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. 2010 Jun;160(3):627–642. doi: 10.1111/j.1476-5381.2010.00681.x

Figure 4.

Figure 4

Co-expression of HA-β2AR and CB1-GFP2 alters receptor efficacy to activate ERK and CREB phosphorylation. (A) Dose–response curves for WIN pERK activation in CB1-GFP2/TreHA-β2AR cells pretreated for 48 h without or with Dox (10 µg·mL−1); n= 8. Inset shows On-Cell Western using an anti-HA primary antibody in CB1-GFP2/TreHA-β2AR cells without or with Dox (10 µg·mL−1, 48 h). (B) Dose–response curves for WIN pCREB activation in CB1-GFP2/Tet-ON/HA-β2AR cells pretreated for 48 h without or with Dox (10 µg·mL−1); n= 4–8. (C) WIN–pCREB responses in 293H cells stably expressing CB1-GFP2 alone or CB1-GFP2 and HA-β2AR. *P < 0.05 compared with 1.0 µM WIN in CB1-GFP2 cells; n= 3. (D) Isoprenaline–pCREB responses in 293H cells stably expressing HA-β2AR and transiently transfected with pcDNA (solid bars) or CB1-GFP2 (open bars). **P < 0.01; P= 7–8. Inset is On-Cell Western using anti-CB1 primary antibody of cells transfected with pcDNA or CB1-GFP2. CREB, cyclic AMP response element binding protein; Dox, doxycycline; ERK, extracellular signal-regulated kinase; WIN, WIN 55,212-2.