Skip to main content
. Author manuscript; available in PMC: 2013 Apr 16.
Published in final edited form as: Cell Metab. 2011 Dec 7;14(6):747–757. doi: 10.1016/j.cmet.2011.11.006

Figure 3. The TGR5 mutant TGR5-A217P, defective in inducing cAMP signaling, fails to inhibit NF-κB activity.

Figure 3

(A-I) Confocal images of empty vector (A-C), mouse TGR5 (D and F), and TGR5-A217P mutant (G-I) -transfected CHO cells stained with DAPI (B, E, H), stained for TGR5 (A, D, G) or shown as merged images (C, F, I). (J) CREB transcriptional activity in CHO cells transfected with both a CRE reporter and TGR5 wildtype (grey squares) or TGR5-A217P mutant (black triangles) in response to INT-777 (n=3). (K) NF-κB transcriptional activity in CHO cells transfected with the NF-κB reporter plasmid in combination with empty vector (white bars), TGR5 (grey bars) and TGR5-A217P (black bars) with or without NF-κB p65 co-transfection (n=3). Results represent the mean ± SEM. * Statistically significant, P<0.05.