| Project/Area Number |
23659056
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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 |
Drug development chemistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
UEDA Hiroshi 長崎大学, 大学院・医歯薬学総合研究科, 教授 (00145674)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUNAGA Hayato 長崎大学, 大学院・医歯薬学総合研究科, 助教 (20437833)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 生物活性物質 / 神経創薬 / DAMPs / プロサイモシンα / 脳虚血 / スクリーニング / 生理活性物質 / 受容体 |
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| Research Abstract |
Prothymosin a (ProTa), a nuclear protein plays multi-functional roles in the nucleus, cytosol, and extracellular environment in terms of auto-protection. We have already revealed that ProTa is released from neurons on ischemic stress through non-vesicular manner and exerts a unique form of neuroprotection through an anti-necrotic mechanism. In addition, extracellular ProTa also exerts an anti-apoptosis through neuroimmunological system. Regarding manner of stress-induced release, ProTa is categorized as novel neuroprotective damage-associated molecular patterns (DAMPs). The extracellular role of ProTa against ischemia-induced damages is mediated through different two plasma membrane receptors. In the present study, we revealed mechanism of ProTa for the neuroprotection via these receptors. Furthermore, we successfully identified functional domains of ProTa as a peptide level on receptor, a candidate druggable target in the treatment of brain infarct.
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