Yeung Shuk Yin M, Lange Wienke, Schwake Michael, Greenwood Iain A
Division of Basic Medical Sciences, Ion Channels and Cell Signalling Research Centre, St. George's, University of London, London SW17 0RE, UK.
Biochem Biophys Res Commun. 2008 Jul 11;371(4):741-6. doi: 10.1016/j.bbrc.2008.04.129. Epub 2008 May 5.
Ion channels encoded by KCNQ genes (1-5) are key regulators of membrane properties in many cell types. The KCNQ5 gene was the last to be identified and has three splice variants that are expressed in human brain and skeletal muscle. The KCNQ5 encoded channel possesses M-current properties and so far no channelopathy has been associated with any of the three variants. We now show that only the shortest KCNQ5 variant, which has exon 9 deleted, was expressed in a variety of murine vascular smooth muscle. In Xenopus oocytes, this variant generated currents with amplitudes, activation kinetics and biophysical properties similar to the full-length variant normally expressed in neuronal tissue. Furthermore sensitivity to block by XE991 and activation by retigabine were also similar between both variants. These data represent an exhaustive characterisation of a truncated KCNQ5 splice variant that may contribute to the native XE991-sensitive channel in murine vasculature.
由KCNQ基因(1-5)编码的离子通道是多种细胞类型中膜特性的关键调节因子。KCNQ5基因是最后被鉴定出来的,有三种剪接变体,在人类大脑和骨骼肌中表达。KCNQ5编码的通道具有M电流特性,到目前为止,尚未发现这三种变体中的任何一种与通道病有关。我们现在表明,只有最短的KCNQ5变体(缺失外显子9)在多种小鼠血管平滑肌中表达。在非洲爪蟾卵母细胞中,该变体产生的电流在幅度、激活动力学和生物物理特性方面与通常在神经元组织中表达的全长变体相似。此外,两种变体对XE991阻断的敏感性和瑞替加滨激活的敏感性也相似。这些数据代表了对截短的KCNQ5剪接变体的详尽表征,该变体可能有助于小鼠脉管系统中天然的XE991敏感通道。