Project/Area Number |
26461444
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Hematology
|
Research Institution | Osaka University |
Principal Investigator |
MAEDA Tetsuo 大阪大学, 医学系研究科, 助教 (00403064)
|
Co-Investigator(Kenkyū-buntansha) |
金倉 譲 大阪大学, 医学系研究科, 教授 (20177489)
齊藤 則充 大阪大学, 医学系研究科, 特任助教(常勤) (30597399)
一井 倫子 大阪大学, 医学系研究科, 寄附講座助教 (30633010)
織谷 健司 大阪大学, 医学系研究科, 准教授 (70324762)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | STAP蛋白 / アダプター蛋白 / STAP / EBウイルス / リンパ腫 / 遺伝子多型 / シグナル / 免疫 / 炎症 / 骨髄微小環境 / リンパ球 |
Outline of Final Research Achievements |
Previously, we have reported that Signal transducing adaptor protein (STAP) binds latent membrane protein-1 in Epstein-Barr virus (EBV), and Bcr-Abl fusion protein, which causes chronic myeloid leukemia (CML). In this study we studied the role of STAP family in various hematological diseases. We found that STAP-1 is down-regulated in EBV-induced post transplantation lymphoproliferative disorder compared with EBV-negative de novo DLBCL. Regarding the effect on CML, STAP-1 deficiency improved the survival of CML model mouse. Further study would clarify the precise molecular mechanisms.
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