| Project/Area Number |
15K15157
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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 |
Immunology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
WATANABE Toshio 奈良女子大学, 大学院人間文化研究科, 教授 (60201208)
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| Research Collaborator |
SUMIYOSHI Mami
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 遺伝子改変動物 / マスト細胞 / PI3K / シグナル伝達 / 小胞輸送 / マスト細胞分化 / mTORC1 / Arfファミリー |
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| Outline of Final Research Achievements |
To understand mast cell biology, we established mast cell lineage specific Cre expressing mice under the control of FcεRIα locus. Among the signaling molecules functioning downstream of PI3K, we focused Tsc1 and Arf1 along with Arf6. Loss of Tsc1, which causes augmentation of mTORC1 signal, led to marked increase of mast cell number in peritoneal cavity. On the other hand, loss of Arf1 along with Arf6, both of which serve as a vesicle trafficking regulator, impaired mast cell development. These results indicate that mTORC1 signal as well as Arf-mediated vesicle trafficking system play a critical role in mast cell development.
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