| Project/Area Number |
26460286
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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 |
General anatomy (including histology/embryology)
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
馬場 良子 産業医科大学, 医学部, 講師 (90271436)
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| Co-Investigator(Renkei-kenkyūsha) |
KOKUBU Keiji 産業医科大学, 医学部, 助教 (00432740)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | PKR / gelsolin / actin / villin / BiFC法 / 小腸吸収上皮細胞 |
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| Outline of Final Research Achievements |
We showed that PKR inhibited the key actin-modifying protein gelsolin which regulate actin dynamics and control its functions. Through this mechanism, PKR counteracted viral entry into the cell. The epithelial cells of small intestine extend microvilli which are closely related to function. Actin filaments play important role in the microvilli, however, the regulation by PKR is not revealed. In this study, we examined an association of PKR and actin-related proteins, and effects of PKR mutation on intestinal epithelium. We morphologically found that PKR and gelsolin bind in cytosol using BiFC method. Both PKR and gelsolin were widely expressed in the intestinal epithelial cells. The expression level differed between the cells from villi and crypt. In the PKR-knockout mice, the shape of villi and expression of villin protein differed from normal mice. These data showed a possibility of important role of PKR on villi and microvilli maintenance.
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