期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 276, 期 18, 页码 15445-15452出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M008961200
关键词
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资金
- NCI NIH HHS [CA62029] Funding Source: Medline
- NIAID NIH HHS [R29 AI038396, AI38396, R01 AI038396] Funding Source: Medline
- NIGMS NIH HHS [R56 GM036927, GM36927, R01 GM036927] Funding Source: Medline
Recent reports have shown that several heterotrimeric protein-coupled receptors that signal through G alpha (q) can induce Rho dependent responses, but the pathways that mediate the interaction between G alpha (q) and Rho have not yet been identified. In this report we present evidence that G alpha (q) expressed in COS-7 cells coprecipitates with the Rho guanine nucleotide exchange factor (GEF) Lbc, Furthermore, G alpha (q) expression enhances Rho-dependent responses. Coexpressed G alpha (q) and Lbc have a synergistic effect on the Rho-dependent rounding of 1321N1 astrocytoma cells. In addition, serum response factor-dependent gene expression, as assessed by the SRE.L reporter gene, is synergistically activated by G alpha (q) and Rho GEFs. The synergistic effect of G alpha (q) on this response is inhibited by C3 exoenzyme and requires phiospholipase C activation. Surprisingly, expression of G alpha (q), in contrast to that of G alpha (12) and G alpha (13), does not increase the amount of activated Rho. We also observe that G alpha (q) enhances SRE.L stimulation by activated Rho, indicating that the effect of G alpha (q) occurs downstream of Rho activation. Thus, G alpha (q) interacts physically and/or functionally with Rho GEFs; however this does not appear to lead to or result from increased activation of Rho. We suggest that G alpha (q)-generated signals enhance responses downstream of Rho activation.
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