Mechanism of neurite outgrowth through chloride ion dependent regulation of G protein signaling
| Project/Area Number |
22790215
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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 |
General physiology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 低分子量Gタンパク質 / クロライドイオン / 神経突起伸長 |
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| Research Abstract |
In rat pheochromocytoma PC12D cells, NGF-induced neurite outgrowth was inhibited in low Cl^-condition. This inhibition was partially rescued by the treatment of cells with Rho kinase inhibitor Y-27632.In parental PC12 cells, NGF-induced neurite outgrowth was also inhibited by in low Cl^-condition. However, in PC12 cells, inhibition of neurite outgrowth in the low Cl^-condition was not rescued by Y-27632 treatment. The protein expression level of RhoA in PC12D cells was higher than that in PC12 cells. These observations suggest that difference of protein expression level in both cells might cause different sensitivity to Rho kinase inhibitor.
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Report
(3 results)
Research Products
(15 results)
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[Journal Article] Regulation of epithelial sodium transport via epithelial Na^+ channel (ENaC)2011
Author(s)
Marunaka Y, Niisato N, Taruno A, Ohta M, Miyazaki H, Hosogi S, Nakajima K, Kusuzaki K, Ashihara E, Nishio K, Iwasaki Y, Nakahari T, Kubota T
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Journal Title
J Biomed Biotechnol
Volume: 2011
Issue: 1
Pages: 978196-978196
DOI
Related Report
Peer Reviewed
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