Coupled gating between cardiac calcium release channels (ryanodine receptors)
Coupled gating between cardiac calcium release channels (ryanodine receptors)
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DOI：
10.1161/hh1101.091268
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发表时间：
2001-06-08
影响因子：
20.1
通讯作者：
Marks, AR
中科院分区：
文献类型：
--
作者：
Marx, SO;Gaburjakova, J;Marks, AR
心肌中的兴奋-收缩偶联需要通过Ca 2+内流激活Ca 2+释放通道/2型兰尼碱受体（RyR 2s）。RyR 2以紧密排列的阵列排列在肌质网状膜上，使得它们的大胞质结构域彼此接触。我们现在表明，多个RyR 2可以在一定条件下分离，使它们保持物理耦合。当在平面脂质双层中检查这些耦合通道时，多个通道表现出同时门控，称为“耦合门控”。去除调节亚基，FK 506结合蛋白（FKBP12.6），功能上而不是物理上解偶联多个RyR 2通道。RyR 2通道之间的偶联门控可能是兴奋-收缩偶联以及涉及细胞内Ca 2+释放的其他信号通路中的重要调节机制。
Excitation-contraction coupling in heart muscle requires the activation of Ca2+-release channels/type 2 ryanodine receptors (RyR2s) by Ca2+ influx. RyR2s are arranged on the sarcoplasmic reticular membrane in closely packed arrays such that their large cytoplasmic domains contact one another. We now show that multiple RyR2s can be isolated under conditions such that they remain physically coupled to one another. When these coupled channels are examined in planar lipid bilayers, multiple channels exhibit simultaneous gating, termed "coupled gating." Removal of the regulatory subunit, the FK506 binding protein (FKBP12.6), functionally but not physically uncouples multiple RyR2 channels. Coupled gating between RyR2 channels may be an important regulatory mechanism in excitation-contraction coupling as well as in other signaling pathways involving intracellular Ca2+ release.