| Project/Area Number |
09670170
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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 |
Pathological medical chemistry
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| Research Institution | Aichi Cancer Center |
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Principal Investigator |
OSADA Hirotaka Aichi Cancer Center, Pathophysiology Unit, Section Head, 病態学研究室, 室長 (30204176)
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| Co-Investigator(Kenkyū-buntansha) |
YATABE Yasushi Aichi Cancer Center, Research Institute, Researcher, 研究所, 研究員 (90280809)
MASUDA Akira Aichi Cancer Center, Laboratory of Ultrastructure Research, Researcher, 超微形態学部, 主任研究員 (50157202)
TAKAHASHI Takashi Aichi Cancer Center, Laboratory of Ultrastructure Research, Laboratory Head, 超微形態学部, 部長 (50231395)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | Lung Cancer / Oncogene / がん遺伝子 |
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| Research Abstract |
We previously isolated the human LIMK2 gene and identified two alternative transcripts, LIMK2a and LIMK2b, which were differentially regulated in a tissue-specific manner. To examine this differential tissue-specific expression in detail, an RNase protection assay was performed, which demonstrated three expression patterns of the LIMK2 isoforms. In digestive organs, the LIMK2a transcripts were preferentially expressed in fetal and adult tissues ; in brain and lung, the LIMK2a transcript was predominantly expressed only in fetal tissue, and in placenta, the LIMK2b transcript was expressed more abundantly than that of LJMK2a. To further investigate this mechanism and the transcription factors involved, we isolated the two distinct 5' upstream regions from the phage genomic library, and found that both LIMK2a and 2b promoters have a single major transcription initiation site and thecharacteristics of a TATA-less promoter. A luciferase reporter assay of the transcriptional activity revealed positive as well as negative regulatory regions within both promoters. The RORalphal may be involved in the positive regulation for the LIMK2b expression, while the MZF-1 might regulate both LIMK2a and 2b in a different manner. The genomic structure of the LIMK2 gene was also determined. These findings should lead to a better understanding of the possibly diverse functions of the LIMK family
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