...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neuron >Calmodulin mediates calcium-dependent inactivation of the cerebellar type 1 inositol 1,4,5-trisphosphate receptor.
【24h】

Calmodulin mediates calcium-dependent inactivation of the cerebellar type 1 inositol 1,4,5-trisphosphate receptor.

机译：钙调蛋白介导小脑1型肌醇1,4,5-三磷酸受体的钙依赖性失活。

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

The dependency of purified mouse cerebellar type 1 inositol 1,4,5-trisphosphate receptor (IP3R1)/Ca2+ channel function on cytoplasmic Ca2+ was examined. In contrast to the channels in crude systems, the purified IP3R1 reconstituted into planar lipid bilayers did not show the bell-shaped dependence on Ca2+. It was activated with increasing Ca2+ sublinearly without inhibition even up to 200 microM. The addition of calmodulin to the cytoplasmic side inhibited the channel at high Ca2+ concentrations. Calmodulin antagonists reversed the Ca2+-dependent inactivation of the native channels in cerebellar microsomes. These results indicate that the bell-shaped dependence on cytoplasmic Ca2+ is not an intrinsic property of the IP3R1, and the Ca2+-dependent inactivation is directly mediated by calmodulin.
机译：检查了纯化的小鼠小脑1型肌醇1,4,5-三磷酸受体（IP3R1）/ Ca2 +通道功能对细胞质Ca2 +的依赖性。与粗体系中的通道相反，纯化的IP3R1重构为平面脂质双层，未显示出对Ca2 +的钟形依赖性。它通过亚线性增加的Ca2 +激活，即使抑制到200 microM，也没有抑制作用。在细胞质侧添加钙调蛋白可抑制高Ca2 +浓度下的通道。钙调蛋白拮抗剂逆转小脑微粒体内天然通道的Ca2 +依赖性失活。这些结果表明，钟形对细胞质Ca2 +的依赖性不是IP3R1的固有特性，而Ca2 +依赖性的失活直接由钙调蛋白介导。

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