| Project/Area Number |
26670142
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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 |
General medical chemistry
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| Research Institution | Kobe University |
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Principal Investigator |
Matozaki Takasi 神戸大学, 医学(系)研究科(研究院), 教授 (80252782)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 腸上皮細胞 / 炎症 / 生体分子 / 腸内細菌 / シグナル伝達 |
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| Outline of Final Research Achievements |
SAP-1 is a receptor-type protein tyrosine phosphatase that is localized specifically at microvilli of the brush border in intestinal epithelial cells. I previously found that SAP-1 ablation results in exacerbation of spontaneous colitis in Il10 knockout mice. In this study, I showed that tyrosine phosphorylation of CEACAM, a dephosphorylation substrate for SAP-1, promotes the activation of downstream molecules, thereby inducing production of chemokines such as IL-8. In addition, I found that SAP-1 specifically interacts with CEACAM and that this interaction is mediated via the ectodomains of both proteins. Thus, SAP-1 in intestinal epithelial cells is likely to regulate the intestinal immunity by controlling the tyrosine phosphorylation level of CEACAM.
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