| Project/Area Number |
15K14344
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Gunma University |
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Principal Investigator |
Shirao Tomoaki 群馬大学, 大学院医学系研究科, 教授 (20171043)
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| Co-Investigator(Renkei-kenkyūsha) |
ISHIZUKA Yuta 群馬大学, 大学院・医学系研究科・神経薬理学, 助教 (50614179)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ドレブリン / コネキシン / アクチン / GAP結合 / GAP 結合 / アストロサイト |
|---|
| Outline of Final Research Achievements |
GAP junction plays a pivotal role for intercellular signaling of glial cells in the central nervous system. The present study indicates that drebrin binds to connexin 43 via actin-binding region 2. This suggests that the drebrin-mediated change of GAP junction function is due to the alteration of molecular interaction between drebrin, connexin43 and actin filaments. Additionally, it is indicated that the phosphorylation of drebrin at Ser 142 does not affect the binding affinity of drebrin to connexin 43 both phospho- and dephospho-mimic mutants of drebrin could bind to connexin 43.
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