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• W2016454749 abstract "The roles of calmodulin (CaM)-dependent protein kinase II (CaMKII) in the maintenance of basal activity and the reversion of run-down of L-type Ca2+ channels were studied in guinea-pig ventricular myocytes by the patch-clamp technique. In the cell-attached configuration, the Ca2+-channel activity was inhibited to 82% – 26% by 1 – 10 μM KN-93 and to 92% – 66% by 0.1 – 1 μM autocamtide-2–related inhibitory peptide (AIP) myristoylated. In the inside-out configuration, the bovine cardiac cytoplasm recovered Ca2+-channel activity to 87% of that recorded in the cell-attached configuration, while the CaMKII inhibitor 281-301 at 10 μM reduced the recovery effect to 19%. CaM + ATP recovered the channel activity to 93% and 28% of that recorded in the cell-attached configuration when applied at 1 and 5 min after run-down, respectively, showing a time-dependent attenuation. However, in the presence of 0.33 μM CaMKII, this attenuation was abolished, showing 85% and 75% recovery when applied at 1 and 5 min after run-down, respectively. This recovery effect was suppressed by 10 μM AIP, applied at 5 min, but not at 1 min after run-down. We concluded that CaMKII activation is required in the maintenance of basal activity of L-type Ca2+ channels." @default.
• W2016454749 created "2016-06-24" @default.
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• W2016454749 date "2008-01-01" @default.
• W2016454749 modified "2023-10-18" @default.
• W2016454749 title "Calmodulin Kinase II Activation Is Required for the Maintenance of Basal Activity of L-Type Ca2+ Channels in Guinea-Pig Ventricular Myocytes" @default.
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• W2016454749 doi "https://doi.org/10.1254/jphs.08101fp" @default.
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