| Project/Area Number |
16K08746
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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 |
Experimental pathology
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
Toyota Hiroko 東京医科大学, 医学部, 助手 (80468660)
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| Co-Investigator(Kenkyū-buntansha) |
矢那瀬 紀子 東京医科大学, 医学部, 講師 (10210303)
秦 喜久美 東京医科大学, 医学部, 講師 (30287156)
古畑 昌枝 東京医科大学, 医学部, 助手 (90468661)
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| Project Period (FY) |
2016-04-01 – 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 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ストレス応答MAPキナーゼJNK / ストレス応答MAPキナーゼ / ストストレス応答性MAPキナーゼ / ストレス応答性MAPキナーゼ / 病理学 |
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| Outline of Final Research Achievements |
The nucleoprotein Thy28 molecule has been shown to control antigen receptor-mediated cell death of B and T cells in vitro. We made Thy28TG mice and examined the role of Thy28. Thymic cell death induced by administration of anti-CD3 is suppressed compared to wild-type mice, and suppression of JNK activation and Bcl-xL down-regulation is observed along with suppression of this anti-CD3-induced cell death. It was speculated that Thy28 TG mice were highly sensitive to EAE induced by self-peptides, and the cause thereof was the increase in IFN-g production induced by CD4-positive naive T cells.
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| Academic Significance and Societal Importance of the Research Achievements |
JNK活性化にも関与するThy28がアポトーシス誘導に関わっていることが示唆された。今後さらに実験を重ねThy28機能的役割を明らかにすることによって、アポトーシス誘導機構、さらには癌、自己免疫疾患などの誘導の解明に寄与すると期待できる。
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