Coupled gating between individual skeletal muscle Ca2+ release channels (ryanodine receptors)
Coupled gating between individual skeletal muscle Ca2+ release channels (ryanodine receptors)
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DOI：
10.1126/science.281.5378.818
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发表时间：
1998-08-07
期刊：
影响因子：
56.9
通讯作者：
Marks, AR
中科院分区：
文献类型：
--
作者：
Marx, SO;Ondrias, K;Marks, AR
骨骼肌的兴奋 - 收缩偶联需要通过肌浆网中的兰尼碱受体（RyR1）通道释放细胞内钙离子（Ca2 +）。一半的RyR1通道由质膜中的电压依赖性Ca2 +通道激活。在平面脂质双分子层中，RyR1通道表现出同时的开放和关闭，称为“偶联门控”。添加通道辅助蛋白FKBP12可诱导偶联门控，去除FKBP12则使通道解偶联。偶联门控提供了一种机制，通过该机制，不与电压依赖性Ca2 +通道相关的RyR1通道可受到调节。
Excitation-contraction coupling in skeletal muscle requires the release of intracellular calcium ions (Ca2+) through ryanodine receptor (RyR1) channels in the sarcoplasmic reticulum. Half of the RyR1 channels are activated by voltage-dependent Ca2+ channels in the plasma membrane, In planar Lipid bilayers, RyR1 channels exhibited simultaneous openings and closings, termed "coupled gating." Addition of the channel accessory protein FKBP12 induced coupled gating, and removal of FKBP12 uncoupled channels, Coupled gating provides a mechanism by which RyR1 channels that are not associated with voltage-dependent Ca2+ channels can be regulated.