Ergocalciferol (vitamin D2) is activated in vivo by hydroxylation to 25-hydroxyergocalciferol and 1α,25-dihydroxycalciferol. Activated Vitamin D2 molecules may be used in a wide range of studies to assess their effects on functions such as immune function and calcium homeostasis.
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New vitamin D analogs are interesting candidates for anticancer treatment, including squamous cell carcinomas (SCCs), especially in combination with cytostatics. In order to evaluate the effect of combined application of cisplatin, imatinib, or docetaxel and new vitamin D analogs [PRI-1906:
Current opinion in nephrology and hypertension, 16(4), 297-304 (2007-06-15)
Vitamin D has diverse biological actions, and consequently the mechanisms behind how it regulates gene transcription are diverse. Unlike its well described positive effects on gene transcription, little is known about how vitamin D induces transcriptional repression. Vitamin D-induced transcriptional
Journal of cellular biochemistry, 88(2), 282-285 (2003-01-10)
1alpha-Hydroxy-23 carboxy-24,25,26,27-tetranorvitamin D(3) (calcitroic acid) is known to be the major water-soluble metabolite produced during the deactivation of 1,25-(OH)(2)D(3). This deactivation process is carried out exclusively by the multicatalytic enzyme CYP24 and involves a series of oxidation reactions at C(24)
1α,25-dihydroxy vitamin D [1,25(OH)(2)D] is the active metabolite of vitamin D. Antibody-based detection methods lack specificity, but when combined with isotope dilution/ultra-performance liquid chromatography (UPLC)-tandem mass spectrometry, immunoextraction provides an attractive method for 1,25(OH)(2)D. We developed a method for simultaneous
Archives of ophthalmology (Chicago, Ill. : 1960), 120(5), 607-612 (2002-05-25)
Although calcitriol (1,25-dihydroxycholecalciferol) and vitamin D(2) inhibit retinoblastoma growth in the athymic (nude) mouse xenograft (Y-79 cell line) model of retinoblastoma, they can cause severe toxicity. To examine the toxicity of and dose-dependent response for the inhibition of tumor growth
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