PKA-dependent regulation of CaV1.2Δ1800 channels via AKAP15 and AKAP79ΔPIX. (A) Representative IBa through CaV1.2Δ1800 and CaV1.2Δ1800 + DCT channels coexpressed with cDNA ratios of either 0.003:1 AKAP15 or 0.01:1 AKAP79ΔPIX in tsA-201 cells in the absence or presence of 5 µM forskolin elicited by a test pulse to 10 mV from a holding potential of −80 mV. (B) Mean current-voltage relationships for CaV1.2Δ1800 and CaV1.2Δ1800 + DCT channels with 0.003:1 AKAP15 or 0.01:1 AKAP79ΔPIX and 5 µM forskolin (Fsk). Dashed black line indicates zero current level. (C) Coupling efficiency (nA/pC) for CaV1.2Δ1800 and CaV1.2Δ1800 + DCT channels with AKAP15 or AKAP79ΔPIX and 5 µM forskolin. Dashed black line indicates mean coupling ratio for unstimulated CaV1.2Δ1800 + DCT. n values and ±SEM are indicated. **, P < 0.01; and *, P < 0.05 versus control. Significance was determined by ANOVA followed by Dunnett’s post-test. (D) Mean current-voltage relationships determined as in B. Fits to current-voltage relationships showed that there was no significant difference in the voltage dependence of activation (P > 0.7). (B and D) Error bars are SEM. (E) Coupling ratio (nA/pC) for CaV1.2Δ1800 and CaV1.2Δ1800 + DCT channels with PKA Cα catalytic subunit plus PKA RIIα regulatory subunit, AKAP15, AKAP79ΔPIX, and 5 µM forskolin. Dashed black line indicates mean coupling ratio for unstimulated CaV1.2Δ1800 + DCT. ***, P < 0.001; and *, P < 0.05 versus controls without forskolin. Significance was determined by Student’s t test. The control results for AKAP15 + DCT are values from the dataset published in Fuller et al. (2010). The experiments presented here overlapped in time with those previously published experiments.
