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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Cell Signal. 2014 Nov 17;27(3):716–726. doi: 10.1016/j.cellsig.2014.11.006

Figure 4. Influence of CRIP1a on CB1R agonist-mediated ERK1/2 phosphorylation.

Figure 4

(A and B) N18TG2 WT, empty vector (Control), CRIP1a XS (A), and CRIP1a KD (B) cells were serum-starved for 16 h, pretreated for 2 h with 1 μM THL, and treated with either vehicle, the CB1R full agonist WIN55212-2 (10 nM), CP55940 (10 nM), or the CB1R partial agonist mAEA (10 nM) for 5 min. Immunoreactive phosphoERK1/2 was determined using the In-cell-Western assay as described in the Materials and Methods. Quantitation of phosphoERK1/2 was calculated as the ratio of immunoreactive phosphoERK1/2 to total ERK, and compared to basal, represented as 100% for each clone. *Indicates significantly different from WT CP55940 treated using one-way ANOVA and Dunnett’s post-hoc test (F3,16=6.36, p<0.05).