| Budget Amount *help |
¥113,360,000 (Direct Cost: ¥87,200,000、Indirect Cost: ¥26,160,000)
Fiscal Year 2009: ¥22,100,000 (Direct Cost: ¥17,000,000、Indirect Cost: ¥5,100,000)
Fiscal Year 2008: ¥22,100,000 (Direct Cost: ¥17,000,000、Indirect Cost: ¥5,100,000)
Fiscal Year 2007: ¥22,100,000 (Direct Cost: ¥17,000,000、Indirect Cost: ¥5,100,000)
Fiscal Year 2006: ¥22,100,000 (Direct Cost: ¥17,000,000、Indirect Cost: ¥5,100,000)
Fiscal Year 2005: ¥24,960,000 (Direct Cost: ¥19,200,000、Indirect Cost: ¥5,760,000)
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| Research Abstract |
α-Klotho binds to Na^+, K^+-ATPase and is rapidly translocated from endosomal organella to the plasma membrane together with Na^+, K^+-ATPase in response to altered extracellular calcium concentration. Increased Na^+ gradient produced by elevated Na^+, K^+-ATPase activity drives PTH secretion and transepithelial transport of calcium. β-Klotho is essential for FGF15 signaling and functions as a key regulator of bile acid/cholesterol metabolism. Detailed analyses revealed a comprehensive regulatory scheme of mineral homeostasis involving the mutually regulated positive/negative feedback actions of α-Klotho, FGF23 and 1,25(OH)_2D and an analogous regulatory network composed of β-Klotho, FGF15/humanFGF19 and bile acids that regulate bile acid/cholesterol metabolism. We also suggested Klotho-independent FGF21 signaling pathway(s). α-Klotho functions as a glyco-recognition/binding protein . The demonstrated molecular functions of α-Klotho provide a new paradigm that may change current concept in mineral homeostasis.
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