| Project/Area Number |
16K08766
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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 |
Parasitology (including sanitary zoology)
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
Tsukui Kumiko 国立感染症研究所, 寄生動物部, 主任研究官 (00420092)
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| Research Collaborator |
MARUMO Konomi
WATANABE Natsuki
MIYAMOTO Eri
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | lysosome / phagosome / Entamoeba histolytica / protease / traffic / receptor |
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| Outline of Final Research Achievements |
We examined the role of cysteine protease binding protein family (CPBF), Entamoeba unique lysosomal hydrolase receptor, and their involvement in the pathogenesis of Entamoeba histolytica, the causative agent of amebiasis. We established small RNA mediated gene silencing strains of all the eleven CPBFs and evaluated invasion efficiency using Matrigel matrix. As a result, CPBF2-silenced strain showed significant reduction in Matrigel invasion. CPBF2 is a receptor of solo α-amylase, however, there was no relation between α-amylase activity, α-amylase molecules and Matrigel invasion. On the other hand, CPBF2-silenced strain showed significant defect in cell motility. These results suggest that the deficiency in Matrigel invasion was caused by the reduced cell motility of CPBF2-silenced strain, independent of its role as a lysosomal hydrolase receptor. We found a novel role of lysosomal hydrolase receptor in the regulation of E. histolytica cell motility.
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| Academic Significance and Societal Importance of the Research Achievements |
リソソーム酵素輸送受容体にこれまで知られていなかった細胞運動制御機能を見いだした。予想外の発見であったが、細胞内シグナル伝達機構が未解明の赤痢アメーバ原虫における運動制御機構に、新しい分子メカニズムを見いだす端緒となった。初期に分化した真核生物である赤痢アメーバでの研究は、真核生物に重要な役割をもつ細胞運動の進化と分化にユニークな知見を与えることが期待される。また、細胞運動は赤痢アメーバの生存および病原性に重要である。赤痢アメーバにユニークな分子機構の解明は宿主への副作用が少ない創薬標的となることが期待される。
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