Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Okazaki, K. et al.

KN-62, a specific Ca++/calmodulin-dependent protein kinase inhibitor, reversibly depresses the rate of beating of cultured fetal mouse cardiac myocytes.

Effects of KN-62 (1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4- phenylpiperazine), a specific Ca++/calmodulin (CaM)-dependent protein kinase inhibitor, were examined on the rate of spontaneous beating and the intracellular Ca++ transient of cultured myocytes from fetal mouse ventricle. KN-62 depressed the rate of beating in a dose-dependent fashion. Spontaneous beating ceased 10 min after the administration of 1 microM KN-62 and recovered gradually after washing with cultured medium. Addition of KN-04 [N-(1-1[P-(5-isoquinolinsulfonyl)benzyl]-2-(4- phenylpiperazinyl)ethyl)-5-isoquinolinsulfonamide; 1 microM], an analog of KN-62, did not change the rate of beating. In the experiment using an intracellular Ca++ fluorescence indicator, fluo-3, KN-62 depressed the fluo-3 intensity at a systolic phase. The kinase activity to syntide-2 of Ca++/CaM kinase II purified from the rabbit heart was inhibited by KN-62, but not by KN-04. Addition of KN-62 inhibited the phosphorylation of phospholamban by Ca++/CaM kinase II in a dose-dependent manner. KN-62 depressed the Ca(++)-pumping ATPase activity in the presence of Ca++ and CaM by 32%. These findings indicate that Ca++/CaM kinase II changes an intracellular Ca++ transient and modulates the rate of beating at least in part.[1]

References

KN-62, a specific Ca++/calmodulin-dependent protein kinase inhibitor, reversibly depresses the rate of beating of cultured fetal mouse cardiac myocytes. Okazaki, K., Ishikawa, T., Inui, M., Tada, M., Goshima, K., Okamoto, T., Hidaka, H. J. Pharmacol. Exp. Ther. (1994) [Pubmed]

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