| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Outline of Final Research Achievements |
Previously, we reported that ZNRF1 ubiquitin ligase promotes Wallerian degeneration by degrading AKT to induce GSK3B activation. ZNRF1 starts to degrade AKT only after neuronal injury, but the mechanism of ZNRF1 activation in response to invasive stimulations has been unclear. Here we show that oxidative stress activates ZNRF1 by inducing its phosphorylation in neurons. We also found by using in vitro and in vivo models that the pathophysiological significance of ZNRF1-mediated signaling in the regulation of murine corticogenesis, and elucidating the underlying the phosphorylation mediated regulatory mechanism of its catalytic activity is useful for a better understanding of corticogenesis by the selective proteolysis of AKT.
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