Roles of endogenous small molecule in autophagy induction
| Project/Area Number |
25282236
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Chemical biology
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥18,460,000 (Direct Cost: ¥14,200,000、Indirect Cost: ¥4,260,000)
Fiscal Year 2015: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2013: ¥6,890,000 (Direct Cost: ¥5,300,000、Indirect Cost: ¥1,590,000)
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| Keywords | オートファジー / 細菌感染 / 8-ニトロcGMP / タンパク質修飾 / 細胞内情報伝達 / 活性酸素 / 医薬品探索 |
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| Outline of Final Research Achievements |
Autophagy is a major intracellular degradation system that serves to maintain homeostasis and to suppress disease progression. Majority of autophagy processes are believed to be non-selective but there are some exceptions. These selective autophagy processes must have different mechanism from canonical autophagy. We have examined in this study whether endogenous small molecules are involved in the selection mechanism. Under the inflammation conditions by bacterial infection, a nitrated nucleotide: 8-nitro-cGMP forms in the host cells. I found this nucleotide accumulated around the invading bacteria cells (group A streptococcus) and this accumulation was found to be an early marker for selective autophagic degradation of the bacterial cells.
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Report
(4 results)
Research Products
(15 results)
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[Journal Article] Endogenous nitrated nucleotide is a key mediator of autophagy and innate defense against bacteria.2013
Author(s)
Ito C, Saito Y, Nozawa T, Fujii S, Sawa T, Inoue H, Matsunaga T, Khan S, Akashi S, Hashimoto R, Aikawa C, Takahashi E, Sagara H, Komatsu M, Tanaka K, Akaike T, Nakagawa I, Arimoto H.
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Journal Title
Mol. Cell
Volume: 52
Issue: 6
Pages: 794-804
DOI
Related Report
Peer Reviewed / Open Access
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