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. Author manuscript; available in PMC: 2009 Jan 1.
Published in final edited form as: Neuropharmacology. 2007 Jun 26;54(1):36–44. doi: 10.1016/j.neuropharm.2007.06.005

Fig. 3. The kinetics of ERK1/2 activation for an internalization-deficient mutant CB1 receptor (D164N) is temporally similar to that of the wild-type receptor.

Fig. 3

(A) 100 nM CP 55,940-induced internalization of wild-type and D164N CB1 receptors. Mutation of aspartate 164 to asparagine prevented receptor internalization in HEK293 cells. Data shown are mean ± SEM; n = 15–20 for three to four experiments. **p<0.01 compared with the extent of wild-type CB1 receptor internalization by unpaired t-test. (B) Activation of ERK1/2 in cells expressing wild-type or D164N CB1 receptors. The time course of D164N CB1 receptor-mediated activation of ERK1/2 was not significantly different from the wild-type receptor. Data shown are mean ± SEM; n = 15–20 for three to four experiments.