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. Author manuscript; available in PMC: 2011 Mar 28.
Published in final edited form as: Sci Signal. 2010 Sep 28;3(141):ra70. doi: 10.1126/scisignal.2001152

Fig. 3.

Fig. 3

Regulation of CaV1.2 channel activity by optimal expression of cDNA encoding AKAP15. (A) Coupling efficiency (nA/pC) for CaV1.2Δ1800 and CaV1.2Δ1800 + DCT channels with and without AKAP15, and 5 μM forskolin. **P < 0.01 versus control without forskolin. Dashed black line indicates mean current for unstimulated CaV1.2Δ1800 + DCT (ITail, peak tail current; Q, total gating current; Vrev, reversal potential). (B) Time course of peak Ba2+ current during perfusion with 5 μM forskolin (Fsk). Pulses to 10 mV before and during application of forskolin. Inset: current traces indicated by a and b. (C) Current-voltage relationships of CaV1.2 channels from (A). (D) Coupling efficiency (nA/pC) for CaV1.2Δ1800 and CaV1.2Δ1800 + DCT channels with PKA Cα catalytic subunit, PKA RIIα regulatory subunit, AKAP15, and 5 μM forskolin. ***P < 0.001 versus control. Dashed black line indicates mean current for unstimulated CaV1.2Δ1800 + DCT. Right, coupling efficiency (nA/pC) of individual experiments in each condition. Red line indicates the maximum current observed with CaV1.2Δ1800 + DCT. (E) Current-voltage relationships of CaV1.2 channels from (D). Significance was determined by ANOVA.