• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >The protein kinase C inhibitor, bisindolylmaleimide (I), inhibits voltage-dependent K+ channels in coronary arterial smooth muscle cells
【24h】

The protein kinase C inhibitor, bisindolylmaleimide (I), inhibits voltage-dependent K+ channels in coronary arterial smooth muscle cells

机译：蛋白激酶C抑制剂bisindolylmaleimide（I）抑制冠状动脉平滑肌细胞中的电压依赖性K +通道

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We examined the effects of the protein kinase C (PKC) inhibitor, bisindolylmaleimide (BIM) (I), on voltage-dependent K+ (K-V) channels in rabbit coronary arterial smooth Muscle Cells using whole-cell patch clamp technique. BIM (1) reversibly and dose-dependently inhibited the K-V currents with an apparent K-d value of 0.27 mu M The inhibition of the K-V current by BIM (I) was highly voltage-dependent between - 30 and +10 mV (voltage range of channel activation), and the additive inhibition of the K-V current by BIM (I) was voltage-dependence in the full activation voltage range. The rate constants of association and dissociation for BIM (1) were 18.4 mu M-1 s(-1) and 4.7 s(-1), respectively. BIM (I) had no effect on the steady-state activation and inactivation of K-V channels. BIM (11) caused use-dependent inhibition of K,,, current, which was consistent with the slow recovery from inactivation in the presence of BIM (I) (recovery time constants were 856.95 +/- 282.6 ms for control, and 1806.38 +/- 110.0 ms for 300 nM BIM (I)). ATP-sensitive K+ (K-ATP), inward rectifier K+ (K-IR). Ca2+ -activated K+ (BKCa) channels, which regulate the membrane potential and arterial tone, were not affected by BIM (1). The PKC inhibitor, chelerythrine, and protein kinase A (PKA) inhibitor, PKA-IP, had little effect on the K-V current and did not alter the inhibitory effects of BIM (1) on the K, current. These results suggest that BIM (1) inhibits K-V channels in a phosphorylation-independent, and voltage-, time- and Use-dependent manner. (c) 2005 Elsevier Inc. All rights reserved.
机译：我们使用全细胞膜片钳技术检查了蛋白激酶C（PKC）抑制剂双吲哚基马来酰亚胺（BIM）（I）对兔冠状动脉平滑肌细胞中电压依赖性K +（K-V）通道的影响。 BIM（1）可逆和剂量依赖性地抑制KV电流，其表观Kd值为0.27μM.BIM（I）对KV电流的抑制在-30至+10 mV（通道电压范围）之间高度依赖电压BIM（I）对KV电流的累加抑制是在整个激活电压范围内的电压依赖性。 BIM（1）的缔合和解离速率常数分别为18.4μM-1 s（-1）和4.7 s（-1）。 BIM（I）对K-V通道的稳态激活和失活没有影响。 BIM（11）导致了对钾电流的使用依赖性抑制，这与存在BIM（I）时从失活中缓慢恢复一致（对照的恢复时间常数为856.95 +/- 282.6 ms，1806.38 +对于300 nM BIM（I）为110.0 ms。 ATP敏感K +（K-ATP），内向整流器K +（K-IR）。调节膜电位和动脉张力的Ca2 +激活的K +（BKCa）通道不受BIM的影响（1）。 PKC抑制剂白屈菜红碱和蛋白激酶A（PKA）抑制剂PKA-IP对K-V电流几乎没有影响，并且没有改变BIM（1）对K电流的抑制作用。这些结果表明，BIM（1）以不依赖磷酸化，依赖电压，依赖时间和依赖使用的方式抑制K-V通道。 （c）2005 Elsevier Inc.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号