| Project/Area Number |
02670294
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | The university of Tokyo, Faculty of medicine. |
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Principal Investigator |
KANEKO Yoshiyasu The University of Tokyo, Faculty of Medicine, Assistant, 医学部(病), 助手 (90124669)
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| Co-Investigator(Kenkyū-buntansha) |
KOIKE Kazuhiko The University of Tokyo, Faculty of Medicine, Assistant, 医学部(病), 助手 (90234658)
NAKAYAMA Toshifumi The University of Tokyo, Faculty of Medicine, Assistant, 医学部(病), 医員 (80150275)
HASHIMOTO Yoshiaki The University of Tokyo, Faculty of Medicine, Assistant, 医学部(病), 助手 (40172879)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1990: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | hepatoma / liver regeneration / tumor promoter / c-kinase / hepatitis virus / c-fos / cell differentiation / 癸癌プロモ-タ- / C・キナ-ゼ / cーfos / 肝細胞 / 蛋白リン酸化 / HBVーX遺伝子 / 核蛋白 / 細胞癌遺伝子 |
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| Research Abstract |
Hepatitis B virus(HBV)and hepatitis C virus(HCV)may cause alterations of signal transduction pathways involved in the regulation of cell proliferation either directly or indirectly. Repeated regeneration of hepatocyte itself may cause alterations of the regulatory mechanism. To investigate the possible mechanism of the alterations of signal transduction pathways we examined the effects of teleocidin on PLC/PRF/5 hepatoma cells which had integrated form of HBV DNA.
Teleocidin, a tumor promoter whose actions are believed to be mediated by protein kinas-e C, acted inhibitory on cell proliferation and altered morphological appearance remarkably. Column chromatography disclosed the presence of three peaks of C-kinase activity. Two of which were down regulated while the third one is not down regulated by prolonged incubation with teleocidin. The C-kinase activity of the third peak was detected in the column fractions into which usual protein kinase C was not eluted, indicating that the molecular structure of the protein kinase was different from those of usual protein kinase C. Those data suggest that C-kinase like protein kinase exists in these hepatoma cells.
Since HBV X gene is known to enhance the expression of other genes, it can be speculated that the expression of X gene may cause the production of this C-kinase like protein. Further investigation is necessary to prove this supposition.
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