| Project/Area Number |
15K11039
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Kagoshima University (2016-2017)
Hiroshima University (2015) |
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Principal Investigator |
HARADA Kae 鹿児島大学, 医歯学域歯学系, 助教 (60432663)
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| Co-Investigator(Kenkyū-buntansha) |
兼松 隆 広島大学, 医歯薬保健学研究科(歯), 教授 (10264053)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | オートファジー / 細菌感染 / 感染 / 細菌排除 |
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| Outline of Final Research Achievements |
Autophagy is an intrinsic host defense system that recognizes and eliminates invading bacterial pathogens. We have identified microtubule-associated protein 1 light chain 3 (LC3), a marker protein of autophagy, as a binding partner of phospholipase C-related catalytically inactive protein (PRIP). To disclose the molecular mechanisms of bacterial elimination by autophagic pathway, we here examined by using a Salmonella Typhimurium infection assay. In mouse embryonic fibroblasts (MEFs) infected with Salmonella, the number of intracellular Salmonella and Salmonella in LC3-positive autophagosome-like vacuoles (SCVs: Salmonella containing vacuoles) were both increased in Prip-knockout (KO) MEFs. In addition, we analyzed autophagic flux, and autophagic flux in Prip-KO MEFs was impaired. Altogether, impaired acidification in SCVs of Prip-KO MEFs may induce abnormality in antibacterial autophagy, resulting in remarkable Salmonella proliferation.
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