| Budget Amount *help |
¥100,360,000 (Direct Cost: ¥77,200,000、Indirect Cost: ¥23,160,000)
Fiscal Year 2012: ¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2011: ¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2010: ¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2009: ¥20,410,000 (Direct Cost: ¥15,700,000、Indirect Cost: ¥4,710,000)
Fiscal Year 2008: ¥23,400,000 (Direct Cost: ¥18,000,000、Indirect Cost: ¥5,400,000)
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| Research Abstract |
In this project, we tried to elucidate a regulatory mechanism for the activation of PRRs, particularly nucleic acid sensors, and the related signaling pathways, leading to the induction of cytokine/chemokine genes in innate immune responses for host defense against viral infection and cancer. First, we found that the poly(ADP-ribose) polymerase (PARP)-13 shorter isoform (ZAPS) critically functions as a potent stimulator of IFN responses in human cells mediated by RIG-I, through the physical association of ZAPS with RIG-I. Next, we revealed that ZAPS is a factor targeted by Influenza viral NS1 protein for viral innate immune evasion. In addition, we showed a role of PARP-7/TIPARP and PARP-12 as a possible negative regulator of RIG-I-meditated innate immune signalings. Furthermore, we also identified a candidate DNA sensor for human cytomegalovirus (HCMV). On the other hand, this project contributed to the research, wherein it has been shown a novel mechanism for the suppression of innate immune signalings mediated by tumor-derived DNA in tumor-infiltrating dendritic cells. These results may provide a therapeutic and preventive insight for the control of viral infection and cancer.
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