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Mouse Anti-CYP24A1 Recombinant Antibody (CBFYC-2569) (V2LY-0125-LY932)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYC-2569
Antibody Isotype
IgG1, κ
Application
WB, IP, IF, ELISA

Basic Information

Immunogen
Amino acids 351-437 mapping near the C-terminus of human CYP24.
Host Species
Mouse
Specificity
Human
Antibody Isotype
IgG1, κ
Clonality
Monoclonal Antibody
Application Notes
ApplicationNote
WB1:100-1:1,000
IP1-2 μg per 100-500 μg of total protein (1 mL of cell lysate)
IF(ICC)1:50-1:500
ELISA1:100-1:1,000

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

Format
Liquid
Buffer
Gelatin & PBS
Preservative
Sodium Azide
Concentration
0.2 mg/mL
Purity
>95% as determined by analysis by SDS-PAGE
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
Entrez Gene ID
1591
UniProt ID
Q07973
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.
More Infomation

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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