| Project/Area Number |
15590350
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Kumamoto University |
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Principal Investigator |
NISHIURA Hiroshi Kumamoto University, Faculty of Medical and Pharmaceutical Sciences, Faculty Member, 大学院・医学薬学研究部, 助手 (90284760)
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| Co-Investigator(Kenkyū-buntansha) |
TANASE Sumio Kumamoto University, School of Medicine, Professor, 医学部, 教授 (20112401)
SHIBUYA Yoko Kumamoto University, University Hospital, Faculty Member, 医学部附属病院, 助手 (70094018)
OGAWA Minetarou Kumamoto University, Institute of Molecular Embryology and Genetics, Professor, 発生医学センター, 教授 (70194454)
ARAKI Kimi Kumamoto University, Institute of Molecular Embryology and Genetics, Assistant Professor, 発生医学センター, 助教授 (90211705)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Ribosomal protein S19 / mouse ES cells / Apoptosis / complement C5a receptor / Akt / ERK / 補体C5aレセプター / JAK-STAT |
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| Research Abstract |
We had a plan to find a biological effect of ribosomal protein S19 (RP S19) dimer in mouse which had an special vector with Q137N mutant RP S19 cDNA. Preliminary, established Q137N mutant-mouse NIH3T3 clones acquired to resistant apoptosis by manganese(II). From this, we suspected the ability to regulate apoptosis by RP S19 dimer-induced C5a receptor (C5aR)-mediated pathway, and reported to Joural. We started to establish mouse ES cell clones to make a mouse model. At the same time, we performed western-blotting analysis to detect a more detail mechanism about C5aR-mediated pathway, especially PI3-K/Akt and ERK pathway. We found following results. (1) Phosphorylated Akt and ERK were decreased during apoptosis. (2) Phosphorylated Akt was maintained during apoptosis in Q137N-mutant clones. (3) RP S19 dimer overcame the acquired resistance to apoptosis in Q137N mutant-clones. From these results, we strongly suggest that RP S19 dimer plays an important role in apoptosis through changing PI3-K/Akt and ERK pathway on C5aR. Now we have a final plan in vitro to discover a regulation molecule. We also still interested in making a mouse model.
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