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Fig. 2. CNP inhibits FGF2-mediated activation of Erk MAP kinase. (A,B) Serum-starved cells were treated with FGF2 and either CNP or pCPT-cGMP for 30 minutes and analyzed for Erk1/2 phosphorylation by WB (A) or Erk activity by kinase assay using Elk as a substrate (B). Elk phosphorylation at Ser383 was determined by WB. Levels of total Erk1/2 serve as a loading control. (C) Cells were treated with FGF2 alone or together with CNP or pCPT-cGMP for different times up to 12 hours and analyzed for Erk phosphorylation by WB. The WB signal was quantified by densitometry and normalized to total Erk expression. The percentage of Erk phosphorylation relative to cells treated with FGF2 alone (100%) for each time point was graphed with the indicated standard deviation. Note that in short-term FGF2 treatment (1 hour), Erk activation was nearly completely inhibited by CNP or pCPT-cGMP in contrast to longer treatments (2-12 hours) where both CNP and pCPT-cGMP only lowered Erk activation by approximately 50%.

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