| Project/Area Number |
13660060
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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 |
蚕糸・昆虫利用学
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| Research Institution | Kyoto Institute of Technology |
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Principal Investigator |
FURUSAWA Toshiharu KYOTO INSTITUTE OF TECHNOLOGY, FACULTY OF TEXTILE SCIENCE, PROFESSOR, 繊維学部, 教授 (70127166)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIMURA Yukio KYOTO INSTITUTE OF TECHNOLOGY, FACULTY OF TEXTILE SCIENCE, PROFESSOR, 繊維学部, 教授 (20273542)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | RNA-binding protein / TIA-1(3) Post-transcription regulation / Gene expression (Bombyx mori) / 発生 / CAT蛋白質 / TRN蛋白質 |
|---|
| Research Abstract |
A cDNA encoding a 388 amimo acid TIA-1-type RNA-binding protein (BmTRN-1) was isolated from midgut cDNAs of the silkworm, Bombyx mod, via homologous cloning, in order to characterize its function. The deduced amino acid sequence, most likely encoded by a single copy gene, has significant homology with human TIA-1 and TIAR known as apoptotic regulators and recently reported to function as important factors for either splicing or translation. RRT-PCR analysis showed that the BmTRN-1 gene was vigorously transcribed in the midgut at the gut purge stage, indicating a possible relation to the tissue-decomposing process in larval-pupal metamorphosis. We also show that inhibition of the expression of BmTRN-1 by a transfected ohgonucleotide encoding the antisense sequence caused a remarkable rise in protein expression from artificially constructed cDNAs encoded by plasmid vectors in Bombyx cells, depending on the constructed ORF sequences of the introduced cDNAs. Furthermore, it was shown that the transcripts iron the cDNAs introduced into the cells increased under the antisense-inhibition of BmTRN-1 when the protein levels of these cDNAs also rose, demonstrating that BmTRN-1 could act as a regulator especially of the mechanism eliminating transcripts with possible targets for BmTRN-1 recognition in the authentic post-transcription process.
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