| Project/Area Number |
26640043
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | University of Hyogo (2016)
Kyoto University (2014-2015) |
|---|
Principal Investigator |
Oinuma Izumi 兵庫県立大学, 生命理学研究科, 教授 (40452297)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | axon / small GTPase / R-Ras / axon regeneration / actin / 神経再生 / 低分子量Gタンパク質 / アクチン細胞骨格 / 選択的スプライシング / ガイダンス因子 / 再生医学 / 神経科学 / ガイダンス分子 / アクチン / afadin / 軸索 |
|---|
| Outline of Final Research Achievements |
We have reported that GTP-bound R-Ras stimulates axonal elongation and branching in cultured neurons. Elucidation of regulatory mechanisms for axonal morphogenesis by active R-Ras is helpful for axonal regenerative study, and we searched for R-Ras-binding proteins responsible for axonal development through yeast-two-hybrid screening. Through the screening, we identified an actin-binding protein, afadin, for R-Ras binding partner mediating axonal branching. We further identified alternative variants for afadin, l-afadin and s-afadin, and their opposite roles for inducing axonal branching.
|
