| Project/Area Number |
24659084
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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 anatomy (including Histology/Embryology)
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| Research Institution | Osaka University |
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Principal Investigator |
HARADA Akihiro 大阪大学, 医学(系)研究科(研究院), 教授 (40251441)
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| Co-Investigator(Kenkyū-buntansha) |
KUNII Masataka 大阪大学, 大学院医学系研究科, 助教 (80614768)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 細胞極性 / SNARE / 極性輸送 / ノックアウトマウス / 上皮形成 |
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| Outline of Final Research Achievements |
Deficiency in syntaxin3, known to be important in apical transport, caused defects in apical transport and cell proliferation in polarized cells. To know the molecular mechanism of these phenotype, we generated an apical marker protein which is expressed after drug administration. As the marker worked well in cell lines, we induced the gene into primary cultured cells and we will look at the transport after getting sufficient amount of cells. To make model system to examine the molecular mechanism, we introduced Cre recombinase into primary cultured cells and we are expanding the cells now. In addition, we successfully generated intestinal cell lines which lacks syntaxin3 by CRISPR method. As we observed similar phenotype in these cell lines, we are planning to use these cells for elucidation of molecular mechanism of apical transport and cell proliferation.
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