Suppr超能文献

细菌钠离子通道 NavAb 晚期缓慢失活所需的门控电荷相互作用。

A gating charge interaction required for late slow inactivation of the bacterial sodium channel NavAb.

机构信息

Department of Pharmacology, University of Washington, Seattle, WA 98195, USA.

出版信息

J Gen Physiol. 2013 Sep;142(3):181-90. doi: 10.1085/jgp.201311012.

Abstract

Voltage-gated sodium channels undergo slow inactivation during repetitive depolarizations, which controls the frequency and duration of bursts of action potentials and prevents excitotoxic cell death. Although homotetrameric bacterial sodium channels lack the intracellular linker-connecting homologous domains III and IV that causes fast inactivation of eukaryotic sodium channels, they retain the molecular mechanism for slow inactivation. Here, we examine the functional properties and slow inactivation of the bacterial sodium channel NavAb expressed in insect cells under conditions used for structural studies. NavAb activates at very negative membrane potentials (V1/2 of approximately -98 mV), and it has both an early phase of slow inactivation that arises during single depolarizations and reverses rapidly, and a late use-dependent phase of slow inactivation that reverses very slowly. Mutation of Asn49 to Lys in the S2 segment in the extracellular negative cluster of the voltage sensor shifts the activation curve ∼75 mV to more positive potentials and abolishes the late phase of slow inactivation. The gating charge R3 interacts with Asn49 in the crystal structure of NavAb, and mutation of this residue to Cys causes a similar positive shift in the voltage dependence of activation and block of the late phase of slow inactivation as mutation N49K. Prolonged depolarizations that induce slow inactivation also cause hysteresis of gating charge movement, which results in a requirement for very negative membrane potentials to return gating charges to their resting state. Unexpectedly, the mutation N49K does not alter hysteresis of gating charge movement, even though it prevents the late phase of slow inactivation. Our results reveal an important molecular interaction between R3 in S4 and Asn49 in S2 that is crucial for voltage-dependent activation and for late slow inactivation of NavAb, and they introduce a NavAb mutant that enables detailed functional studies in parallel with structural analysis.

摘要

电压门控钠离子通道在重复去极化期间经历缓慢失活,这控制了动作电位爆发的频率和持续时间,并防止兴奋性细胞死亡。尽管同源四聚体细菌钠离子通道缺乏引起真核钠离子通道快速失活的细胞内连接同源域 III 和 IV,但它们保留了缓慢失活的分子机制。在这里,我们研究了在用于结构研究的条件下在昆虫细胞中表达的细菌钠离子通道 NavAb 的功能特性和缓慢失活。NavAb 在非常负的膜电位下激活(大约-98 mV 的 V1/2),并且具有在单个去极化期间产生并迅速逆转的早期缓慢失活相,以及缓慢失活的晚期使用依赖性相。在电压传感器的细胞外负簇中的 S2 片段中,将 Asn49 突变为 Lys 会将激活曲线向更正的电位移动约 75 mV,并消除晚期缓慢失活相。门控电荷 R3 与 NavAb 晶体结构中的 Asn49 相互作用,该残基突变为 Cys 会导致激活和晚期缓慢失活相阻断的电压依赖性发生类似的正移,就像 N49K 突变一样。诱导缓慢失活的延长去极化也会引起门控电荷移动的滞后,这导致需要非常负的膜电位才能将门控电荷恢复到其静息状态。出乎意料的是,N49K 突变不会改变门控电荷移动的滞后,即使它阻止了晚期缓慢失活相。我们的结果揭示了 S4 中的 R3 和 S2 中的 Asn49 之间的重要分子相互作用,这对于电压依赖性激活和 NavAb 的晚期缓慢失活至关重要,并且它们引入了一个 NavAb 突变体,该突变体能够与结构分析并行进行详细的功能研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/deb8/3753604/d1d728eb6780/JGP_201311012_Fig1.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验