Regulation of L-type Ca^<2+> channel activity by calmodulin

我们使用膜片钳技术（由内到外模式）测量了l型Ca^<2+>通道及其突变体c端缺失（δ CT）和δ CT与钙调蛋白（CaM）连接的活性。我们发现CaM与通道的结合是通道活性所必需的。与野生型通道不同，突变体不需要ATP来维持通道活性。这表明CaM和ATP与c端近端相互作用，产生通道活性，而通道活性被c端远端负调节。

We measured activity of L-type Ca^<2+> channel and its mutants, C-terminal deletion (delta CT) and delta CT linked with calmodulin (CaM), using patch-clamp technique (inside-out mode). We found that binding of CaM to the channel was required for the channel activity. Unlike the wild type channel, the mutants did not require ATP for the channel activity. It was suggested that CaM and ATP interacted with a proximal part of C-terminal thereby producing the channel activity, which was modulated negatively by a distal part of C-terminal.