| Project/Area Number |
24500362
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Bioinformatics/Life informatics
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| Research Institution | Osaka University |
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Principal Investigator |
DAIYASU Hiromi 大阪大学, 情報科学研究科, 特任研究員 (40362397)
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| Co-Investigator(Kenkyū-buntansha) |
TOH Hiroyuki 独立行政法人産業技術総合研究所, ゲノム情報研究センター, 副研究センター長 (70192656)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | ケモカイン受容体 / ウイルス由来受容体 / シグナル伝達 / 機能分化 / 分子進化 |
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| Outline of Final Research Achievements |
Chemokine receptors (CKRs), which are involved in homeostasis, inflammation, and immune response, constitute a subfamily of the G protein-coupled receptors. Both decoy and viral receptors are the homologs of CKRs, but their functions are different not only from those of the typical CKRs, but also from each other. To identify the changes which have induced the functional differentiation of the CKR homologs during the molecular evolution, we compared the three groups with bioinformatics methods.
From amino acid or nucleotide sequence comparisons and model structure buildings, we found that the several sites, which might be involved in the ligand binding and/or the signal transduction in the CKRs, had changed in each group. The results of our analyses would be expected to the modification of GPCR functions and the drug development.
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