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Sci. STKE, 3 July 2007 PERSPECTIVESThe Surprising Catch of a Voltage-Gated Potassium Channel in a Neuronal SNAREDurga P. Mohapatra, Helene Vacher, and James S. Trimmer* Department of Pharmacology, School of Medicine, University of California, Davis, CA 95616, USA. Abstract:
Among ion channels, voltage-gated calcium channels have been considered unique in their ability to mediate signaling events independent of the flow of ions through their pore. A voltage-gated potassium channel termed Kv2.1 has been identified as playing a role remarkably similar to one ion-independent function of calcium channels, facilitating regulated exocytosis through a direct interaction with a t-SNARE [soluble NSF (N-ethylmaleimidesensitive factor) attachment protein receptor] component of the vesicle release machinery. Kv2.1 overexpression enhances depolarization-induced secretion from the neuroendocrine-like PC12 cell line, and a nonconducting Kv2.1 mutant can accomplish the same feat. Kv2.1 interacts directly with syntaxin 1A, a plasma membrane t-SNARE component of the vesicle docking and fusion apparatus. Deletion of the syntaxin 1Abinding segment from Kv2.1 abolishes its ability to promote vesicle release, supporting a mechanism whereby Kv2.1 presumably transfers voltage-dependent conformational changes induced by membrane depolarization to interacting t-SNAREs to affect exocytosis. Kv2.1, a major mediator of electrical events in central neurons, cardiac and smooth muscle, and pancreatic *Corresponding author. Department of Pharmacology, School of Medicine, University of California, Davis, CA 95616, USA. Telephone, 530-754-6075; fax, 530-754-6079; e-mail, jtrimmer{at}ucdavis.edu
Citation: D. P. Mohapatra, H. Vacher, J. S. Trimmer, The Surprising Catch of a Voltage-Gated Potassium Channel in a Neuronal SNARE. Sci. STKE 2007, pe37 (2007). The editors suggest the following Related Resources on Science sites:In Science Signaling
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