Abstract
Ion channels are essential for basic cellular function and for processes including sensory perception and intercellular communication in multicellular organisms. Voltage-gated potassium (Kv) channels facilitate dynamic cellular repolarization during an action potential, opening in response to membrane depolarization to facilitate K+efflux. In both excitable and nonexcitable cells other, constitutively active, K+channels provide a relatively constant repolarizing force to control membrane potential, ion homeostasis, and secretory processes. Of the forty known human Kv channel pore-formingαsubunits that coassemble in various combinations to form the fundamental tetrameric channel pore and voltage sensor module, KCNQ1 is unique. KCNQ1 stands alone in having the capacity to form either channels that are voltage-dependent and require membrane depolarization for activation, or constitutively active channels. In mammals, KCNQ1 regulates processes including gastric acid secretion, thyroid hormone biosynthesis, salt and glucose homeostasis, and cell volume and in some species is required for rhythmic beating of the heart. In this review, the author discusses the unique functional properties, regulation, cell biology, diverse physiological roles, and involvement in human disease states of this chameleonic K+channel.
Highlights
Ion channels facilitate the transmembrane movement of aqueous ions across lipid bilayers and down an electrochemical gradient at rates that can approach the diffusion limit
We discovered that the molecular basis for this is that KCNQ1-KCNE2 is expressed in the basolateral membrane of thyrocytes and is required for normal production of thyroid hormone by the thyroid gland (Figure 5(b)) [140]
Following the original MDCK study of KCNE-KCNQ1 targeting [234], we examined the influence of Kcne2 and Kcne3 on Kcnq1 localization in parietal cells using singleand double-knockout mice [141]
Summary
Ion channels facilitate the transmembrane movement of aqueous ions across lipid bilayers and down an electrochemical gradient at rates that can approach the diffusion limit. Voltage-gated ion channels share a defining feature—a voltage sensor module or paddle that contains at its heart a transmembrane helix (segment 4 or S4) with periodic basic residues [8]. These basic residues “sense” membrane potential by moving across the membrane electric field in response to membrane potential changes (Figures 1(c)–1(e)). Kir (and potentially K2P) channels contribute to correcting the hyperpolarization that occurs, for example, between cardiac myocyte action potentials by allowing K+ influx at voltages negative to EK Kir variants such as the KATP channels couple membrane potential to cellular metabolic state [46]
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