| Project/Area Number |
16390398
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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 | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
SHIOSE Akira (2005) KYUSHU UNIVERSITY, Graduate school of Medicine, Research associate, 大学院医学研究院, 助手 (30363336)
森田 茂樹 (2004) 九州大学, 大学院・医学研究院, 助教授 (70243938)
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| Co-Investigator(Kenkyū-buntansha) |
TOMITA Yukihiro KYUSHU UNIVERSITY, Department of cardiovascular surgery, faculty of Medicine, Research Associate, 大学病院, 講師 (90180174)
TANOUE Yoshihisa KYUSHU UNIVERSITY, Department of cardiovascular surgery, faculty of Medicine, Research Associate, 大学病院, 助手 (40372742)
SUMIMOTO Hideki KYUSHU UNIVERSITY, Medical Institute of Bioregulation, professor, 生体防御医学研究所, 教授 (30179303)
HARADA Mine KYUSHU UNIVERSITY, Graduate School of Medicine, professor, 大学院医学研究院, 教授 (00019621)
ITO Hiroyuki KYUSHU UNIVERSITY, Graduate School of Medicine, Research associate, 大学院医学研究院, 助手 (70336022)
塩瀬 明 九州大学, 大学院・医学研究院, 助手 (30363336)
西田 誉浩 九州大学, 大学院・医学研究院, 助手 (50284500)
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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 |
¥14,200,000 (Direct Cost: ¥14,200,000)
Fiscal Year 2005: ¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 2004: ¥7,100,000 (Direct Cost: ¥7,100,000)
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| Keywords | cyclin D1 / cardiomyocyte / サイクリンD1 / 心筋細胞増殖 |
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| Research Abstract |
Cardiomyocytes withdraw from the cell-cycle after birth and are in non-proliferative state. One of this mechanism was suggested that cyclin D, which promotes cell-cycle from G0-1 phase to S phase, could not import to nucleus. In this study, we studied the cell-cycle regulation by cyclin D1 using lentivirus vector and plasmid vector, and tried to promote cell-cycle progression. Recently it was reported that cyclin D1 fused nucleor localization signals(NLS) could transfer to the nucleus of cardiomyocytes, but in our study, exogenous cyclin D1 could localize in nucleus at least in a part. Additionally, proliferative marker Ki67 was expressed in the 40% of cardiomyocytes of which cyclin D1 could localize in nucleus. These results showed that cyclin D1 could localize in nucleus partially and cell-cycle could progress by expressing exogenous cyclin D1.
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