Young J D, Cohn Z A, Gilula N B
Cell. 1987 Mar 13;48(5):733-43. doi: 10.1016/0092-8674(87)90071-7.
Gap junctions isolated from rat liver were incorporated into planar lipid bilayers. A channel activity that was directly dependent on voltage was recorded. Changes of pH and (Ca2+) had no direct effect on channel activity; however, they modulated the voltage-dependent gating of the gap junction channels differently. Single-channel fluctuations showed large scatter with peak amplitudes of 140 and 280 picoSiemmens in 0.1 M NaCl. The major protein of gap junctions (Mr of 27 kd) was also reconstituted into bilayers, giving channel properties similar to those of intact gap junctions. Polyclonal antibodies specific for this protein caused inhibition of the junctional conductance in bilayers. These data provide direct evidence that the 27 kd protein is the molecular species responsible for gap junction communication between cells.
从大鼠肝脏分离出的间隙连接被整合到平面脂质双分子层中。记录到一种直接依赖于电压的通道活性。pH值和（Ca2+）的变化对通道活性没有直接影响；然而，它们对间隙连接通道的电压依赖性门控有不同的调节作用。单通道波动显示出较大的离散性，在0.1 M NaCl中峰值幅度为140和280皮西门子。间隙连接的主要蛋白质（分子量为27 kd）也被重组到双分子层中，产生了与完整间隙连接相似的通道特性。针对这种蛋白质的多克隆抗体导致双分子层中连接电导的抑制。这些数据提供了直接证据，证明27 kd蛋白质是负责细胞间间隙连接通讯的分子种类。
