Marx S O, Ondrias K, Marks A R
Molecular Cardiology Program, Divisions of Cardiology and Circulatory Physiology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
Science. 1998 Aug 7;281(5378):818-21. doi: 10.1126/science.281.5378.818.
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.
骨骼肌中的兴奋-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通道表现出同时开放和关闭，称为“耦合门控”。添加通道辅助蛋白FKBP12会诱导耦合门控，而去除FKBP12会使通道解偶联。耦合门控提供了一种机制，通过该机制，与电压依赖性Ca2+通道无关的RyR1通道可以受到调节。
