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. 2014 Sep 27;468:490–503. doi: 10.1016/j.virol.2014.09.005

Fig. 1.

Fig. 1

ERK1/2 signaling is activated in TC-83 infected cells (A) Schematic of ERK signal transduction cascade – upstream activators and downstream targets. (B) Quantification of fold changes in phosphorylation status of target proteins in infected cells over uninfected cells as observed by RPPA. Signal intensities pertaining to phosphorylated forms of proteins were calculated for mock-infected lysates and TC-83 infected lysates following imaging and quantification of the RPPA slides. The values were then used to calculate the fold change in phosphorylation in the infected samples over the mock-infected samples. (C) Western blot validation of ERK phosphorylation in U87MG cells after infection with TC-83. Infected and mock uninfected cell lysates were collected at the time points indicated. β-actin was used as a loading control, and three independent experiments were conducted. (D) Western blot validation of downstream substrate p90RSK phosphorylation. (E) Quantification p-ERK1 and p-ERK2 in infected cells from three independent experiments, normalized to β-actin and then compared to the mock at each time point. Bars indicate the mean and error bars represent standard error.