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. Author manuscript; available in PMC: 2011 Mar 5.
Published in final edited form as: Circ Res. 2010 Jan 28;106(4):748–756. doi: 10.1161/CIRCRESAHA.109.213363

Figure 4. Displacing CaM from the IQ domain of Cav1.2 increases coupled gating of WT and TS Cav1.2 channels.

Figure 4

(A) Ca2+ sparklet records from tsA-201 and arterial myocytes showing induction of coupled gating by W7 (100 µmol/L). κ values are shown above each trace. (B) Number of coupled sites per cell before and after W7. (C) Cartoon of Cav1.2-EGFP and CaM-tRFP. Right, images of Cav1.2-EGFP in tsA-201 cells under control conditions, during W7 treatment, and following CaM-tRFP photobleaching. (D) Cav1.2-EGFP fluorescence intensity at an example cross section of the membrane marked by the white line in each of the images in panel C. Dotted lines show the FDA and FA values used to calculate effective FRET=1-(FDA/FA). (E) FRET in specific sites before and after W7 (center, lower row) or PDBu (right, lower row) application. Yellow bars are mean values. (F) Ca2+ sparklet records with coupled Cav1.2 channels from tsA-201 cells expressing Cav1.2-TS and hypertensive smooth muscle. (G) Representative Cav1.2 channel currents evoked by depolarization from −80 to −30 mV in patches (cell-attached) from tsA-201 cells expressing WT (upper trace) and Cav1.2-TS channels (lower trace). The close state is denoted by a “c” and the open state by an “o”. (H) Number of sites with coupled Cav1.2 channels per cell in cells expressing WT and TS Cav1.2 and in normotensive (NT) and hypertensive (HTN) smooth muscle. (I) FRET data between EGFP-tagged WT or TS Cav1.2 and CaM-tRFP.