| Project/Area Number |
10558105
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Functional biochemistry
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
KITAGAWA Masatoshi Medical Institute of Bioregulation, Kyushu University, Professor, 生体防御医学研究所, 助教授 (50294971)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAYAMA Keiichi Medical Institute of Bioregulation, Kyushu University, Professor, 生体防御医学研究所, 教授 (80291508)
HATAKEYAMA Shigetsugu Medical Institute of Bioregulation, Kyushu University, Research Assoc., 生体防御医学研究所, 助手 (70294973)
NAKAYAMA Keiko Medical Institute of Bioregulation, Kyushu University, Assoc. Prof., 生体防御医学研究所, 助教授 (60294972)
HIRAI Aizan Chiba Prefectural Togane Hospital, President, 院長
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥9,800,000 (Direct Cost: ¥9,800,000)
Fiscal Year 1999: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1998: ¥6,000,000 (Direct Cost: ¥6,000,000)
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| Keywords | p27ィイD1Kip1ィエD1 / ubiquitination / proteasome / lung cancer / cyclin-dependent kinase / サイクリン依存性キナーゼ阻害分子 / ユビキチン-プロテアソーム / 蛋白分解 / プロセッシング |
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| Research Abstract |
It has been reported that the cyclin dependent kinase inhibitory proteins (CDK inhibitor) , such as p27ィイD1Kip1ィエD1 negatively regulates the G1-CDK activity in normal cells. In most cancer cells, up-regulation of G1-cyclin dependent kinase (G1-CDK) activity contributes in their malignant growth. First of all, we study the expression of p27ィイD1Kip1ィエD1 in human lung cancer using immunohistoichemistry. We found that p27ィイD1Kip1ィエD1 labeling index was decreased and p27ィイD1Kip1ィエD1 degradation activity was up-regulated in cancerious lung tissues, compared with nonneoplastic lung tissues. Therefore, it is important to study the mechanisms of p27ィイD1Kip1ィエD1 degradation. In the next study, we found that p27ィイD1Kip1ィエD1 was eliminated by two independent mechanisms, ubiquitin-mediated degradation and ubiquitin-independent processing. These tow activity was significantly high during progression from G1 to S phase. These finding suggested that inhibitor of p27ィイD1Kip1ィエD1 degradation is a potential drug for cancer therapy.
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