Vitamin-D

Vitamin-D refers to the secosteroid prohormone that a series of cytochrome P450 hydroxylases converts, by 25- and 1α-hydroxylation, into 1α,25-dihydroxyvitamin D₃, the ligand of the vitamin D receptor (VDR), and later inactivates by 24-hydroxylation. Preclinical research has used VDR knockout mice to separate ligand-dependent from ligand-independent receptor actions in bone and skin, and human cell lines to map VDR target genes such as the cathelicidin antimicrobial peptide gene. Research Market supplies vitamin D with lot data on the certificate of analysis. It is sold strictly for laboratory research use.

Chemical structure and identification

• Compound class: Secosteroid (vitamin D)
• Chemical form: The product listing does not state which form (for example cholecalciferol, D₃, or ergocalciferol, D₂); the form is reported on the batch certificate of analysis
• Form: Supplied in a sealed research vial
• Analytical methods: Identity and purity data reported on the batch certificate of analysis

Research applications

• Cytochrome P450 metabolism: Reviewed for the P450 enzymes behind 25- and 1α-hydroxylation that generate 1α,25-dihydroxyvitamin D₃ and the 24- and 23-hydroxylases that start its inactivation, drawing on crystal structures and knockout animals [1]
• VDR knockout mice: VDR-null mice developed hypocalcemia, hyperparathyroidism, hypophosphatemia and rickets; a high-calcium, high-phosphorus, lactose diet prevented the mineral and growth-plate changes, pointing to intestinal receptor action [2]
• Ligand-independent VDR action: Alopecia in VDR-null mice persisted after five generations without dietary or UV-derived vitamin D, and hair-reconstitution assays traced the defect in anagen initiation to VDR-null keratinocytes [3]
• VDR target genes: 1,25-Dihydroxyvitamin D₃ induced the human cathelicidin antimicrobial peptide (CAMP) gene through a VDR-bound vitamin D response element in myeloid, keratinocyte and colon cancer cell lines; the element was absent from mouse, rat and dog genomes [4]

Reference citations

1. Jones G. et al. (2014). Cytochrome P450-mediated metabolism of vitamin D. J Lipid Res, 55(1):13–31. PMID 23564710 · DOI
2. Demay M.B. (2006). Mechanism of vitamin D receptor action. Ann N Y Acad Sci, 1068:204–213. PMID 16831920 · DOI
3. Sakai Y. et al. (2001). Metabolic and cellular analysis of alopecia in vitamin D receptor knockout mice. J Clin Invest, 107(8):961–966. PMID 11306599 · DOI
4. Gombart A.F. et al. (2005). Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. FASEB J, 19(9):1067–1077. PMID 15985530 · DOI

Literature summaries describe published preclinical research and are not claims about this product’s effects in humans or animals.