Lipid-mediated inactivation of colicin E1 channels by calcium ions.
Lipid-mediated inactivation of colicin E1 channels by calcium ions.
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钙离子导致的脂质介导的大肠菌素 E1 通道失活。
DOI：
10.1134/s0006297906010159
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Antonenko,YN
中科院分区：
文献类型：
--
作者：
Sobko,AA;Kotova,EA;Zakharov,SD;Cramer,WA;Antonenko,YN
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。在电生理学实验中，Ca 2+抑制了大肠杆菌素E1通道在由二植烷酰磷脂酰甘油形成的膜中的活性，而没有从膜表面发生蛋白质的解吸。没有观察到Ca 2+对二植烷酰磷脂酰胆碱形成的膜的影响。单通道测量结果表明，Ca 2+诱导的大肠杆菌素诱导的电流减少跨带负电荷的膜是由于开放的大肠杆菌素通道的数量减少，而不是它们的性质的变化。根据环形模型，Ca 2+对大肠杆菌素El通道形成活性的影响被解释为由Ca 2+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的改变。
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 El channel-forming activity is explained by alteration of the membrane lipid curvature caused by electrostatic interaction of Ca2+with negatively charged lipid head groups.