| 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: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Outline of Final Research Achievements |
The purpose of this study was to elucidate the molecular mechanism(s) of HCV-mediated activation of the transcription factor FoxO1 that is associated with increased gluconeogenesis and induction of apoptosis through oxidative stress and JNK activation. The results obtained demonstrated that HCV infection induces oxidative stress (production of reactive oxygen species [ROS]) and JNK activation, which leads to increased expression of the phosphatase MKP3 to mediate dephosphorylation (activation) and nuclear localization of FoxO1, thereby promoting gluconeogenesis. Also, HCV-induced oxidative stress and JNK activation lead to increased expression of the pro-apoptotic protein Bim and activation of another pro-apoptotic protein Bax, thereby triggering mitochondrion-mediated apoptosis.
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