Regulation and biological significance of mitochondrial c-Src.
Project/Area Number |
26460372
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General medical chemistry
|
Research Institution | Fukushima Medical University |
Principal Investigator |
Homma Yoshimi 福島県立医科大学, 医学部, 教授 (60192324)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | ミトコンドリア / 活性酸素 / チロシンキナーゼ / B細胞 / リン酸化 / プロテオーム解析 / トランスジェニックマウス / B細胞 / シグナル伝達 / プロテオーム |
Outline of Final Research Achievements |
Suppression of c-Src activity enhances production of radical oxygen species (ROS) in mitochondria. We identified flotillin-1 as a c-Src substrate that prevent ROS production. We produced transgenic (Tg) mice expressing a phosphorylation-defective mutant of succinate dehydrogenase A in B cells. Splenic B cells in male, but not female, Tg mice produced enhanced ROS, and exhibited decreased humoral immune response.
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Report
(4 results)
Research Products
(5 results)