| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2018: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2017: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
Fiscal Year 2016: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
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| Outline of Final Research Achievements |
A pro-inflammatory cytokine IL-1b requires caspase-1 activation through NLRP3 inflammasome formation to be secreted extracellularly. We have previously reported that a non-receptor tyrosine kinase BTK is essential for NLRP3 inflammasome activation. At the beginning, in this study we had tried to determine amino acid residues of NLRP3 phosphorylated by BTK and to clarify its physiological significance. However, we met technical difficulties to purify a sufficient amount of phosphorylated NLRP3 for LC/LC-MS analysis and another research group reported the significance of phosphorylated NLRP3. Thus, we made an alternative of identifying a partner of NLRP3 in macrophages. As a result, we have found that an actin-modulating factor gelsolin negatively regulates NLRP3 inflammasome activation as well as apoptosis on the mitochondria.
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