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Lu, Ling,Zhang, Qian,Timofeyev, Valeriy,Zhang, Zhao,Young, J. Nilas,Shin, Hee-Sup,Knowlton, Anne A.,Chiamvimonvat, Nipavan Ovid Technologies Wolters Kluwer -American Heart A 2007 Circulation research Vol.100 No.1
<P>Cytoskeletal proteins are known to sculpt the structural architecture of cells. However, their role as bridges linking the functional crosstalk of different ion channels is unknown. Here, we demonstrate that a small conductance Ca(2+)-activated K(+) channels (SK2 channel), present in a variety of cells, where they integrate changes in intracellular Ca(2+) concentration [Ca(2+)(i)] with changes in K(+) conductance and membrane potential, associate with L-type Ca(2+) channels; Ca(v)1.3 and Ca(v)1.2 through a physical bridge, alpha-actinin2 in cardiac myocytes. SK2 channels do not physically interact with L-type Ca(2+) channels, instead, the 2 channels colocalize via their interaction with alpha-actinin2 cytoskeletal protein. The association of SK2 channel with alpha-actinin2 localizes the channel to the entry of external Ca(2+) source, which regulate the channel function. Furthermore, we demonstrated that the functions of SK2 channels in atrial myocytes are critically dependent on the normal expression of Ca(v)1.3 Ca(2+) channels. Null deletion of Ca(v)1.3 channel results in abnormal function of SK2 channel and prolongation of repolarization and atrial arrhythmias. Our study provides insight into the molecular mechanisms of the coupling of SK2 channel with voltage-gated Ca(2+) channel, and represents the first report linking the coupling of 2 different types of ion channels via cytoskeletal proteins.</P>
Zhang, Zhao,He, Yuxia,Tuteja, Dipika,Xu, Danyan,Timofeyev, Valeriy,Zhang, Qian,Glatter, Kathryn A.,Xu, Yanfang,Shin, Hee-Sup,Low, Reginald,Chiamvimonvat, Nipavan Ovid Technologies Wolters Kluwer -American Heart A 2005 CIRCULATION - Vol.112 No.13
<P>Previous data suggest that L-type Ca2+ channels containing the Cav1.3(alpha(1D)) subunit are expressed mainly in neurons and neuroendocrine cells, whereas those containing the Cav1.2(alpha1C) subunit are found in the brain, vascular smooth muscle, and cardiac tissue. However, our previous report as well as others have shown that Cav1.3 Ca2+ channel-deficient mice (Cav1.3(-/-)) demonstrate sinus bradycardia with a prolonged PR interval. In the present study, we extended our study to examine the role of the Cav1.3(alpha1D) Ca2+ channel in the atria of Cav1.3(-/-) mice.</P>