| Project/Area Number |
10044307
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
HOMMA Yoshimi Fukushima Medical Univeirsity School of Medicine, Department of Biomolecular Science, Professor, 医学部, 教授 (60192324)
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| Co-Investigator(Kenkyū-buntansha) |
SEKIMATA Masayuki FukushimaMedical University School of Medicine, lecturer, 医学部, 講師 (80250190)
SUEOKA Nobor 米国コロラド大学, 分子細胞生物学部, 教授
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1999: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1998: ¥400,000 (Direct Cost: ¥400,000)
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| Keywords | intracellular signaling / cell differentiation / transcription / glia cell / gene expression / silencer protein |
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| Research Abstract |
Clonal cell lines from an ethylnitrosourea-induced rat peripheral neurotumor, RT4, were established by Prof. Sueoka (cooperative investigator in this project). The RT4 cell line family has a stem cell type, RT4-AC, where daughter cells spontaneously and irreversibly differentiate into one of three derivative cell types: a glial cell type, 4T4-P, and two neuronal types, RT4-E and RT4-B. The aims of this cooperative study were: 1) to transfer cell lines of the RT4 family to this laboratory of Fukushinia1 Medical University and confirm expression levels of marker proteins in these cells, 2) to analyze molecular basis on regulation of GFAP expression using these cell lines. Following results were obtained from this research project.
1) Stable expression pattern of marker proteins was observed in all of four cell lines transferred. Scince this pattern was similar to that reported previously.
2) The expression of GFAP was negatively regulated by a sis-element, GDR1. Using GDR1 seuence, we detected proteins specifically bound to this sequence in non-glial RT4-E and hepatoma HTC. Identification of the proteins has been still on going.
3) Using a cDNA subtraction method, kinds of transcripts were specifically isolated from the cDNA libraries. GCM and DNMT1 were identified from the RT4-AG minus RT4-D library
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