Abstract
The calciotropic hormone 1alpha, 25-dihydroxyvitamin D(3) [1alpha, 25 (OH)(2)D(3)] regulates many biological actions such as calcium homeostasis, cell differentiation and proliferations. Most of the biological actions of 1alpha, 25 (OH)(2)D(3) are thought to be mediated by the vitamin D receptor (VDR) , which is a member of a nuclear receptor superfamily acting as a ligand-inducible transcription factor. VDR deficient mice (conventional-VDRKO mice) appear the typical phenotype of vitamin D dependent type II rickets. However, no defect in conventional-VDRKO mice was observed in osteoblast specific-conditional VDRKO mice. Here, we introduce VDR function in bone involving such difference phenotype in these mice.
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