| Project/Area Number |
22590274
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General medical chemistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
KITAZATO Kaio 長崎大学, 医歯薬学総合研究科, 准教授 (50372769)
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| Co-Investigator(Renkei-kenkyūsha) |
KOMATSU Masaaki 東京都医学研究機構, 東京都臨床医学総合研究所, 副参事研究員 (90356254)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 細胞医化学 / ウイルス複製 / オートファジー / 宿主標的 / インフルエンザウイルス / ウイルスＲＮＡ合成 / ウイルスタンパク質翻訳 / Hsp90 / mTORシグナル / 中国 / 国際情報交換 / PGG / 微小管結合タンパク質MIP-T3 |
|---|
| Research Abstract |
In this study, we established a cell line that constitutively expresses GFP-LC3, the molecular marker of autophagy, which can visualize the dynamics of autophagosome formation during influenza virus infection. We found that viral protein expression reduced in autophagy-deficient MEFs (MEFsAtg7-/-) which is relevant to the reduction in viral RNA synthesis including mRNA and genomic RNA. However, viral replication did not significantly affected by autophagy deficiency. Furthermore, viral entry into cell did not affected by autophagy deficiency, but Hsp 90 induction in response to viral infection and mTOR signalling were altered in MEFsAtg7-/-, suggesting that these autophagy-deficiency-induced host aberrant response might be responsive to the reduction of viral RNA synthesis.
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