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. 2013 May 2;288(24):17803–17811. doi: 10.1074/jbc.M113.477182

FIGURE 2.

FIGURE 2.

Activation of adenosine A2A receptors in PC12 cells causes proteasome-dependent degradation of EF2K. A, PC12 cells were stimulated for 3 or 6 h with CGS 21680 (100 nm) with or without MG132 (25 μm), and EF2K, p-tyrosine hydroxylase (p-TH), which served as a positive control for PKA activation downstream of A2A receptors, and GAPDH levels were assessed by SDS-PAGE and immunoblot. B, graph of summary data. A two-way ANOVA revealed significant main effects of CGS 21680 treatment and MG132, as well as a significant interaction between CGS 21680 and MG132. Bonferroni post-hoc tests revealed that either 3 or 6 h treatment with CGS 21680 reduced EF2K levels relative to control (CGS 3 h: 65.95 ± 9.89, n = 3, **, p < 0.01; CGS 6 h: 49.31 ± 12.02, n = 3, ***, p < 0.001), and this effect was blocked by the addition of MG132 at both time points (CGS+MG132 3 h: 126.44 ± 13.87, n = 3; CGS+MG132 6 h: 106.45 ± 16.35, n = 3).