FIGURE 2.
PKCζ is required for Gq-coupled GPCR stimulation of the ERK5 pathway. A, NIH 3T3-m1R cells, preincubated or not with a myristoylated PKCζ pseudosubstrate inhibitor (10 μm), were challenged with the agonist carbachol, and ERK5 activation (P-ERK5) was determined as detailed under ”Experimental Procedures.“ Blot bands were quantified by laser-scanner densitometry, and data (mean ± S.E. of 3 independent experiments) were expressed as a percentage of activated kinase (P-ERK5) versus total ERK5. B, MEFs obtained from WT or PKCζ-deficient mice (PKCζ−/−) were challenged with S1P, and ERK5 activation was assessed at different times as in previous panels. Data (mean ± S.E. of 3 independent experiments) were expressed as -fold activation when compared with the absence of agonist.