| Project/Area Number |
08671023
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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 |
Radiation science
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
MISAKI Takashi Kyoto University Graduate School of Medicine, Nuclear Medicine and Diagnostic Imaging, Instructor, 医学研究科, 助手 (60181872)
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| Co-Investigator(Kenkyū-buntansha) |
KASAGI Kanji Kyoto University Graduate School of Medicine, Nuclear Medicine and Diagnostic Im, 医学研究科, 助教授 (20115819)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | interferons / thyrocytes / staurosporine / protein kinase C / iodine / C型り酸化酵素 |
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| Research Abstract |
In rat thyroid cell line FRTL5, thyroid stimulating hormone (TSH) stimulated protein kinase C (PKC) measured by binding of phorbol-dibutylate. Interferon (IFN) gamma dose dependently suppressed this stimulation. The suppression was reproduced by non-gamma IFN, and potentiated by tumor necrosis factor. On the other hand, inhibitors of PKC such as staurosporine, H-7, and H-9 stimulated iodine uptake in TSH-deprived FRTL5 cells, additive to IFN-driven enhancement. The 3 PKC inhibitors suppressed TSH stimulation of iodine uptake, while IFN act synergistically with TSH in this regard. The results imply IFN inhibits PKC activity via mechanisms different from that of other inhibitors.
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