| Project/Area Number |
13680783
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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 |
Cell biology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
MAEDA Akito FACULTY OF MEDICINE INSTRUCTORS, 医学研究科, 助手 (50298882)
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| Co-Investigator(Kenkyū-buntansha) |
KINASHI Tatsuo FACULTY OF MEDICINE PROFESSOR, 医学研究科, 教授 (30202039)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2001: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Rap1 / Cell migration / Integrin |
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| Research Abstract |
In search for effectors of the Ras-related GTPase Rap1, we used the yeast two-hybrid system and isolated a cDNA encoding a protein p30 that interacts with Rap1. P30 consists of 265 amino acids, has the Ras/Rap banding domain and coiled-coil region, and selectively associates with activated form of Rapl. P30 is expressed predominantly in Leukocyte. Next, we examined the effect of p30 on cell migration and adhesion. The p30-overexpressing cells moved on ICAM-1 faster than wild type upon stimulation with a chemokine, that was accompanied with the activation of Rap1. And the p30-overexpressing cells also increased adhesion to ICAM-1. Moreover, analysis of the p30 mutants function revealed that the truncated p30 interfere cell migration and adhesion. These results that p30 may play a role in the regulation of the Integrin activation in association with Rap1
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