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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 6. Effect of CRIP1a on the kinetics of ERK1/2 phosphorylation.

Figure 6

N18TG2 WT and CRIP1a XS (A) and N18TG2 WT and CRIP1a KD clones (B) were serum starved for 16 h, treated with THL for 2 h, and pretreated for 30 min in the absence or presence of the dynamin inhibitor Dynasore (80 μM), and then challenged with the CB1R agonist CP55940 (10 nM) for the indicated times. PhosphoERK1/2 levels were determined as the ratio of immunoreactive phosphoERK1/2:DRAQ5. PhosphoERK values were represented as a percent change relative to basal, expressed as 100% for WT cells. No significant differences in total ERK levels from time 0 were detected in time course data for untreated or Dynasore-treated cells (data not shown). Data are presented as the mean ± S.E.M. from four independent experiments performed in duplicate. *p<0.05 indicates significant difference from WT using a two-way ANOVA and Bonferroni post-hoc.