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孔道细胞内口处的正电荷调节CFTR氯离子通道中的阴离子传导。

Positive charges at the intracellular mouth of the pore regulate anion conduction in the CFTR chloride channel.

作者信息

Aubin Chantal N St, Linsdell Paul

机构信息

Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia B3H 1X5, Canada.

出版信息

J Gen Physiol. 2006 Nov;128(5):535-45. doi: 10.1085/jgp.200609516. Epub 2006 Oct 16.

Abstract

Many different ion channel pores are thought to have charged amino acid residues clustered around their entrances. The so-called surface charges contributed by these residues can play important roles in attracting oppositely charged ions from the bulk solution on one side of the membrane, increasing effective local counterion concentration and favoring rapid ion movement through the channel. Here we use site-directed mutagenesis to identify arginine residues contributing important surface charges in the intracellular mouth of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel pore. While wild-type CFTR was associated with a linear current-voltage relationship with symmetrical solutions, strong outward rectification was observed after mutagenesis of two arginine residues (R303 and R352) located near the intracellular ends of the fifth and sixth transmembrane regions. Current rectification was dependent on the charge present at these positions, consistent with an electrostatic effect. Furthermore, mutagenesis-induced rectification was more pronounced at lower Cl(-) concentrations, suggesting that these mutants had a reduced ability to concentrate Cl(-) ions near the inner pore mouth. R303 and R352 mutants exhibited reduced single channel conductance, especially at negative membrane potentials, that was dependent on the charge of the amino acid residue present at these positions. However, the very low conductance of both R303E and R352E-CFTR could be greatly increased by elevating intracellular Cl(-) concentration. Modification of an introduced cysteine residue at position 303 by charged methanethiosulfonate reagents reproduced charge-dependent effects on current rectification. Mutagenesis of arginine residues in the second and tenth transmembrane regions also altered channel permeation properties, however these effects were not consistent with changes in channel surface charges. These results suggest that positively charged arginine residues act to concentrate Cl(-) ions at the inner mouth of the CFTR pore, and that this contributes to maximization of the rate of Cl(-) ion permeation through the pore.

摘要

许多不同的离子通道孔被认为在其入口周围聚集有带电荷的氨基酸残基。这些残基所贡献的所谓表面电荷在从膜一侧的本体溶液中吸引带相反电荷的离子、增加有效局部抗衡离子浓度以及促进离子快速通过通道方面可能发挥重要作用。在这里,我们使用定点诱变来鉴定在囊性纤维化跨膜电导调节因子(CFTR)氯离子通道孔的细胞内口处贡献重要表面电荷的精氨酸残基。虽然野生型CFTR在对称溶液中与线性电流 - 电压关系相关,但在位于第五和第六跨膜区域细胞内末端附近的两个精氨酸残基(R303和R352)诱变后观察到强烈的外向整流。电流整流取决于这些位置存在的电荷,这与静电效应一致。此外,诱变诱导的整流在较低的氯离子浓度下更为明显,这表明这些突变体在内孔口附近浓缩氯离子的能力降低。R303和R352突变体表现出单通道电导降低,特别是在负膜电位下,这取决于这些位置存在的氨基酸残基的电荷。然而,通过提高细胞内氯离子浓度,R303E和R352E - CFTR两者非常低的电导都可以大大增加。用带电荷的甲硫基磺酸盐试剂修饰303位引入的半胱氨酸残基可重现对电流整流的电荷依赖性影响。第二和第十跨膜区域中精氨酸残基的诱变也改变了通道渗透特性,然而这些效应与通道表面电荷的变化不一致。这些结果表明带正电荷的精氨酸残基起到在CFTR孔的内口处浓缩氯离子的作用,并且这有助于使氯离子通过孔的渗透速率最大化。

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