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Papers In Press, published online ahead of print July 4, 2006
Institut für Pharmakologie und Toxikologie, TU-München, München 80802
Corresponding Author: welling{at}ipt.med.tu-muenchen.de
Calcium-dependent facilitation of L-type calcium channels has been reported to depend on the function of Calmodulin kinase II. In contrast, the mechanism for voltage-dependent-facilitation is not clear. In HEK 293 cells expressing Cav1.2, Cav
J. Biol. Chem, 10.1074/jbc.M508661200
Submitted on August 5, 2005
Revised on May 22, 2006
Accepted on July 4, 2006
Calmodulin kinase II is involved in voltage-dependent facilitation of the L-type Cav1.2 calcium channel. Identification of the phosphorylation sites
2a and Calmodulin kinase II, the calcium current measured at +30 mV was facilitated up to 1.5- fold by a 200 ms long prepulse to +160 mV. This voltage-dependent facilitation was prevented by the Calmodulin kinase II inhibitors KN93 and the autocamtide-2-related peptide. In cells expressing the Cav1.2 mutation I1649E, a residue critical for the binding of Ca2+-bound calmodulin, facilitation was also abolished. Calmodulin kinase II was coimmunoprecipitated with the Cav1.2 channel from murine heart and HEK 293 cells expressing Cav1.2 and Calmodulin kinase II. The precipitated Cav1.2 channel was phosphorylated in the presence of calmodulin and Ca2+. Fifteen putative Calmodulin kinase II phosphorylation sites were identified mostly in the carboxyterminal tail of Cav1.2. Neither truncation at amino acid 1728 nor changing the II-III loop serines 808 and 888 to alanines affected facilitation of the calcium current. In contrast, facilitation was decreased by the single mutations S1512A and S1570A and abolished by the double mutation S1512/1570A. These serines flank the carboxyterminal EF hand motif. Immunoprecipitation of Calmodulin kinase II with the Cav1.2 channel was not affected by the mutation S1512/1570A. The phosphorylation of the Cav1.2 protein was strongly decreased in the S1512/1570A double mutant. These results suggest that voltage-dependent facilitation of the Cav1.2 channel depends on the phosphorylation of S1512/1570 by Calmodulin kinase II.
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