infantile, 1 and Idiopathic Infantile Hypercalcemia. Among its related pathways are Metabolism and Cytochrome P450 - arranged by substrate type. Gene Ontology (GO) annotations related to this gene include oxidoreductase activity and heme binding. An important paralog of this gene is CYP27A1.
Entrez Gene ID
1591
UniProt ID
Q07973
Alternative Names
Cytochrome P450 Family 24 Subfamily A Member 1; Cytochrome P450, Subfamily XXIV (Vitamin D 24-Hydroxylase); Cytochrome P450, Family 24, Subfamily A, Polypeptide 1; Vitamin D(3) 24-Hydroxylase; Cytochrome P450 24A1; Cytochrome P450-CC24; 24-OHase; CYP24; 1,25-Dihydroxyvitamin D(3) 24-Hydroxylase, Mitochondrial;
Function
A cytochrome P450 monooxygenase with a key role in vitamin D catabolism and calcium homeostasis. Via C24- and C23-oxidation pathways, catalyzes the inactivation of both the vitamin D precursor calcidiol (25-hydroxyvitamin D3) and the active hormone calcitriol (1-alpha,25-dihydroxyvitamin D3) (PubMed:24893882, PubMed:15574355, PubMed:8679605, PubMed:11012668, PubMed:16617161, PubMed:29461981).

With initial hydroxylation at C-24 (via C24-oxidation pathway), performs a sequential 6-step oxidation of calcitriol leading to the formation of the biliary metabolite calcitroic acid (PubMed:24893882, PubMed:15574355).

With initial hydroxylation at C-23 (via C23-oxidation pathway), catalyzes sequential oxidation of calcidiol leading to the formation of 25(OH)D3-26,23-lactone as end product (PubMed:11012668, PubMed:8679605).

Preferentially hydroxylates at C-25 other vitamin D active metabolites, such as CYP11A1-derived secosteroids 20S-hydroxycholecalciferol and 20S,23-dihydroxycholecalciferol (PubMed:25727742).

Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via FDXR/adrenodoxin reductase and FDX1/adrenodoxin (PubMed:8679605).
Biological Process
Fatty acid omega-oxidation Source: GO_Central
Osteoblast differentiation Source: BHF-UCL
Response to vitamin D Source: BHF-UCL
Vitamin D catabolic process Source: UniProtKB
Vitamin D metabolic process Source: Reactome
Vitamin D receptor signaling pathway Source: BHF-UCL
Vitamin metabolic process Source: Reactome
Cellular Location
Mitochondrion
Involvement in disease
Hypercalcemia, infantile, 1 (HCINF1):
A disorder characterized by abnormally high level of calcium in the blood, failure to thrive, vomiting, dehydration, and nephrocalcinosis.

Yasuda, K., Nishikawa, M., Okamoto, K., Horibe, K., Mano, H., Yamaguchi, M., ... & Sakaki, T. (2021). Elucidation of metabolic pathways of 25-hydroxyvitamin D3 mediated by CYP24A1 and CYP3A using Cyp24a1 knockout rats generated by CRISPR/Cas9 system. Journal of Biological Chemistry, 296.

Meyer, M. B., & Pike, J. W. (2020). Mechanistic homeostasis of vitamin D metabolism in the kidney through reciprocal modulation of Cyp27b1 and Cyp24a1 expression. The Journal of steroid biochemistry and molecular biology, 196, 105500.

Cavalier, E., Huyghebaert, L., Rousselle, O., Bekaert, A. C., Kovacs, S., Vranken, L., ... & Ladang, A. (2020). Simultaneous measurement of 25 (OH)-vitamin D and 24, 25 (OH) 2-vitamin D to define cut-offs for CYP24A1 mutation and vitamin D deficiency in a population of 1200 young subjects. Clinical Chemistry and Laboratory Medicine (CCLM), 58(2), 197-201.

Cappellani, D., Brancatella, A., Kaufmann, M., Minucci, A., Vignali, E., Canale, D., ... & Marcocci, C. (2019). Hereditary hypercalcemia caused by a homozygous pathogenic variant in the CYP24A1 gene: a case report and review of the literature. Case Reports in Endocrinology, 2019.

Cai, H., Jiao, Y., Li, Y., Yang, Z., He, M., & Liu, Y. (2019). Low CYP24A1 mRNA expression and its role in prognosis of breast cancer. Scientific reports, 9(1), 1-11.

Sun, H., Jiang, C., Cong, L., Wu, N., Wang, X., Hao, M., ... & Cong, X. (2018). CYP24A1 Inhibition facilitates the antiproliferative effect of 1, 25 (OH) 2D3 through downregulation of the WNT/β-Catenin pathway and methylation-mediated regulation of CYP24A1 in colorectal cancer cells. DNA and Cell Biology, 37(9), 742-749.

Agnello, L., Scazzone, C., Lo Sasso, B., Ragonese, P., Milano, S., Salemi, G., & Ciaccio, M. (2018). CYP27A1, CYP24A1, and RXR-α Polymorphisms, Vitamin D, and multiple sclerosis: a pilot study. Journal of Molecular Neuroscience, 66(1), 77-84.

Pronicka, E., Ciara, E., Halat, P., Janiec, A., Wójcik, M., Rowińska, E., ... & Litwin, M. (2017). Biallelic mutations in CYP24A1 or SLC34A1 as a cause of infantile idiopathic hypercalcemia (IIH) with vitamin D hypersensitivity: molecular study of 11 historical IIH cases. Journal of applied genetics, 58(3), 349-353.

Carpenter, T. O. (2017). CYP24A1 loss of function: clinical phenotype of monoallelic and biallelic mutations. The Journal of steroid biochemistry and molecular biology, 173, 337-340.

Hawkes, C. P., Li, D., Hakonarson, H., Meyers, K. E., Thummel, K. E., & Levine, M. A. (2017). CYP3A4 induction by rifampin: an alternative pathway for vitamin D inactivation in patients with CYP24A1 mutations. The Journal of Clinical Endocrinology & Metabolism, 102(5), 1440-1446.

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

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