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The role of vitamin D in calcium metabolism has been recognized and studied since the beginning of the century. After its production in the skin or its intestinal absorption, cholecalciferol needs metabolic activation in the liver and kidney. The production of the active hormone, calcitriol, is tightly feedback-regulated and is one of the key regulators of plasma calcium/phosphate and bone homeostasis through genomic (in)activation of a number of genes in its target tissues (intestine, bone, kidney, parathyroid gland). Indeed, calcitriol exerts its effects via a specific vitamin D receptor (VDR), a member of the superfamily of steroid/ thyroid/vitamin A hormone receptors (1), leading to gene regulation mediating various biological responses. Recently, interactions between the VDR and one of the retinoid acid receptors, retinoid X receptor (RXR), also a member of the same superfamily of steroid receptors, have been described (2, 3). These interactions, namely the formation of heterodimers between activated
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