Regulatory Mechanisms of Ca2+-activated Ion Channels and Their Impacts on Physiological/Pathophysiological Functions

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Background

Ca2+ influx through Ca2+ channels localized in the plasma membrane and organelle membrane is involved in robust physiological reactions as a second messenger. In excitable cells such as neurons and myocytes, voltage dependent Ca2+ channels propagate electrical signals by forming action potentials and at the same time initiate Ca2+ signaling. On the other hand, in non-excitable cells such as immune cells and chondrocytes, voltage independent Ca2+ channels such as TRP channels and Ca2+ release-activated Ca2+ channels are responsible for Ca2+ signaling. Ca2+ influx through these Ca2+ channels is critically regulated by Ca2+-activated K+ (KCa) channels: membrane hyperpolarization due to the activation of KCa channels suppresses Ca2+ influx in excitable cells but promotes it in non-excitable cells. KCa channels are classified into three subtypes: BK, IK, and SK channels. KCa channels are often localized near Ca2+ channels in the cell membrane or organelle membrane and form Ca2+ microdomains because of rapid removal of free Ca2+ from cytosol. This enables KCa channels to be efficiently activated at physiological membrane potential, convert local Ca2+ signals into electrical signals, and modulate Ca2+ channel activity as feedback mechanisms. As for BK channel, its activity, e.g. voltage dependence, Ca2+ sensitivity and drug sensitivity, and intracellular localization are largely modified by (i) accessory subunits such as β and γ subunits and (ii) alternative splicing. Thus, BK channel can acquire tissue specificity. Furthermore, BK channel activity is also modulated by kinases/phosphatases, reactive oxygen species, and endogenous ligands. In addition to KCa channels, Ca2+-activated Cl- channels such as TMEM16A are also involved in the conversion of Ca2+ into electrical signals. Ryanodine receptors amplify an increase in intracellular Ca2+ concentration by means of Ca2+-induced Ca2+ release and cause membrane hyperpolarization via activation of KCa channels. Various kinds of Ca2+-activated ion channels construct complicated network and finely control membrane potential, intracellular Ca2+ signaling and thus physiological responses.

This topic focuses on novel mechanisms that control KCa channel functions and their outputs as physiological or pathophysiological responses at molecular, organellar, cellular, tissue, and whole body-levels. Especially, it appears crucial to collect more information on protein-protein interaction as well as functional coupling via Ca2+ that characterize KCa channel functions in each tissue. The goal of this Research Topic is to build the latest platform of knowledge on KCa channels and other Ca2+-activated ion channels and contribute to the further progress of this research area. 

Scope of this Research Topic may include (but is not limited to) (i) regulatory mechanisms that modulate gene/protein levels, intracellular localization and functions of KCa channels by alternative splicing, accessory subunits, protein-protein interactions with cellular components such as Ca2+ channels and scaffold proteins, (ii) physiological impact of KCa channels based on above mechanisms, and (iii) roles of KCa channels in intracellular organelles such as mitochondria, lysosome and nucleus. Original research and review article submissions are welcome in this Research Topic. Articles regarding other Ca2+-activated ion channels are also acceptable.

Keywords: KCa channel, BK channel, IK channel, SK channel, Ca2+ signaling

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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