| Budget Amount *help |
¥71,370,000 (Direct Cost: ¥54,900,000、Indirect Cost: ¥16,470,000)
Fiscal Year 2012: ¥13,520,000 (Direct Cost: ¥10,400,000、Indirect Cost: ¥3,120,000)
Fiscal Year 2011: ¥13,520,000 (Direct Cost: ¥10,400,000、Indirect Cost: ¥3,120,000)
Fiscal Year 2010: ¥14,300,000 (Direct Cost: ¥11,000,000、Indirect Cost: ¥3,300,000)
Fiscal Year 2009: ¥13,520,000 (Direct Cost: ¥10,400,000、Indirect Cost: ¥3,120,000)
Fiscal Year 2008: ¥16,510,000 (Direct Cost: ¥12,700,000、Indirect Cost: ¥3,810,000)
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| Research Abstract |
Cross-talk between reactive oxygen species (ROS) and cellular signaling systems, including NF-kB pathway, plays an important role in inflammation and cell death. IKKb phosphorylates IkB and activates NF-kB when cells are treated with proinflammatory cytokines. We found that the nuclear IKKb acts as an adaptor protein for IkBa ubiquitination and degradation for oxidative stress-induced NF-kB activation. NF-kB activation by the nuclear IKKb suppresses anti-apoptotic gene expression and promotes cell death. NF-kB-mediated suppression of anti-apoptotic genes is involved in acetaminophen-induced liver injury in mice. ROS promote extracellular secretion of RIP3 and then regulate necroptosis.
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