| Project/Area Number |
16590079
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Gifu University |
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Principal Investigator |
UEDA Hiroshi Gifu University, Faculty of Engineering, associate professor, 工学部, 助教授 (50253779)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2004: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | G protein / Rho / Rac / SRE / RhoGEF / actin |
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| Research Abstract |
We have previously reported that G protein signaling regulated cell spreading or cell shape change through activation of Rho family GTPases in cultured cells. In order to examine the molecular mechanism of Rho family GTPase activation by G protein, we have attempted to identify the Rho family GTPase-specific guanine nucleotide exchange factor (RhoGEF) regulated by G protein. Rho family GTPase activation was evaluated by luciferase reporter assay using serum response element (SRE). Among a number of RhoGEF molecules tested, co-expression of ARHGEF9 with Gβγ or a GTPase deficient mutant of Gαs (GαsQL) activated SRE-dependent transcription in NIH3T3 fibroblast cells. Such activation was also observed in _Neuro2A neuroblastoma cells transfected with GαsQL but not with Gβγ. In Neuro2A cells, a dominant negative mutant of Rac blocked GαsQL/ARHGEF9-activated SRE-dependent transcription, but those of RhoA and Cdc42 were without effects. Isoproterenol activated SRE-dependent transcription through ARHGEF9 in Neuro2A cells transfected with β-adrenergic receptor, which couples with Gs. These results indicate that Gαs regulates SRE-dependent transcription through ARHGEF9/Rac in Neuro2A neuroblastoma cells.
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