| Project/Area Number |
24659485
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Infectious disease medicine
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
KOSHINO Ichiro 東京女子医科大学, 医学部, 助教 (80328377)
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| Co-Investigator(Kenkyū-buntansha) |
TAKAKUWA Yuichi 東京女子医科大学, 医学部, 教授 (40113740)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | マラリア原虫 / 膜骨格 / ATP |
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| Research Abstract |
It was demonstrated that: i) ATP was released from infected erythrocytes upon burst. ii) ATP-stimulation resulted in phosphorylation of dematin, leading to loosening of membrane skeleton. iii) P2Y11 receptor antagonists inhibited malaria parasite invasion of erythrocytes. iv) The parasite invasion was inhibited in the presence of ATP-hydrolyzing enzymes. Altogether, it was strongly implicated that invasion process of erythrocytes by Plasmodium falciparum requires host erythrocyte-derived ATP, which then stimulates P2Y11-mediated signaling pathway, leading to phosphorylation of dematin, and loosening of erythroycte membrane skeleton. Drugs which shut down the above-mentioned signaling pathway might provide a novel strategy to protect humans from malaria.
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