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Pubmed ID :29743299
Publication Date : //

The AKAP Cypher/Zasp contributes to β-adrenergic/PKA stimulation of cardiac Ca1.2 calcium channels.


Stimulation of the L-type Ca current conducted by Ca1.2 channels in cardiac myocytes by the β-adrenergic/protein kinase A (PKA) signaling pathway requires anchoring of PKA to the Ca1.2 channel by an A-kinase anchoring protein (AKAP). However, the AKAP(s) responsible for regulation in vivo remain unknown. Here, we test the role of the AKAP Cypher/Zasp in β-adrenergic regulation of Ca1.2 channels using physiological studies of cardiac ventricular myocytes from young-adult mice lacking the long form of Cypher/Zasp (LCyphKO mice). These myocytes have increased protein levels of Ca1.2, PKA, and calcineurin. In contrast, the cell surface density of Ca1.2 channels and the basal Ca current conducted by Ca1.2 channels are significantly reduced without substantial changes to kinetics or voltage dependence. β-adrenergic regulation of these L-type Ca currents is also significantly reduced in myocytes from LCyphKO mice, whether calculated as a stimulation ratio or as net-stimulated Ca current. At 100 nM isoproterenol, the net β-adrenergic-Ca current conducted by Ca1.2 channels was reduced to 39 ± 12% of wild type. However, concentration-response curves for β-adrenergic stimulation of myocytes from LCyphKO mice have concentrations that give a half-maximal response similar to those for wild-type mice. These results identify Cypher/Zasp as an important AKAP for β-adrenergic regulation of cardiac Ca1.2 channels. Other AKAPs may work cooperatively with Cypher/Zasp to give the full magnitude of β-adrenergic regulation of Ca1.2 channels observed in vivo.

Authors : Yu Haijie , Yuan Can , Westenbroek Ruth E , Catterall William A ,

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