| Project/Area Number |
25650036
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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 |
Functional biochemistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
MATSUNAGA Hayato 長崎大学, 医歯薬学総合研究科(薬学系), 客員研究員 (20437833)
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| Co-Investigator(Renkei-kenkyūsha) |
UEDA Hiroshi 長崎大学, 医歯薬学総合研究科(薬学系), 教授 (00145674)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | DAMPs / 生理活性物質 / 受容体 / 核シャトル / 脳・神経 |
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| Outline of Final Research Achievements |
Prothymosin-alpha (PTMA), a nuclear protein has a multitude of cell-protective functions against cell stress in nuclear, intracellular, and extracellular. Stress-induced extracellular release of ProTα is observed in neurons among components of brain cells. Extracellular PTMA is a ligand for the two types of receptors: a TLR4/MD2 involved in innate immunity response and novel identified cell membrane proteins, whereas extracellularly released PTMA is reimported to the nucleus in a certain type of cells. Neuroprotective cytokines were upregulated by the exogenous PTMA treatment in recipient cells bearing nuclear shuttle action of PTMA, suggesting that recipient cells would be involved in the maintenance for the cell communities. Neuroprotective mechanisms of PTMA against brain stresses, such as an ischemic stroke have been proposed to require for the cell membrane receptor signaling pathway and the direct epigenomic regulation of gene expression via a nuclear shuttling of PTMA.
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