| Project/Area Number |
25893021
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Akita University |
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Principal Investigator |
ASANUMA ken 秋田大学, 医学(系)研究科(研究院), 技術職員 (50710125)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | がん / イノシトールリン脂質 / Pten / PIK3C3 / Akt / PI(3,4,5)P3 |
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| Outline of Final Research Achievements |
The class III phosphoinositide 3-kinase, PIK3C3 is known to contribute to autophagy and regulate intracellular membrane trafficking. However, the role of PIK3C3 in tumorigenesis is little known. In the study, we elucidate that development of T cell lymphoma in T cell specific Pten deficient mouse was suppressed by crossing with T cell specific Pik3c3 deficient mice. In addition, Akt was little phosphorylated in thymus of Pten; Pik3c3 double knockout mice. These findings suggest that PIK3C3 might be a positive regulator for Akt signaling.
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