首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Cloning and expression of a Kv1.2 class delayed rectifier K+ channel from canine colonic smooth muscle.
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Cloning and expression of a Kv1.2 class delayed rectifier K+ channel from canine colonic smooth muscle.

机译:犬结肠平滑肌的Kv1.2类延迟整流K +通道的克隆和表达。

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摘要

A cDNA (CSMK1) encoding a delayed rectifier K+ channel of the Kv1.2 class was cloned from canine colonic circular smooth muscle and expressed in Xenopus oocytes. These channels appear to be uniquely expressed in gastrointestinal muscles and may participate in the electrical slow wave activity. Functional expression of CSMK1 in Xenopus oocytes demonstrated a K+ current that activated in a voltage-dependent manner upon depolarization. This current was highly sensitive to 4-aminopyridine (IC50, 74 microM). A low-conductance K+ channel was identified in inside-out patches from oocytes injected with CSMK1. This channel displayed a linear current-voltage relation with a slope conductance of 14 pS. The channels were blocked in a concentration-dependent manner by 4-aminopyridine. Northern blot analysis demonstrated that CSMK1 is expressed in a wide variety of gastrointestinal smooth muscles. Portal vein, renal artery, and uterus do not express CSMK1, suggesting that, among smooth muscles, expression of this K+ channel may be restricted to gastrointestinal smooth muscles. CSMK1 is 91% homologous to RAK, a delayed rectifier K+ channel cloned from rat heart, but displays unique pharmacological properties and tissue distribution.
机译:从犬结肠结肠平滑肌克隆了一个编码Kv1.2类延迟整流K +通道的cDNA(CSMK1),并在非洲爪蟾卵母细胞中表达。这些通道似乎在胃肠道肌肉中独特表达,并可能参与电慢波活动。 CSMK1在非洲爪蟾卵母细胞中的功能性表达显示出K +电流,该电流在去极化时以电压依赖性方式激活。该电流对4-氨基吡啶(IC50,74 microM)高度敏感。在注射CSMK1的卵母细胞的内向外斑片中鉴定出低电导K +通道。该通道显示出线性电流-电压关系,斜率电导为14 pS。该通道被4-氨基吡啶以浓度依赖性方式阻断。 Northern印迹分析表明,CSMK1在各种各样的胃肠道平滑肌中表达。门静脉,肾动脉和子宫不表达CSMK1,这表明在平滑肌中,该K +通道的表达可能仅限于胃肠道平滑肌。 CSMK1与RAK(从大鼠心脏克隆的延迟整流子K +通道)同源91%,但显示出独特的药理特性和组织分布。

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