Deletion of the distal C terminus of CaV1.2 channels leads to loss of beta-adrenergic regulation and heart failure in vivo.

@article{Fu2011DeletionOT,
  title={Deletion of the distal C terminus of CaV1.2 channels leads to loss of beta-adrenergic regulation and heart failure in vivo.},
  author={Ying Fu and Ruth E. Westenbroek and Frank H. Yu and John Patrick Clark and Misty R. Marshall and Todd Scheuer and William A. Catterall},
  journal={The Journal of biological chemistry},
  year={2011},
  volume={286 14},
  pages={12617-26}
}
L-type calcium currents conducted by CaV1.2 channels initiate excitation-contraction coupling in cardiac and vascular smooth muscle. In the heart, the distal portion of the C terminus (DCT) is proteolytically processed in vivo and serves as a noncovalently associated autoinhibitor of CaV1.2 channel activity. This autoinhibitory complex, with A-kinase anchoring protein-15 (AKAP15) bound to the DCT, is hypothesized to serve as the substrate for β-adrenergic regulation in the fight-or-flight… CONTINUE READING
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