Article
Deletion of the distal C terminus of CaV1.2 channels leads to loss of beta-adrenergic regulation and heart failure in vivo.
The Journal of biological chemistry - 8 Apr 2011
Fu Ying, Westenbroek Ruth E, Yu Frank H, Clark John P, Marshall Misty R, Scheuer Todd, Catterall William A
Abstract excerpt
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...
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