| Project/Area Number |
20790247
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Gunma University |
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Principal Investigator |
NAKAGAWA Yuko Gunma University, 生体調節研究所, 助教 (90422500)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | がん / Ca^<2+>透過性チャネル / チャネル / カルシウム |
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| Research Abstract |
The present study was conducted to characterize the regulation and function of TRPV2 channel in highly malignant tumor cell. The expression of TRPV2 was not only detected in the normal cell, but also in the tumor cell. We then determined localization of TRPV2 using metastatic B16 melanoma murine cells transfected with TRPV2-EGFP. In serum-free condition, most of the TRPV2 signal was located in the cytoplasm. Treatment with serum induced translocation of some of the TRPV2-EGFP to the plasma membrane. Serum-induced translocation was blocked by transfection of short-form TRPV2 (s-TRPV2) lacking a pore-forming region and the sixth transmembrane domain. These data conformed to that of macrophage TtT/M87 cell. To determine the function of migration for the TRPV2, we performed the wound healing assay. The ruthenium red, TRPV family inhibitor, blocked the migration of B6 cell. However s-TRPV2 couldn't inhibit the cell migration.
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