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Significance The strengthening of heart contraction by epinephrine (adrenaline) and norepinephrine starts with the activation of β-adrenergic receptors and culminates in a protein kinase A–mediated increase in Ca2+ influx through the voltage-gated Ca2+ channel, CaV 1.2, into cardiomyocytes. Many crucial molecular details of this vital physiological regulation remained enigmatic for decades, not the least owing to the difficulty of reconstituting the regulation in model cells. Capitalizing on the recent discovery of the central role of the CaV 1.2-associated protein, Rad, we present a report of full reconstitution of the β-AR–CaV 1.2 cascade in a model system, theXenopus oocyte, and investigate crucial aspects of regulation such as the roles of auxiliary subunits and diverse forms of the channel protein.

Reconstitution of β-adrenergic regulation of Ca V 1.2: Rad-dependent and Rad-independent protein kinase A mechanisms

Reconstitution of β-adrenergic regulation of Ca _V 1.2: Rad-dependent and Rad-independent protein kinase A mechanisms