| Project/Area Number |
23570173
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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 |
Functional biochemistry
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| Research Institution | Nippon Veterinary and Life Science University (2013)
Tokyo Women's Medical University (2011-2012) |
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Principal Investigator |
ARIMURA Yutaka 日本獣医生命科学大学, 応用生命科学部, 准教授 (10281677)
|
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| Co-Investigator(Kenkyū-buntansha) |
YAGI Junji 東京女子医科大学, 医学部・微生物学免疫 学教室, 教授 (70182300)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
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| Keywords | チロシンホスファターゼ / 免疫シグナル / 細胞死 / 国際情報交換 / ホスファターゼ |
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| Research Abstract |
In the beginning, we obtained a result suggesting that protein tyrosine phosphatase named PTP-PEST induced a novel type of cell death upon its gene transduction into immune T cells, in this study. To clarify the underlying molecular mechanisms, we started exploration, and conducted various experiments such as cell death, cell division, cell number counting, gene introduction of partially deleted gene to define the responsive position within the gene, co-transfection of associating molecules. As the results, our initial observation was interpreted as follows: PTP-PEST does not seem to induce cell death, but suppress expression of internal vector markers by inhibiting one of possible pathways of signal transduction to LTR promoter of retrovirus vector used here, and thus the gene-introduced cells appear to decrease in number superficially. Accordingly, possibility that some past reports have also misunderstood cell death was raised.
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