| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Outline of Final Research Achievements |
Vitamin D is a primary regulator in many biological phenomena such as calcium homeostasis and bone formation. Such actions are thought to be mediated through transcriptional controls by the vitamin D receptor (VDR). Ligand-induced function of VDR have been well established, however, the physiological impact of unliganded VDR still remains unclear. Here we report that VDR helix 12 deletion (ΔAF2) mutant mice fed with high calcium diet exhibited impaired bone formation unlike VDRKO mice. Trabeculae in VDRΔAF2 mice were filled with fibroblast-like cells instead of bone marrow. Microarray and real-time RT-PCR analyses of kidney in VDRKO and VDRΔAF2 mice reveal distinct gene expression profiles. Six putative target genes regulated by unliganded VDR and responsible for impaired bone formation were identified.
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