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• W2185255623 abstract "Rationale: L-type Ca (CaV1.2) channels shape the cardiac action potential waveform and are essential for excitation–contraction coupling in heart. A gain-of-function G406R mutation in a cytoplasmic loop of CaV1.2 channels causes long QT syndrome 8 (LQT8), a disease also known as Timothy syndrome. However, the mechanisms by which this mutation enhances CaV1.2-LQT8 currents and generates lethal arrhythmias are unclear. Objective: To test the hypothesis that the anchoring protein AKAP150 modulates CaV1.2-LQT8 channel gating in ventricular myocytes. Methods and Results: Using a combination of molecular, imaging, and electrophysiological approaches, we discovered that CaV1.2-LQT8 channels are abnormally coupled to AKAP150. A pathophysiological consequence of forming this aberrant ion channel-anchoring protein complex is enhanced CaV1.2-LQT8 currents. This occurs through a mechanism whereby the anchoring protein functions like a subunit of CaV1.2-LQT8 channels that stabilizes the open conformation and augments the probability of coordinated openings of these channels. Ablation of AKAP150 restores normal gating in CaV1.2-LQT8 channels and protects the heart from arrhythmias. Conclusion: We propose that AKAP150-dependent changes in CaV1.2-LQT8 channel gating may constitute a novel general mechanism for CaV1.2-driven arrhythmias. (Circ Res. 2011;109:255-261.)" @default.
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• W2185255623 date "2011-01-01" @default.
• W2185255623 modified "2023-09-24" @default.
• W2185255623 title "Brief UltraRapid Communication Restoration of Normal L-Type Ca 2 Channel Function During Timothy Syndrome by Ablation of an Anchoring Protein" @default.
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