Modulatory mechanisms of cardiac ion channels.

与H.A.Fozzard教授的合作在表达通道功能和结构确认的技术成果方面取得了很大进展。我们还获得了ATP敏感性K^+通道的克隆。现在，我们已经准备好表达这些K^+通道，酪氨酸磷酸化对HERG K通道的功能调节正在研究中。HERG K^+通道的突变是长QT综合征的病因之一。因此，我们开始检查突变通道的功能异常。与H.C.Hartzell教授的联合研究在ryanodine受体通道蛋白的纯化方面取得了很大进展，这使我们能够以更高的成功率研究它们的功能。由于这一联合研究的成果，现在人们用精细的技术和新的信息研究了蛋白磷酸化和磷酸酶对Ca^<2+>激活的Cl^-通道和L型Ca^<2+>通道的调节。

The collaboration with Professor H.A.Fozzard has made a great advance in the technical achievements of the expressed channels functions and structural confirmation. We also acquired the clones of ATP-sensitive K^+ channel. Now, we are ready to express these K^+ channels and functional modulation of HERG K channel by tyrosin phosphorylation is under investigation. Furthermore, mutation of HERG K^+ channels is one of etiological factors for long QT syndrome. Therefore, we started to examine functional abnormality of the mutated channels. The joint research with Professor H.C.Hartzell has made a great advance for the purification of ryanodine receptor channel proteins, which enables us to study their function with much higher success rate. Modulation of Ca^<2+> -activated Cl^- -channel and L-type Ca^<2+> channel by protein phosphorylation and phosphatases is now studied with refined technique and new information owing to the fruits of this joint research.