| Budget Amount *help |
¥117,910,000 (Direct Cost: ¥90,700,000、Indirect Cost: ¥27,210,000)
Fiscal Year 2016: ¥23,530,000 (Direct Cost: ¥18,100,000、Indirect Cost: ¥5,430,000)
Fiscal Year 2015: ¥24,440,000 (Direct Cost: ¥18,800,000、Indirect Cost: ¥5,640,000)
Fiscal Year 2014: ¥25,350,000 (Direct Cost: ¥19,500,000、Indirect Cost: ¥5,850,000)
Fiscal Year 2013: ¥25,220,000 (Direct Cost: ¥19,400,000、Indirect Cost: ¥5,820,000)
Fiscal Year 2012: ¥19,370,000 (Direct Cost: ¥14,900,000、Indirect Cost: ¥4,470,000)
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| Outline of Final Research Achievements |
Fujita has elucidated that DHX36 and Pumilio play critical role in recognition of viral RNA in antiviral stress granule (avSG) by RIG-I-Like Receptor (RLR). They discovered that Picornaviruses evade RLR function by cleaving G3BP, an important component of avSG, to evade immune response. They discovered that viral poly A+ RNA is recognized in avSG to enhance host immune responses. IPS-1 is a critical adaptor for RLR signaling. They discovered that aggregation of TRAF binding domain is sufficient for signaling.
Takaori-Kondo has elucidated that the upregulation of intracellular level of HIV-1 Vif by CBF-β is mainly caused by suppressing MDM2-mediated proteasomal degradation and that expression of APOBEC3B is augmented by activation of the classical NF-κB pathways.
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