| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
We have reported that Ras-PI3K signaling mediates endocytosis, and influenza viruses exploit this pathway to expedite their efficient incorporation into cells. Moreover, calcium signaling, triggered by the viruses, has been identified as an upstream regulator of Ras-PI3K signaling. In this study, we explored in detail the mechanism by which calcium signaling is activated upon the viral infection. First, we performed high-speed imaging experiments with fluorescently labeled virus particles to gain further insight into the spatiotemporal dynamics of Ca2+ responses upon virus entry. Immediately after infection, localized and modest Ca2+ elevations, prior to the aforementioned robust Ca2+ release from endoplasmic reticulum, were detected in the regions where the labeled particles were adsorbed. Moreover, we identified the membrane protein, which is involved in the Ca2+ elevation by the viruses.
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