Abstract
The L-type calcium channel plays a critical role in excitation-contraction coupling by mediating calcium influx into cardiomyocytes. In vivo, beta-adrenergic receptor stimulation is proposed to increase the activity of the channel via cAMP-dependent protein kinase A (PKA) phosphorylation. It is not clear whether direct phosphorylation of the channel protein is sufficient to alter function. In addition, while several consensus phosphorylation sites exist, the site/s responsible for increased channel activity remains unknown.