| Budget Amount *help |
¥20,280,000 (Direct Cost: ¥15,600,000、Indirect Cost: ¥4,680,000)
Fiscal Year 2013: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2012: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥10,660,000 (Direct Cost: ¥8,200,000、Indirect Cost: ¥2,460,000)
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| Outline of Final Research Achievements |
Proinflammatory stimuli, including tumor necrosis factor α (TNFα), activate IκB kinase (IKK) complex and induces NF-κ activation. We previously found that nuclear IKKβ acts as an adaptor protein for IκBα degradation and NF-κB activation. To elucidate the role of IKKβ in vivo, we developed mice expressing nuclear-localized IKKβ and lacking cytoplasmic IKKβ in hepatocytes. These mice showed massive hepatic necrosis and developed liver cirrhosis. Whereas, liver failure of these mice was ameliorated by crossing with mice expressing cytoplasmic-localized IKKβ. These results suggest that nuclear IKKβ promote cell death and cytoplasmic IKKβ protect cells from death in vivo. The opposite effect of IKKβ in the nucleus and cytoplasm is closely linked to hepatitis and hepatocellular carcinoma.
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