Establishment of assay system for drugs that regulate microglia via transcription factors
| Project/Area Number |
26670036
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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 |
Pharmacology in pharmacy
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| Research Institution | Kumamoto University |
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Principal Investigator |
KATSUKI Hiroshi 熊本大学, 大学院生命科学研究部(薬), 教授 (40240733)
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| Co-Investigator(Renkei-kenkyūsha) |
SEKI Takahiro 熊本大学, 大学院生命科学研究部, 准教授 (50335650)
Otsuka Masami 熊本大学, 大学院生命科学研究部, 教授 (40126008)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ミクログリア / 核内受容体 / 神経保護 / 一酸化窒素合成酵素 / サイトカイン / アルギナーゼ / 転写因子 / ケモカイン / MAPキナーゼ / オルタナティブ活性化 / パーキンソン病 |
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| Outline of Final Research Achievements |
The present study focused on several members of nuclear receptor family that acted as ligand-regulated transcription factors, and found that a natural compound macelignan with PPARγ agonist activity protected dopaminergic neurons in midbrain tissues via promotion of M2 activation of microglia. On the other hand, the present study also demonstrated that agonists at VDR / RXR and an agonist at RAR suppressed M1 activation of microglia via inhibition of recruitment of another transcription factor NF-κB, in a MAP kinase-dependent manner and a MAP kinase-independent manner, respectively.
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Report
(3 results)
Research Products
(52 results)
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[Journal Article] Effects of cyclodextrins on GM1-gangliosides in fibroblasts from GM1-gangliosidosis patients.2015
Author(s)
Maeda Y, Motoyama K, Higashi T, Horikoshi Y, Takeo T, Nakagata N, Kurauchi Y, Katsuki H, Ishitsuka Y, Kondo Y, Irie T, Furuya H, Era T, Arima H.
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Journal Title
J Pharm Pharmacol.
Volume: 67
Issue: 8
Pages: 1133-1142
DOI
Related Report
Peer Reviewed / Open Access
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