ATP Release Channels
Department of Molecular Cell Physiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan
Int. J. Mol. Sci. 2018, 19(3), 808; https://doi.org/10.3390/ijms19030808
Received: 1 February 2018 / Revised: 28 February 2018 / Accepted: 9 March 2018 / Published: 11 March 2018
(This article belongs to the Special Issue Ion Transporters and Channels in Physiology and Pathophysiology)
Adenosine triphosphate (ATP) has been well established as an important extracellular ligand of autocrine signaling, intercellular communication, and neurotransmission with numerous physiological and pathophysiological roles. In addition to the classical exocytosis, non-vesicular mechanisms of cellular ATP release have been demonstrated in many cell types. Although large and negatively charged ATP molecules cannot diffuse across the lipid bilayer of the plasma membrane, conductive ATP release from the cytosol into the extracellular space is possible through ATP-permeable channels. Such channels must possess two minimum qualifications for ATP permeation: anion permeability and a large ion-conducting pore. Currently, five groups of channels are acknowledged as ATP-release channels: connexin hemichannels, pannexin 1, calcium homeostasis modulator 1 (CALHM1), volume-regulated anion channels (VRACs, also known as volume-sensitive outwardly rectifying (VSOR) anion channels), and maxi-anion channels (MACs). Recently, major breakthroughs have been made in the field by molecular identification of CALHM1 as the action potential-dependent ATP-release channel in taste bud cells, LRRC8s as components of VRACs, and SLCO2A1 as a core subunit of MACs. Here, the function and physiological roles of these five groups of ATP-release channels are summarized, along with a discussion on the future implications of understanding these channels.
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Keywords:
ATP; purinergic signaling; ion channel; connexin; pannexin; CALHM; VRAC; VSOR; maxi-anion channel
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MDPI and ACS Style
Taruno, A. ATP Release Channels. Int. J. Mol. Sci. 2018, 19, 808.
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