Suppr超能文献

CLC 通道的功能及其在健康和疾病中的异常。

CLC channel function and dysfunction in health and disease.

机构信息

Institute of Complex Systems-Zelluläre Biophysik (ICS-4), Forschungszentrum Jülich Jülich, Germany.

Institut für Neurophysiologie, Medizinische Hochschule Hannover Hannover, Germany.

出版信息

Front Physiol. 2014 Oct 7;5:378. doi: 10.3389/fphys.2014.00378. eCollection 2014.

Abstract

CLC channels and transporters are expressed in most tissues and fulfill diverse functions. There are four human CLC channels, ClC-1, ClC-2, ClC-Ka, and ClC-Kb, and five CLC transporters, ClC-3 through -7. Some of the CLC channels additionally associate with accessory subunits. Whereas barttin is mandatory for the functional expression of ClC-K, GlialCam is a facultative subunit of ClC-2 which modifies gating and thus increases the functional variability within the CLC family. Isoform-specific ion conduction and gating properties optimize distinct CLC channels for their cellular tasks. ClC-1 preferentially conducts at negative voltages, and the resulting inward rectification provides a large resting chloride conductance without interference with the muscle action potential. Exclusive opening at voltages negative to the chloride reversal potential allows for ClC-2 to regulate intracellular chloride concentrations. ClC-Ka and ClC-Kb are equally suited for inward and outward currents to support transcellular chloride fluxes. Every human CLC channel gene has been linked to a genetic disease, and studying these mutations has provided much information about the physiological roles and the molecular basis of CLC channel function. Mutations in the gene encoding ClC-1 cause myotonia congenita, a disease characterized by sarcolemmal hyperexcitability and muscle stiffness. Loss-of-function of ClC-Kb/barttin channels impairs NaCl resorption in the limb of Henle and causes hyponatriaemia, hypovolemia and hypotension in patients suffering from Bartter syndrome. Mutations in CLCN2 were found in patients with CNS disorders but the functional role of this isoform is still not understood. Recent links between ClC-1 and epilepsy and ClC-Ka and heart failure suggested novel cellular functions of these proteins. This review aims to survey the knowledge about physiological and pathophysiological functions of human CLC channels in the light of recent discoveries from biophysical, physiological, and genetic studies.

摘要

CLC 通道和转运蛋白在大多数组织中表达,具有多种功能。人类有四种 CLC 通道,CLC-1、CLC-2、CLC-Ka 和 CLC-Kb,还有五种 CLC 转运蛋白,CLC-3 到 -7。一些 CLC 通道还与辅助亚基结合。巴特氏蛋白是 CLC-K 功能性表达所必需的,而胶质钙黏蛋白是 CLC-2 的可选亚基,它调节门控,从而增加 CLC 家族的功能变异性。同种型特异性离子传导和门控特性使不同的 CLC 通道能够优化其细胞任务。CLC-1 优先在负电压下传导,由此产生的内向整流为氯离子提供了较大的静息电导,而不会干扰肌肉动作电位。CLC-2 仅在氯离子反转电位负值的电压下打开,从而能够调节细胞内氯离子浓度。CLC-Ka 和 CLC-Kb 同样适合内向和外向电流,以支持跨细胞氯离子通量。人类每一种 CLC 通道基因都与一种遗传性疾病有关,对这些突变的研究提供了许多关于 CLC 通道功能的生理作用和分子基础的信息。CLC-1 基因的突变导致先天性肌强直症,其特征是肌细胞膜过度兴奋和肌肉僵硬。CLC-Kb/barttin 通道的功能丧失会损害 Henle 肢段中 NaCl 的重吸收,导致 Bartter 综合征患者低血钠、低血容量和低血压。CLCN2 基因突变见于中枢神经系统疾病患者,但该同工型的功能作用仍不清楚。最近发现 CLC-1 与癫痫有关,CLC-Ka 与心力衰竭有关,这表明这些蛋白具有新的细胞功能。本综述旨在根据生物物理、生理和遗传研究的最新发现,综述人类 CLC 通道的生理和病理生理功能的知识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c242/4188032/891ecff84291/fphys-05-00378-g0001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验