Analysis of membrane deforming proteins in Malaria parasite
| Project/Area Number |
17K08808
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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 | Okayama University |
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Principal Investigator |
Yamada Hiroshi 岡山大学, 医歯薬学総合研究科, 准教授 (80325092)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | マラリア / 膜輸送 / 膜変形 / ダイナミン / リン脂質 / 感染症 |
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| Outline of Final Research Achievements |
Malaria parasite live with erythrocyte and form parasitophorous vacuole (PV) around the parasite. And the parasite develops membrane trafficking system to get nutrients and transport many proteins. In this study, we tried to examine whether or not malarial proteins could participate in these membrane remodeling. We found that the candidate protein directly bound to liposomes and deformed them. The activity of membrane deformation by the protein was altered in the presence of GTP. We are now investigating the detailed mechanism of membrane deformation by the protein using electron microscopy and high speed atomic force microscopy.
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| Academic Significance and Societal Importance of the Research Achievements |
マラリアは３大感染症の一つであり、世界で最も被害の大きい寄生虫感染症である。抗マラリア薬は主要な治療法であるが、薬剤耐性の出現、拡散により、その対応が急務である。熱帯熱マラリア原虫は、赤血球に寄生すると膜輸送を発達させ栄養分を取り込み、また複雑な膜輸送を伴う寄生環境を構築する。この膜輸送に必須である膜制御タンパク候補をみつけ、その性状を解析した。このタンパクの機能阻害は、膜輸送の不全を引き起こすと考えられる。この知見から、これらタンパクを標的に抗マラリア薬の創製が可能となった。本研究の進展は、原虫生理の理解と創薬の展開に大きく寄与していくものと考えられ、その医学薬学的意義も深い。
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Report
(4 results)
Research Products
(22 results)
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[Journal Article] Initial phospholipid-dependent Irgb6 targeting to Toxoplasma gondii vacuoles mediates host defense.2019
Author(s)
Lee, Y., Yamada, H., Pradipta, A., Ma, J.S., Okamoto, M., Nagaoka, H., Takashima, E., Standley, D.M., Sasai, M., Takei, K., Yamamoto, M.
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Journal Title
Life Science Alliance
Volume: 3
Issue: 1
Pages: 000-000
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] ATP6AP2 variant impairs CNS development and neuronal survival to cause fulminant neurodegeneration2019
Author(s)
Takuo Hirose, Alfredo Cabrera-Socorro, David Chitayat, Thomas Lemonnier, Olivier Feraud, Carmen Cifuentes-Diaz, Nicolas Gervasi, Cedric Mombereau, Tanay Ghosh, Loredana Stoica, Al Bacha Jeanne d'arc, Hiroshi Yamada et al.
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Journal Title
Journal of Clinical Investigation
Volume: 130
Issue: 5
Pages: 2145-2162
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Dynamic clustering of dynamin-amphiphysin helices regulates membrane constriction and fission coupled with GTP hydrolysis2018
Author(s)
Tetsuya Takeda, Toshiya Kozai, Huiran Yang, Daiki Ishikuro, Kaho Seyama, Yusuke Kumagai, Tadashi Abe, Hiroshi Yamada, Takayuki Uchihashi, Toshio Ando, Kohji Takei
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Journal Title
eLife
Volume: 7
Pages: 1-19
DOI
NAID
Related Report
Peer Reviewed / Open Access
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