| Project/Area Number |
22681034
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Living organism molecular science
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| Research Institution | The Institute of Physical and Chemical Research |
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Principal Investigator |
KAWATANI Makoto 独立行政法人理化学研究所, 化合物ライブラリー評価研究チーム, 専任研究員 (50391925)
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| Research Collaborator |
MUROI Makoto 独立行政法人理化学研究所, 化合物ライブラリー評価研究チーム, 専任研究員 (30261168)
FUTAMURA Yushi 独立行政法人理化学研究所, 化学情報・化合物創製チーム, 協力研究員 (70525857)
KAZAMI Sayaka 独立行政法人理化学研究所, 化合物ライブラリー評価研究チーム, 協力技術員
HONDA Kaori 独立行政法人理化学研究所, 化合物ライブラリー評価研究チーム, 協力技術員
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥23,400,000 (Direct Cost: ¥18,000,000、Indirect Cost: ¥5,400,000)
Fiscal Year 2012: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2011: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2010: ¥12,480,000 (Direct Cost: ¥9,600,000、Indirect Cost: ¥2,880,000)
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| Keywords | 癌 / 小分子化合物 / エンドサイトーシス |
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| Research Abstract |
The purpose of this study is to construct a cell morphology-based high-content screening system and to develop anti-cancer agents targeting the endocytic pathway. We constructed a chemical-genetic phenotype profiling system based on the high-content cell morphology database, Morphobase. We showed that NPD1801, which perturbs the endocytic pathway, targeted calmodulin, caused the activation of Ras-Raf pathway, the inhibition of the fusion of late endosome and lysosome, and the dysfunction of lysosome, and resulted in the cancer cell death.
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