| Project/Area Number |
12F02736
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| Research Category |
Grant-in-Aid for JSPS Fellows
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| Allocation Type | Single-year Grants |
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| Section | 外国 |
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| Research Field |
Immunology
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| Research Institution | Osaka University |
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Principal Investigator |
審良 静男 (2012-2013) 大阪大学, 免疫学フロンティア研究センター, 教授
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KEBER Rok 大阪大学, 免疫学フロンティア研究センター, 特任研究員 (50745578)
KEBER Rok 大阪大学, 免疫学フロンティア研究センター, 外国人特別研究員
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2014: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2013: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2012: ¥100,000 (Direct Cost: ¥100,000)
|
|---|
| Keywords | Regnase1 / Autoimmunity / RNA degradation / Regulatory T cells / Renase-1 / RNA stabilit / Cyp51 / Regnase-1 / MyD88 |
|---|
| Outline of Annual Research Achievements |
During the pevious FY, several important steps to help identify immune cell-specific targets of Regnase-1 have been performed. Regnase-1 supresses autoimmunity by controlling the stability of mRNAs that encode immune-related factors. To examine tissue specificity of this protein and determine cruical targets that cause the autoinflamatory phenotype, we examined phenotype of two immune cell types; cytotoxic T cells (CD8) and regulatory T-cells (Treg) in the absence of regnase1. Deep RNA sequencing of Regnase1-deficient cells, followed by overlay of upregulated targets in both types of cells revealed a smaller number of potential target genes. This set of genes was tested by 3UTR luciferase assay. An ubiquitous antiapoptotic and proproliferative factor was detected as most prominent target.
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| Research Progress Status |
26年度が最終年度であるため、記入しない。
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| Strategy for Future Research Activity |
26年度が最終年度であるため、記入しない。
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Report
(3 results)
Research Products
(1 results)
