| Project/Area Number |
06680670
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Molecular biology
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| Research Institution | KYUSHU INSTITUTE OF TECHNOLOGY |
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Principal Investigator |
NIKAWA Junichi KYUSHU INSTITUTE OF TECHNOLOGY.FACULTY OF COMPUTER SCIENCE AND SYSTEMS ENGINEERING,ASSOCIATE PROFESSOR, 情報工学部, 助教授 (00134271)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Inositol / Signal transduction / Transcriptional regulation / Human cDNA / 情報伝達 / 酵母 |
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| Research Abstract |
The Saccharomyces cerevisiae ire15 mutant has a defect in the expression of INO1, showing an inositol auxotrophic phenotype. We isolated and characterized the yeast SCS2 gene and human HCP1 gene, both can suppress the growth defect of yeast ire15 mutant. Sequence analysis revealed that SCS2 and human HCP1 encode 244 and 360 amino acids, respectively. Both gene products are highly conserved among species. Yeast homolog of HCP1 was isolated and tested for its ability to suppress the ire15 mutation. The results show that the yeast HCP1 also suppress the ire15 mutation. Northern blot analysis revealed that the introduction of these genes into ire15 mutant clearly restored the expression of INO1. These results indicate that these gene products are involved in the regulation of INO1 expression.
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