Sobko A A, Kotova E A, Zakharov S D, Cramer W A, Antonenko Y N
Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia.
Biochemistry (Mosc). 2006 Jan;71(1):99-103. doi: 10.1134/s0006297906010159.
Based on the model of a toroidal protein-lipid pore, the effect of calcium ions on colicin E1 channel was predicted. In electrophysiological experiments Ca2+ suppressed the activity of colicin E1 channels in membranes formed of diphytanoylphosphatidylglycerol, whereas no desorption of the protein occurred from the membrane surface. The effect of Ca2+ was not observed on membranes formed of diphytanoylphosphatidylcholine. Single-channel measurements revealed that Ca2+-induced reduction of the colicin-induced current across the negatively charged membrane was due to a decrease in the number of open colicin channels and not changes in their properties. In line with the toroidal model, the effect of Ca2+ on the colicin E1 channel-forming activity is explained by alteration of the membrane lipid curvature caused by electrostatic interaction of Ca2+ with negatively charged lipid head groups.
基于环形蛋白质-脂质孔模型，预测了钙离子对大肠杆菌素E1通道的影响。在电生理实验中，Ca2+抑制了由二植烷酰磷脂酰甘油形成的膜中大肠杆菌素E1通道的活性，而蛋白质并未从膜表面解吸。在由二植烷酰磷脂酰胆碱形成的膜上未观察到Ca2+的作用。单通道测量表明，Ca2+诱导的跨带负电荷膜的大肠杆菌素诱导电流的降低是由于开放的大肠杆菌素通道数量减少，而非其特性改变。与环形模型一致，Ca2+对大肠杆菌素E1通道形成活性的影响是由Ca2+与带负电荷的脂质头部基团的静电相互作用引起的膜脂质曲率改变所解释的。
