| Project/Area Number |
17K18122
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Basic / Social brain science
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | Teikyo University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2017-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | グルタチオン / microRNA / RNA結合タンパク質 / 神経変性疾患 / 酸化ストレス / miR96 / GTRAP3-18 / 発現制御 / タンパク質 / 脳神経疾患 / 蛋白質 |
|---|
| Outline of Final Research Achievements |
Glutathione is an important endogenous antioxidant against oxidative stress which causes neurodegenerative diseases. Glutathione level is regulated by membrane transporter EAAC1 and its negative regulator GTRAP3-18. They are regulated by same microRNA, however, regulatory mechanism of GTRAP3-18 by microRNA is suggested to be different from that of EAAC1 and other proteins, which is speculated to be mediated by RNA-binding protein. So, we have tried to identify the RNA binding proteins of GTRAP3-18 and analyzed its regulatory mechanism. As a result, we found GTRAP3-18 is negatively regulated by one of its RNA binding proteins. Furthermore, GTRAP3-18 is suggested to be regulated by microRNA through this RNA binding protein.
|
| Academic Significance and Societal Importance of the Research Achievements |
神経変性疾患の治療は投薬により一時的に症状を改善させることは可能であるが、病気の進行を抑制することはできない。種々の神経変性疾患に共通して見られるのが酸化ストレスの亢進と抗酸化機構の破綻である。本研究では、miR96による脳グルタチオン量調節機構が新規エピジェネティック制御機構によるものと明らかにした学術的意義と、この制御機構の解明が分子標的薬や遺伝子治療の開発に繋がり得るという臨床的意義を併せ持つ。今後の更なる研究が未だ根治が不可能な神経変性疾患における根本治療開発の一助になり得ると考えている。
|
