The regulatory mechanisms of tumor metastasis via ASK family proteins
| Project/Area Number |
15K14445
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Molecular biology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Naguro Isao 東京大学, 大学院薬学系研究科(薬学部), 准教授 (80401222)
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| Research Collaborator |
KAMIYAMA Miki
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | がん転移 / ASK1 / シグナル伝達 |
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| Outline of Final Research Achievements |
Based on our previous data that ASK1 knockout mice are highly resistant to tumor metastasis, we investigated in which cells ASK1 functions during metastasis with focusing on the molecular mechanisms. Using tissue-specific conditional knockout mice, we revealed that ASK1 in multiple cells, at least in the platelet and the endothelial cells, is involved in tumor metastasis. Furthermore, ASK1-knockout platelets showed deficiency in multiple kinase signal transductions, resulting in the defect in platelet functions. Also, we found that a phosphorylation site in an ADP receptor P2Y12 was attenuated in ASK1-deficient platelets, which is attributable to the defect of a kinase signal transduction.
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Report
(3 results)
Research Products
(14 results)
