Study on elucidation of the pathophysiology of rare intractable diseases (reticular dysgenesis) with severe combined immunodeficiency and development of therapeutic methods
Project/Area Number |
15K11072
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pathobiological dentistry/Dental radiology
|
Research Institution | The University of Tokushima |
Principal Investigator |
NOMA Takafumi 徳島大学, 大学院医歯薬学研究部(歯学系), 教授 (40189428)
|
Co-Investigator(Kenkyū-buntansha) |
谷村 綾子 徳島大学, 大学院医歯薬学研究部(歯学系), 助教 (10610199)
堀口 大吾 徳島大学, 大学院医歯薬学研究部(歯学系), 助教 (70304532)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | 幹細胞 / ミトコンドリア / エネルギー代謝 / 血球細胞分化制御 / 重症複合型免疫不全症 / 細網異形成症 / AK2 / 遺伝子変異 / 細胞分化 / 組織特異的遺伝子発現 / アデニル酸キナーゼ2 / 制御性T細胞 / FoxP3遺伝子 / テトラサイクリン / 誘導型発現ベクター |
Outline of Final Research Achievements |
The inducible FOXP3 expression vector was transduced into T cell-derived Jurkat cells by several methodology. After selection with puromycin,47 clones were obtained. Although all clones were analyzed for FoxP3 inducibility, no clone effectively induced FOXP3 gene expression by addition of doxycycline. From the verification experiments, it was suggested that the expression efficiency of the full - length isoform (v1) of FOXP3 gene in Jurkat cells is considerably lower than that of the v2 isoform lacking exon 2, possibly due to the involvement of cell - specific stability.
|
Report
(4 results)
Research Products
(5 results)