| Project/Area Number |
15590862
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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 |
Kidney internal medicine
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
TSUCHIYA Ken Tokyo Women's Medical University, Department of Medicine, Associate professor, 医学部, 講師 (00246472)
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| Co-Investigator(Kenkyū-buntansha) |
TSUCHIYA Mariko Tokyo Women's Medical University, Department of Medicine, Associate professor, 医学部, 講師 (00266826)
MOCHIZUKI Toshio Hokkaido University School of Medicine, Department of Medicine, Associate professor, 医学部, 講師 (00277120)
西村 佐代子 東京女子医科大学, 医学部, 助手 (00349721)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | knockout mouse / polycystic kidney / RNAi / microarray / left-right asymmetry / cilia / 遺伝子 / 発生 分化 / 内臓逆位 / のう胞腎 / RNA i / 内蔵逆位 / 体軸 |
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| Research Abstract |
We identified the inv gene which decides the left and right asymmetry and regulates kidney development based on the information of the inv mutant mouse (Nature 395, 1998). The mouse inv gene encodes 1062 amino acid protein containing 15 tandem repeats of the ankyrin motif. However, functional properties and the modulator of gene expression of inv have been unclear.
In this project, we constructed the targeting vector of inv gene for producing inv knockout mouse. Simultaneously, we analyzed the function of inv protein by modulation of gene expression level using overexpression and RNAi technique. The cultured renal tubular cell in which the expression level of inv mRNA was modified by transfection or siRNA and the alternation of gene expression profile was analyzed by microarray system. Several genes related to structural protein of the matrix were downregulated, and in contrast, repairing related genes were upregulated. Moreover, we identified and analyzed some genes closely related to the inv, such as CD2AP or transcription factor mafs.
Near future, we analyzed knockout mouse that we established in this project and will try to reveal the essential role and function of inv protein.
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