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. Author manuscript; available in PMC: 2006 Feb 17.
Published in final edited form as: Circ Res. 2005 Dec 29;98(3):386–393. doi: 10.1161/01.RES.0000201956.86258.e1

Figure 4.

Figure 4

MEKs influence basal KChIP2 mRNA expression and mediate protein kinase C-induced downregulation. A, Neonatal myocytes were treated with 100 μmol/L PE, its corresponding vehicle (0.1 mmol/L ascorbic acid), or 100 nmol/L PMA for 8 hours in the presence or absence of 10 μmol/L U0126 or U0124. RT-PCR data for KChIP2 variants and GAPDH are shown. B, Total KChIP2 mRNA level was determined by real-time PCR. *P<0.05 and **P<0.01 (2-tailed t test, n≥6 for each condition). C, Myo-cytes were infected with adenoviruses carrying a dominant-negative (Ad-dnMEK-hrGFP) or constitutively active (Ad-caMEK-hrGFP) MEK1 or no additional insert (Ad-hrGFP). Infected cells were then untreated (None) or treated with 100 μmol/L PE or 100 nmol/L PMA for 8 hours. #P<0.05 (Wilcoxon signed-rank test, n≥6 for each condition). D, Relative reductions in total KChIP2 mRNA level were obtained from the data in B and C. *P<0.05 and **P<0.01 (Bonferroni test, n≥6 for each condition).