| Project/Area Number |
03455023
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
広領域
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| Research Institution | UNIVERSITY OF TOKYO (1992)
Okazaki National Research Institutes (1991) |
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Principal Investigator |
FURICHI Teiichi UNIVERSITY OF TOKYO, INSTITUTE OF MEDICAL SCIENCE, ASSOCIATE PROFESSOR, 医科学研究所, 助教授 (50219094)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1992: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1991: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Inositol 1,4,5-trisphosphate / IP_3 receptor / Ca^<2+> channel / Drosophila / Cytosolic free calcium / Signal transduction / 細胞内情報伝達 / イノシト-ル3リン酸受容体 / イノシト-ルリン脂質代謝 / カルシウムチャネル |
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| Research Abstract |
We focus our research on the structural and functional analyses of inositol 1,4,5- trisphosphate receptor (IP_3R)
1. Functional domain of IP_3 ligand binding domain: By the expression system of various mutant IP_3Rs in cultured cells, we found the IP_3-binding domain in the N-terminal 650 amino acids of IP_3R.
2. Splicing subtypes: We found two splicing subtypes whose gene expressions are regulated tissue-specific and development-specific manner.
3. Molecular cloning of Drosophila IP_3R: We cloned Drosophila IP_3R cDNA and deduced its receptor structure. We analyzed the expression sites of IP_3R mRNA and mapped the gene on the chromosome 3.
4. Localization of neuronal IP_3R types in mouse brain: We localized neuronal IP_3Rs in mouse brain and showed that IP_3R type 1 is predominant type and the expression of type 2 and type 3 are less efficient. We mapped type 1 gene to the mouse chromosome 6.
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