The beta subunit increases Ca2+ currents and gating charge movements of human cardiac L-type Ca2+ channels.
The beta subunit increases Ca2+ currents and gating charge movements of human cardiac L-type Ca2+ channels.
复制标题
β 亚基可增加 Ca2 电流并控制人类心脏 L 型 Ca2 通道的电荷运动。
DOI：
10.1016/s0006-3495(96)79685-6
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Varadi,G
中科院分区：
文献类型：
--
作者：
Josephson,IR;Varadi,G
使用哺乳动物表达系统研究了人类心脏 L 型 Ca2- 通道的门控电流（非线性电荷运动）的特性及其与 Ca2+ 通道（离子）电流激活的关系。克隆的人心脏α1+兔α2亚基或人心脏α1+兔α2+人β3亚基在HEK293细胞中瞬时表达。最大 Ca2+ 电流密度从 α 1 + α 2 亚基的 -3.9 +/- 0.9 pA/pF 增加到 α 1 + α 2 + β 3 亚基的 -11.6 +/- 2.2 pA/pF。添加 5 mM Co2+ 后，使用 -P/5 方案记录钙通道门控电流。最大非线性电荷运动 (Qmax) 从 alpha 1 + alpha 2 亚基表达的 2.5 +/- 0.3 nC/muF 增加到 alpha 1 + alpha 2 + beta 3 亚基表达的 12.1 +/- 0.3 nC/muF。两个亚基组合的 QON 等于 QOFF。与 Ca2+ 电导激活的电压依赖性相比，QON-Vm 数据由两个玻尔兹曼表达式之和拟合，并且范围更大的负电势。我们得出的结论是：1) β 亚基增加了这些细胞质膜中表达的功能性 α 1 亚基的数量，2) 人类心脏 L 型钙通道的电压依赖性激活涉及至少两个不相同且功能不同的门控结构的运动。
The properties of the gating currents (nonlinear charge movements) of human cardiac L-type Ca2- channels and their relationship to the activation of the Ca2+ channel (ionic) currents were studied using a mammalian expression system. Cloned human cardiac alpha1 + rabbit alpha 2 subunits or human cardiac alpha 1 + rabbit alpha 2 + human beta 3 subunits were transiently expressed in HEK293 cells. The maximum Ca2+ current density increased from -3.9 +/- 0.9 pA/pF for the alpha 1 + alpha 2 subunits to -11.6 +/- 2.2 pA/pF for alpha 1 + alpha 2 + beta 3 subunits. Calcium channel gating currents were recorded after the addition of 5 mM Co2+, using a -P/5 protocol. The maximum nonlinear charge movement (Qmax) increased from 2.5 +/- 0.3 nC/muF for alpha 1 + alpha 2 subunit to 12.1 +/- 0.3 nC/muF for alpha 1 + alpha 2 + beta 3 subunit expression. The QON was equal to the QOFF for both subunit combinations. The QON-Vm data were fit by a sum of two Boltzmann expressions and ranged over more negative potentials, as compared with the voltage dependence for activation of the Ca2+ conductance. We conclude that 1) the beta subunit increases the number of functional alpha 1 subunits expressed in the plasma membrane of these cells and 2) the voltage-dependent activation of the human cardiac L-type calcium channel involves the movements of at least two nonidentical and functionally distinct gating structures.