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. Author manuscript; available in PMC: 2013 Aug 1.
Published in final edited form as: Biochim Biophys Acta. 2012 May 18;1823(8):1273–1284. doi: 10.1016/j.bbamcr.2012.05.012

Figure 6. Transcriptional inhibition abolishes the cAMP-induced increase in HERG abundance.

Figure 6

Part A, a series of immunoblots from HEK-HERG stable cells of HERG and tubulin under control (DMSO), CPT-cAMP treated, actinomycin-D treated, and combination cAMP and actinomycin-D treatment at three time points 6, 12, and 24 hours. HERG appears as a doublet and tubulin was used as the loading control. Lower panels show blots of PKA catalytic subunit-α, PKA regulatory subunit RIIα and multiple isoforms of 14-3-3. Part B shows quantification and summary data for the experiment. Fold change in the ratio of HERG protein over tubulin is plotted per treatment condition for each of the three time points. Control levels are normalized to 1.0 for all time points. Differences between the control and CPT-cAMP treated conditions are significant as indicated, n=5 and * p-value < 0.05, ** p-value < 0.01. Differences between the control and act-D conditions were not statistically significant. Differences between the control and combination treatment conditions were also not statistically significant. There were no significant changes with treatments compared to control for the levels of PKAcat, PKA RIIα and 14-3-3.