The actions of the kinase A anchoring protein, AKAP79, a key element in the regulation of the cardiac L-type Ca2+ channel, were assessed on skeletal muscle Ca2+ channels expressed in Xenopus oocytes. The channels were reconstituted by expressing the pore forming alpha(1s) subunit and its accessory subunits, alpha(2)-delta, beta, and gamma We report, for the first time, that peak Ca2+ channel currents are greatly increased (3.5-fold) by AKAP79 when co-expressed with the truncated form of the alpha(1s) subunit. Immunoblots revealed that the increase in current amplitude is not accompanied by a corresponding increase in the membrane levels of the alpha(1s) subunit. This suggests that AKAP79 does not increase the trafficking of the channel. In addition, we show that the transcript of AKAP 150, the rat ortholog of the human AKAP79, is expressed in rat skeletal muscle and propose that AKAP79/150 modulates Ca2+ channel function. (C) 2004 Elsevier Inc. All rights reserved.