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The regular vitamin D metabolic profiles illustrated with either wild-type mouse VDR or VDR null mice transgenic for the wild-type human VDR, but not the ligand binding-defective form of the protein, this suggests the essential roles of VDR on VD metabolism 25
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reported that combined treatment of CUR and sunitinib increased the expression of the ADAMTS18 gene and significantly decreased the expression level of NCOA4, FTH1 and p53, indicating that CUR could lower the mRNA and protein expression levels of NCOA4, FTH1, and P53, which suggested that CUR may drive ferroptosis by increasing ADAMTS18 gene expression (111)
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