Figure 1.
Figure 1. vGPCR induces IL-6 secretion by stimulating the transcription factor NF-κB. (A) Secretion of IL-6 in media conditioned by 293T cells expressing GFP (control), vGPCR (vGPCR), or the inactive mutant vGPCR R143A (R143A). (B) Transcriptional activation of the IL6 promoter induced by vGPCR is dependent on the κB site in COS-7 cells. (C) Expression of vGPCR, but not vGPCR R143A (R143A) or GFP (control), in COS-7 cells induces the translocation of RelA (p65) to the nucleus. (D) Inhibition of vGPCR induction of pIL6-CAT by overexpression of increasing concentrations of the NF-κB inhibitor, IκBαA32A36, in COS-7 cells. Data represent the mean ± SEM of triplicate samples from a typical experiment and are expressed as fold induction with respect to control.

vGPCR induces IL-6 secretion by stimulating the transcription factor NF-κB. (A) Secretion of IL-6 in media conditioned by 293T cells expressing GFP (control), vGPCR (vGPCR), or the inactive mutant vGPCR R143A (R143A). (B) Transcriptional activation of the IL6 promoter induced by vGPCR is dependent on the κB site in COS-7 cells. (C) Expression of vGPCR, but not vGPCR R143A (R143A) or GFP (control), in COS-7 cells induces the translocation of RelA (p65) to the nucleus. (D) Inhibition of vGPCR induction of pIL6-CAT by overexpression of increasing concentrations of the NF-κB inhibitor, IκBαA32A36, in COS-7 cells. Data represent the mean ± SEM of triplicate samples from a typical experiment and are expressed as fold induction with respect to control.

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