2014 Fiscal Year Annual Research Report
| Project/Area Number |
12F02736
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| Research Institution | Osaka University |
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| 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)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | Regnase1 / Autoimmunity / RNA degradation / Regulatory T cells |
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| 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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