| Project/Area Number |
23590726
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pain science
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| Research Institution | Osaka Institute of Technology |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ITO Seiji 関西医科大学, 医学部, 教授 (80201325)
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| Co-Investigator(Renkei-kenkyūsha) |
TOMINAGA Makoto 自然科学研究機構, 岡崎統合バイオサイエンスセンター, 教授 (90260041)
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| Research Collaborator |
OKUDA Saori 大阪工業大学, 大学院工学研究科, 大学院生
OKAMOTO Kazuya 大阪工業大学, 大学院工学研究科, 大学院生
MATSUYAMA Junichi 大阪工業大学, 大学院工学研究科, 大学院生
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ノシスタチン / ノシスタチン結合タンパク質 / TRPV6 / HSP60 / 疼痛反応 / 痛覚 |
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| Research Abstract |
We identified a pain-regulated peptide nocistatin-interacting protein (Nocistatin binding protein, NSP1). NSP1 bound a molecular chaperone HSP60 and a highly selective Ca2+ channel TRPV6. The interaction of NSP1 and HSP60 was observed in the kidney but not the central nervous system. On the other hand,TRPV6 was expressed in the brain and spinal cord in addition to kidney, and TRPV6 splice variants were specifically expressed in the central nervous system. NSP1 inhibited the TRPV6 activity through the translocation of TRPV6 to the cell membrane. The changes of NSP1 and TRPV6 splice variants expression were observed in inflammatory pain.
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