| Project/Area Number |
15K08088
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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 |
Medical pharmacy
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| Research Institution | Health Sciences University of Hokkaido (2016-2017)
Hokkaido University (2015) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
ISEKI Ken 北海道大学, 大学院薬学研究院 臨床薬剤学講座, 教授 (40203062)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 大腸がん / 染色体 / コンデンシン / マイクロRNA / 遺伝子編集 |
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| Outline of Final Research Achievements |
To investigate the function of SMC4, transformed cell deficits SMC4 gene was planned to produce using genome editing technology. The CRISPR/Cas9 vector plasmid involves gRNA or CRISPR/Cas9 knockout plasmid were transfected into the cells using the lipofection method. However, transformed cells were not produced. Next, we employed the lentiviral vector, transformed cells were obtained by selection with puromycin. However, the resistant cells expressed no Cas9. From these results, we estimated that the production of CRISPR/Cas9 including SMC4 gRNA was difficult. We performed an experiment to transfect siRNA of SMC4 into the cells, and the siRNA transfection showed excellent knockdown effect of SMC4 mRNA expression.
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