| Project/Area Number |
16570168
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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 |
Cell biology
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| Research Institution | Yamagata University School of Medicine |
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Principal Investigator |
KITANAKA Chifumi Yamagata University School of Medicine, Molecular Cancer Science, Professor, 医学部, 教授 (70260320)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Cell-Death / Apoptosis / Cancer / Ras / Hrk / p32 |
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| Research Abstract |
Thus far, we have demonstrated that deregulated Ras activation causes a non-apoptotic type of programmed death in glioma and neuroblastoma cells and that such Ras-mediated non apoptotic programmed cell death has an important role as a tumor suppressor mechanims and in the pathogenesis of neurodegenerative diseases. And as a next step, we have been dissecting the molecular mechanism of Ras-mediated non-apoptotic cell death. The purpose of this current project is to extend our study on the molecular mechanism of Ras-mediated non-apoptotic cell death. In this project, we focused ourselves on JNK, which has been shown to be activated by Ras and to be involved in the regulation of some types of non-apoptotic cell death. Results of this project research revealed that JNK is indeed activated in the course of Ras-induced non-apoptotic cell death, and activation of JNK closely paralleled or preceded cell death. Inhibition of JNK activity by use of a pharmacological inhibitor or a dominant negative mutant of JNK inhibited Ras-induced non-apoptotic cell death. These findings suggest that JNK is critically involved in Ras-induced non-apoptotic cell death. Thus, in this project, we could successfully elucidate a novel aspect of molecular regulation of Ras-mediated non-apoptotic cell death.
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