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1

Voronina, Y. A., A. M. Karhov, and V. S. Kuzmin. "Chloride channels and transporters – role in the electrical activity of pacemaker and working myocardium." Uspehi fiziologičeskih nauk 55, no. 4 (2024): 75–90. https://doi.org/10.31857/s0301179824040041.

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Chlorine anions have a significant influence on the electrophysiological properties of excitable tissues, including myocardium. Chlorine anions and transmembrane chloride currents (ICl) determine the configuration of action potentials (AP) in various regions of hearts. Disruption of transmembrane chloride transport leads to alterations in normal electrical activity, resulting in cardiac pathologies and arrhythmias. Currently, chloride conductivity and expression in the heart and a functional role have been confirmed for several types of macromolecules. These channels include CFTR, ClC-2, CaCC
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2

Lísal, Jiří, and Merritt Maduke. "Proton-coupled gating in chloride channels." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1514 (2008): 181–87. http://dx.doi.org/10.1098/rstb.2008.0123.

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The physiologically indispensable chloride channel (CLC) family is split into two classes of membrane proteins: chloride channels and chloride/proton antiporters. In this article we focus on the relationship between these two groups and specifically review the role of protons in chloride-channel gating. Moreover, we discuss the evidence for proton transport through the chloride channels and explore the possible pathways that the protons could take through the chloride channels. We present results of a mutagenesis study, suggesting the feasibility of one of the pathways, which is closely relate
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3

Kim, Hyeong Jae, Peter Chang-Whan Lee, and Jeong Hee Hong. "Chloride Channels and Transporters: Roles beyond Classical Cellular Homeostatic pH or Ion Balance in Cancers." Cancers 14, no. 4 (2022): 856. http://dx.doi.org/10.3390/cancers14040856.

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The canonical roles of chloride channels and chloride-associated transporters have been physiologically determined; these roles include the maintenance of membrane potential, pH balance, and volume regulation and subsequent cellular functions such as autophagy and cellular proliferative processes. However, chloride channels/transporters also play other roles, beyond these classical function, in cancerous tissues and under specific conditions. Here, we focused on the chloride channel-associated cancers and present recent advances in understanding the environments of various types of cancer caus
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4

Jentsch, Thomas J. "Chloride channels." Current Opinion in Neurobiology 3, no. 3 (1993): 316–21. http://dx.doi.org/10.1016/0959-4388(93)90123-g.

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5

Duan, Dayue Darrel. "Phenomics of Cardiac Chloride Channels." Comprehensive Physiology 3, no. 2 (2013): 667–92. https://doi.org/10.1002/j.2040-4603.2013.tb00499.x.

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AbstractForward genetic studies have identified several chloride (Cl−) channel genes, including CFTR, ClC‐2, ClC‐3, CLCA, Bestrophin, and Ano1, in the heart. Recent reverse genetic studies using gene targeting and transgenic techniques to delineate the functional role of cardiac Cl− channels have shown that Cl− channels may contribute to cardiac arrhythmogenesis, myocardial hypertrophy and heart failure, and cardioprotection against ischemia reperfusion. The study of physiological or pathophysiological phenotypes of cardiac Cl− channels, however, is complicated by the compensatory changes in t
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6

Kicińska, A., G. D bska, W. Kunz, and A. Szewczyk. "Mitochondrial potassium and chloride channels." Acta Biochimica Polonica 47, no. 3 (2000): 541–51. http://dx.doi.org/10.18388/abp.2000_3977.

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Channels selective for potassium or chloride ions are present in inner mitochondrial membranes. They probably play an important role in mitochondrial events such as the formation of delta pH and regulation of mitochondrial volume changes. Mitochondrial potassium and chloride channels could also be the targets for pharmacologically active compounds such as potassium channel openers and antidiabetic sulfonylureas. This review describes the properties, pharmacology, and current observations concerning the functional role of mitochondrial potassium and chloride channels.
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7

Duszyk, Marek, Andrew S. French, and S. F. Paul Man. "Cystic fibrosis affects chloride and sodium channels in human airway epithelia." Canadian Journal of Physiology and Pharmacology 67, no. 10 (1989): 1362–65. http://dx.doi.org/10.1139/y89-217.

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Abnormalities of epithelial function in cystic fibrosis (CF) have been linked to defects in cell membrane permeability to chloride or sodium ions. Recently, a class of chloride channels in airway epithelial cells have been reported to lack their usual sensitivity to phosphorylation via cAMP-dependent protein kinase, suggesting that CF could be due to a single genetic defect in these channels. We have examined single chloride and sodium channels in control and CF human nasal epithelia using the patch-clamp technique. The most common chloride channel was not the one previously associated with CF
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8

Uchida, Shinichi. "In vivo role of CLC chloride channels in the kidney." American Journal of Physiology-Renal Physiology 279, no. 5 (2000): F802—F808. http://dx.doi.org/10.1152/ajprenal.2000.279.5.f802.

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Chloride channels in the kidney are involved in important physiological functions such as cell volume regulation, acidification of intracellular vesicles, and transepithelial chloride transport. Among eight mammalian CLC chloride channels expressed in the kidney, three (CLC-K1, CLC-K2, and CLC-5) were identified to be related to kidney diseases in humans or mice. CLC-K1 mediates a transepithelial chloride transport in the thin ascending limb of Henle's loop and is essential for urinary concentrating mechanisms. CLC-K2 is a basolateral chloride channel in distal nephron segments and is necessar
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9

Wilczyński, Bartosz, Alicja Dąbrowska, Jolanta Saczko, and Julita Kulbacka. "The Role of Chloride Channels in the Multidrug Resistance." Membranes 12, no. 1 (2021): 38. http://dx.doi.org/10.3390/membranes12010038.

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Nowadays, one of medicine’s main and most challenging aims is finding effective ways to treat cancer. Unfortunately, although there are numerous anti-cancerous drugs, such as cisplatin, more and more cancerous cells create drug resistance. Thus, it is equally important to find new medicines and research the drug resistance phenomenon and possibilities to avoid this mechanism. Ion channels, including chloride channels, play an important role in the drug resistance phenomenon. Our article focuses on the chloride channels, especially the volume-regulated channels (VRAC) and CLC chloride channels
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10

Zhao, Piao, Cheng Tang, Yuqin Yang, et al. "A new polymodal gating model of the proton-activated chloride channel." PLOS Biology 21, no. 9 (2023): e3002309. http://dx.doi.org/10.1371/journal.pbio.3002309.

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The proton–activated chloride (PAC) channel plays critical roles in ischemic neuron death, but its activation mechanisms remain elusive. Here, we investigated the gating of PAC channels using its novel bifunctional modulator C77304. C77304 acted as a weak activator of the PAC channel, causing moderate activation by acting on its proton gating. However, at higher concentrations, C77304 acted as a weak inhibitor, suppressing channel activity. This dual function was achieved by interacting with 2 modulatory sites of the channel, each with different affinities and dependencies on the channel’s sta
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11

Fahlke, Christoph, Timothy Knittle, Christina A. Gurnett, Kevin P. Campbell, and Alfred L. George. "Subunit Stoichiometry of Human Muscle Chloride Channels." Journal of General Physiology 109, no. 1 (1997): 93–104. http://dx.doi.org/10.1085/jgp.109.1.93.

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Voltage-gated Cl− channels belonging to the ClC family appear to function as homomultimers, but the number of subunits needed to form a functional channel is controversial. To determine subunit stoichiometry, we constructed dimeric human skeletal muscle Cl− channels in which one subunit was tagged by a mutation (D136G) that causes profound changes in voltage-dependent gating. Sucrose-density gradient centrifugation experiments indicate that both monomeric and dimeric hClC-1 channels in their native configurations exhibit similar sedimentation properties consistent with a multimeric complex hav
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12

Gabriel, S. E., E. M. Price, R. C. Boucher, and M. J. Stutts. "Small linear chloride channels are endogenous to nonepithelial cells." American Journal of Physiology-Cell Physiology 263, no. 3 (1992): C708—C713. http://dx.doi.org/10.1152/ajpcell.1992.263.3.c708.

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We used both single-channel and whole cell patch-clamp techniques to characterize chloride channels and currents endogenous to Sf9 cells, 3T3 fibroblasts, and Chinese hamster ovary cells. In cell-attached patches from these cell types, anion channels were observed with low ohmic conductance (4-11 ps), linear current-voltage relationships, and little time- or voltage-dependent behavior. These channels are very similar to the Cl- channels reported to appear concomitant with the expression of cystic fibrosis transmembrane conductance regulator (CFTR) in these cell lines. The presence of such endo
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13

Fahlke, Christoph. "Ion permeation and selectivity in ClC-type chloride channels." American Journal of Physiology-Renal Physiology 280, no. 5 (2001): F748—F757. http://dx.doi.org/10.1152/ajprenal.2001.280.5.f748.

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Voltage-gated anion channels are present in almost every living cell and have many physiological functions. Recently, a novel gene family encoding voltage-gated chloride channels, the ClC family, was identified. The knowledge of primary amino acid sequences has allowed for the study of these anion channels in heterologous expression systems and made possible the combination of site-directed mutagenesis and high-resolution electrophysiological measurements as a means of gaining insights into the molecular basis of channel function. This review focuses on one particular aspect of chloride channe
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14

Debska, G., A. Kicińska, J. Skalska, and A. Szewczyk. "Intracellular potassium and chloride channels: an update." Acta Biochimica Polonica 48, no. 1 (2001): 137–44. http://dx.doi.org/10.18388/abp.2001_5120.

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Channels selective for potassium or chloride ions are present in all intracellular membranes such as mitochondrial membranes, sarcoplasmic/endoplasmic reticulum, nuclear membrane and chromaffin granule membranes. They probably play an important role in events such as acidification of intracellular compartments and regulation of organelle volume. Additionally, intracellular ion channels are targets for pharmacologically active compounds, e.g. mitochondrial potassium channels interact with potassium channel openers such as diazoxide. This review describes current observations concerning the prop
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15

Higgins, Chris. "Chloride channels revisited." Nature 358, no. 6387 (1992): 536. http://dx.doi.org/10.1038/358536a0.

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16

Vinson, V. "Controlling Chloride Channels." Science Signaling 3, no. 146 (2010): ec338-ec338. http://dx.doi.org/10.1126/scisignal.3146ec338.

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17

Bretag, A. H. "Muscle chloride channels." Physiological Reviews 67, no. 2 (1987): 618–724. http://dx.doi.org/10.1152/physrev.1987.67.2.618.

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18

Ackerman, Michael J., and David E. Clapham. "Cardiac chloride channels." Trends in Cardiovascular Medicine 3, no. 1 (1993): 23–28. http://dx.doi.org/10.1016/1050-1738(93)90024-z.

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19

Darvish, N., J. Winaver, and D. Dagan. "Diverse modulations of chloride channels in renal proximal tubules." American Journal of Physiology-Renal Physiology 267, no. 5 (1994): F716—F724. http://dx.doi.org/10.1152/ajprenal.1994.267.5.f716.

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Cl- selective channels were detected and characterized in apical membranes of cultured rat renal proximal convoluted tubule cells (PCT) using patch-clamping methods. Subpopulations of Cl- channels modulated by cyclic nucleotides, Ca2+, or voltage were identified. Two different 30-pS, voltage-independent, Cl- channels modulated by adenosine 3',5'-cyclic monophosphate (cAMP) or Ca2+ were seen most frequently. The cAMP-dependent channel was activated by membrane-permeable analogues of cAMP, dibutyryl-cAMP or 8-bromo-cAMP. Catalytic subunit of protein kinase A (PKA) applied to detached inside-out
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20

Thompson, Gregory W., Magda Horackova, and J. Andrew Armour. "Ion channel modifying agents influence the electrical activity generated by canine intrinsic cardiac neurons in situ." Canadian Journal of Physiology and Pharmacology 78, no. 4 (2000): 293–300. http://dx.doi.org/10.1139/y99-138.

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This study was designed to establish whether agents known to modify neuronal ion channels influence the behavior of mammalian intrinsic cardiac neurons in situ and, if so, in a manner consistent with that found previously in vitro. The activity generated by right atrial neurons was recorded extracellularly in varying numbers of anesthetized dogs before and during continuous local arterial infusion of several neuronal ion channel modifying agents. Veratridine (7.5 µM), the specific modifier of Na+-selective channels, increased neuronal activity (95% above control) in 80% of dogs tested (n = 25)
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21

al-Awqati, Q., J. Barasch, and D. Landry. "Chloride channels of intracellular organelles and their potential role in cystic fibrosis." Journal of Experimental Biology 172, no. 1 (1992): 245–66. http://dx.doi.org/10.1242/jeb.172.1.245.

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Chloride channels were previously purified from bovine kidney cortex membranes using a drug affinity column. Reconstitution of the purified proteins into artificial liposomes and planar bilayers yielded chloride channels. A 64 x 10(3) M(r) protein, p64, identified as a component of this chloride channel, was used to generate antibodies which depleted solubilized kidney membranes of all chloride channel activity. This antibody has now been used to identify a clone, H2B, from a kidney cDNA library. Antibodies, affinity-purified against the fusion protein of H2B, from a kidney cDNA library. Antib
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22

Hussy, N. "Calcium-activated chloride channels in cultured embryonic Xenopus spinal neurons." Journal of Neurophysiology 68, no. 6 (1992): 2042–50. http://dx.doi.org/10.1152/jn.1992.68.6.2042.

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1. Single-channel currents were recorded from Xenopus spinal neurons developing in vitro using the patch-clamp technique, to identify the channels underlying the large and small macroscopic Ca(2+)-activated Cl- currents (ICl(Ca)) present in these cells. 2. Channels of large (maxi-channels; 310 pS) and smaller conductance (mini-channels; 50-60 pS) are activated by elevation of cytoplasmic Ca2+ concentration. Channel activity is not altered by subsequent removal of Ca2+ from the bath, arguing against a direct ligand-type Ca2+ dependence. The much higher incidence of channel activation in cell-at
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23

Schwiebert, E. M., T. Flotte, G. R. Cutting, and W. B. Guggino. "Both CFTR and outwardly rectifying chloride channels contribute to cAMP-stimulated whole cell chloride currents." American Journal of Physiology-Cell Physiology 266, no. 5 (1994): C1464—C1477. http://dx.doi.org/10.1152/ajpcell.1994.266.5.c1464.

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From whole cell patch-clamp recordings at 35 degrees C utilizing either nystatin perforation or conventional methods with 5 mM MgATP in the pipette solution, it was demonstrated that both cystic fibrosis transmembrane conductance regulator (CFTR) chloride (Cl-) channels and outwardly rectifying Cl- channels (ORCC) contribute to adenosine 3',5'-cyclic monophosphate (cAMP)-activated whole cell Cl- currents in cultured human airway epithelial cells. These results were similar whether recordings were performed on two normal human cell lines or on two cystic fibrosis (CF) cell lines stably compleme
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24

Kulawiak, Bogusz, and Piotr Bednarczyk. "Reconstitution of brain mitochondria inner membrane into planar lipid bilayer." Acta Neurobiologiae Experimentalis 65, no. 3 (2005): 271–76. http://dx.doi.org/10.55782/ane-2005-1562.

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Ion channels are present in the inner mitochondrial membrane. They play an important role in cellular processes. Potassium and chloride channels are involved in regulation of mitochondrial volume, membrane potential and acidification. The mitochondrial potassium channels have been suggested as triggers and end effectors in cytoprotection. In our study we measured single channel activities after reconstitution of submitochondrial particles from rat brain mitochondria into planar lipid membranes. After incorporation, two different potassium selective currents were recorded with single channel co
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25

Gray, R., and D. Johnston. "Rectification of single GABA-gated chloride channels in adult hippocampal neurons." Journal of Neurophysiology 54, no. 1 (1985): 134–42. http://dx.doi.org/10.1152/jn.1985.54.1.134.

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The properties of single chloride channels activated by gamma-aminobutyric acid (GABA) were investigated with hippocampal slices from adult guinea pigs. After the slices were treated with proteolytic enzymes, gigaseal recordings were made from excised patches of pyramidal or granule cell membranes. This newly developed preparation permits the application of patch-clamp techniques to the adult mammalian central nervous system. Guinea pig hippocampal slices were prepared in a conventional manner. Once prepared, the slices were treated with two different enzymes for brief periods and gently agita
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26

Gulbins, E., A. Jekle, K. Ferlinz, H. Grassmé, and F. Lang. "Physiology of apoptosis." American Journal of Physiology-Renal Physiology 279, no. 4 (2000): F605—F615. http://dx.doi.org/10.1152/ajprenal.2000.279.4.f605.

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Ion fluxes and volume changes of the whole cell as well as of organelles belong to the hallmarks of apoptosis; however, the molecular mechanism regulating these changes is only poorly characterized. Several ion channels in the plasma membrane, in particular the N-type K+channel, the chloride channel cystic fibrosis conductance regulator, and an outward rectifying chloride channel, as well as the mitochondrial permeability transition pore, have been implicated to be involved in signal transduction cascades regulating apoptosis. Furthermore, Bcl-2-like proteins have been suggested to function, a
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27

Wang, Wei, Claudia Oliva, Ge Li, Arne Holmgren, Christopher Horst Lillig, and Kevin L. Kirk. "Reversible Silencing of CFTR Chloride Channels by Glutathionylation." Journal of General Physiology 125, no. 2 (2005): 127–41. http://dx.doi.org/10.1085/jgp.200409115.

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The cystic fibrosis transmembrane conductance regulator (CFTR) is a phosphorylation- and ATP-dependent chloride channel that modulates salt and water transport across lung and gut epithelia. The relationship between CFTR and oxidized forms of glutathione is of potential interest because reactive glutathione species are produced in inflamed epithelia where they may be modulators or substrates of CFTR. Here we show that CFTR channel activity in excised membrane patches is markedly inhibited by several oxidized forms of glutathione (i.e., GSSG, GSNO, and glutathione treated with diamide, a strong
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28

THORESON, WALLACE B., RON NITZAN, and ROBERT F. MILLER. "Chloride efflux inhibits single calcium channel open probability in vertebrate photoreceptors: Chloride imaging and cell-attached patch-clamp recordings." Visual Neuroscience 17, no. 2 (2000): 197–206. http://dx.doi.org/10.1017/s0952523800172025.

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The present study uses cell-attached patch-recording techniques to study the single-channel properties of Ca2+ channels in isolated salamander photoreceptors and investigate their sensitivity to reductions in intracellular Cl−. The results show that photoreceptor Ca2+ channels possess properties similar to L-type Ca2+ channels in other preparations, including (1) enhancement of openings by the dihydropyridine agonist, (−)BayK8644; (2) suppression by a dihydropyridine antagonist, nisoldipine; (3) single-channel conductance of 22 pS with 82 mM Ba2+ as the charge carrier; (4) mean open probabilit
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29

Elorza-Vidal, Xabier, Héctor Gaitán-Peñas, and Raúl Estévez. "Chloride Channels in Astrocytes: Structure, Roles in Brain Homeostasis and Implications in Disease." International Journal of Molecular Sciences 20, no. 5 (2019): 1034. http://dx.doi.org/10.3390/ijms20051034.

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Astrocytes are the most abundant cell type in the CNS (central nervous system). They exert multiple functions during development and in the adult CNS that are essential for brain homeostasis. Both cation and anion channel activities have been identified in astrocytes and it is believed that they play key roles in astrocyte function. Whereas the proteins and the physiological roles assigned to cation channels are becoming very clear, the study of astrocytic chloride channels is in its early stages. In recent years, we have moved from the identification of chloride channel activities present in
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30

Berndt, Andre, Soo Yeun Lee, Jonas Wietek, et al. "Structural foundations of optogenetics: Determinants of channelrhodopsin ion selectivity." Proceedings of the National Academy of Sciences 113, no. 4 (2015): 822–29. http://dx.doi.org/10.1073/pnas.1523341113.

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The structure-guided design of chloride-conducting channelrhodopsins has illuminated mechanisms underlying ion selectivity of this remarkable family of light-activated ion channels. The first generation of chloride-conducting channelrhodopsins, guided in part by development of a structure-informed electrostatic model for pore selectivity, included both the introduction of amino acids with positively charged side chains into the ion conduction pathway and the removal of residues hypothesized to support negatively charged binding sites for cations. Engineered channels indeed became chloride sele
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31

Wang, Liwei, Wenbo Ma, Linyan Zhu, et al. "ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells." American Journal of Physiology-Cell Physiology 303, no. 1 (2012): C14—C23. http://dx.doi.org/10.1152/ajpcell.00145.2011.

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Acid-activated chloride currents have been reported in several cell types and may play important roles in regulation of cell function. However, the molecular identities of the channels that mediate the currents are not defined. In this study, activation of the acid-induced chloride current and the possible candidates of the acid-activated chloride channel were investigated in human nasopharyngeal carcinoma cells (CNE-2Z). A chloride current was activated when extracellular pH was reduced to 6.6 from 7.4. However, a further decrease of extracellular pH to 5.8 inhibited the current. The current
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32

Vaisey, George, Alexandria N. Miller, and Stephen B. Long. "Distinct regions that control ion selectivity and calcium-dependent activation in the bestrophin ion channel." Proceedings of the National Academy of Sciences 113, no. 47 (2016): E7399—E7408. http://dx.doi.org/10.1073/pnas.1614688113.

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Cytoplasmic calcium (Ca2+) activates the bestrophin anion channel, allowing chloride ions to flow down their electrochemical gradient. Mutations in bestrophin 1 (BEST1) cause macular degenerative disorders. Previously, we determined an X-ray structure of chicken BEST1 that revealed the architecture of the channel. Here, we present electrophysiological studies of purified wild-type and mutant BEST1 channels and an X-ray structure of a Ca2+-independent mutant. From these experiments, we identify regions of BEST1 responsible for Ca2+ activation and ion selectivity. A “Ca2+ clasp” within the chann
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33

Tsai, L. M., M. Dillard, R. L. Rosenberg, R. J. Falk, M. L. Gaido, and A. L. Finn. "Reconstitution of an epithelial chloride channel. Conservation of the channel from mudpuppy to man." Journal of General Physiology 98, no. 4 (1991): 723–50. http://dx.doi.org/10.1085/jgp.98.4.723.

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We have previously shown that monoclonal antibody E12 (MAb E12), one of several such antibodies raised against theophylline-treated Necturus gallbladder (NGB) epithelial cells, inhibits the chloride conductance in the apical membrane of that tissue. Since chloride channels are critical to the secretory function of epithelia in many different animals, we have used this antibody to determine whether the channels are conserved, and in an immunoaffinity column to isolate the channel protein. We now demonstrate that MAb E12 cross-reacts with detergent-solubilized extracts of different tissues from
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34

Kolesnikov, D. O., E. R. Grigorieva, M. A. Nomerovskaya, D. S. Reshetin, A. V. Shalygin, and E. V. Kaznacheyeva. "The Mechanism of Calcium-Activated Chloride ANO6 Channel Inhibition by CaCCinh-A01." Биологические мембраны Журнал мембранной и клеточной биологии 41, no. 2 (2024): 133–38. http://dx.doi.org/10.31857/s0233475524020046.

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Proteins of the anoctamine family (ANO) form calcium-activated chloride channels (CaCC) and phospholilpid scramblases. The ANO6 (TMEM16F) protein, which combines the functions of a calcium-dependent scramblase and those of an ion channel, is considered as a molecular target for the treatment of blood clotting disorders, COVID-19-associated pneumonia, neurodegenerative diseases, and other pathologies. CaCCinh-A01, which is a channel blocker of the ANO family, is studied as a potential pharmacological drug. Previously, the effect of this inhibitor was studied using methods representing the integ
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35

Sonnhof, U. "Single voltage-dependent K+ and Cl− channels in cultured rat astrocytes." Canadian Journal of Physiology and Pharmacology 65, no. 5 (1987): 1043–50. http://dx.doi.org/10.1139/y87-165.

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The kinetic reactions of a voltage-dependent K+ channel, which constituted about 14% of all the recorded K+ channels in the membrane of cultured rat astrocytes were studied in detail. A scheme of one open and three closed states is necessary to describe the kinetic reactions of this channel. The channel contributes little to the resting membrane potential. Its steady state open probability (Po) is 0.06 at −70 mV. When the cell is depolarized to 0 mV, Po approaches 1. This represents a 17-fold increase. Such channels could contribute to the potassium clearance by enhancing the effect of "spatia
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36

Hao, Feng, Zhong Hai Yuan, Zhi Xin Wang, et al. "Plasmid Construction of TMEM16A-pcDNA3.1 and its Application to Transient and Stable Transfection of FRT Cells." Advanced Materials Research 554-556 (July 2012): 1734–37. http://dx.doi.org/10.4028/www.scientific.net/amr.554-556.1734.

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Calcium-activated chloride channels (CaCCs) play pivotal roles in many physiological Activities, including transepithelial fluid secretion, smooth muscle contraction and sensory transduction. TMEM16A is a bona fide calcium-activated chloride channel,which was discovered by three independent labs in 2008 after Calcium-activated chloride channel current was recorded about thirty years ago. In this study, DNA fragments encoding mouse TMEM16A with green fluorescence protein (GFP) fusion protein were subcloned into pcDNA3.1/Zeo. Transient transfection condition was optimized and Fischer Thyroid epi
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37

Lidofsky, Steven D., and Richard M. Roman. "Alanine uptake activates hepatocellular chloride channels." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 4 (1997): G849—G853. http://dx.doi.org/10.1152/ajpgi.1997.273.4.g849.

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Cells involved in the retrieval and metabolic conversion of amino acids undergo significant increases in size in response to amino acid uptake. The resultant adaptive responses to cell swelling are thought to include increases in membrane K+ and Cl− permeability through activation of volume-sensitive ion channels. This viewpoint is largely based on experimental models of hypotonic swelling, but few mammalian cells experience hypotonic challenge in vivo. Here we have examined volume regulatory responses in a physiological model of cell-swelling alanine uptake in immortalized hepatocytes. Alanin
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38

Clancy, J. P., J. D. McCann, M. Li, and M. J. Welsh. "Calcium-dependent regulation of airway epithelial chloride channels." American Journal of Physiology-Lung Cellular and Molecular Physiology 258, no. 2 (1990): L25—L32. http://dx.doi.org/10.1152/ajplung.1990.258.2.l25.

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To determine how cell calcium ([Ca2+]c) regulates apical Cl- channels, we measured the rate of 125-Iodide (125I-) efflux to assay Cl- channel activity in intact cells and examined cell-free membrane patches from cultured canine tracheal epithelial cells. The Ca2+ elevating agonist bradykinin and the calcium ionophore A23187 increased 125I- efflux. This response did not require prostaglandin production. Under several conditions, changes in [Ca2+]c were temporally dissociated from changes in channel activation: a transient increase in [Ca2+]c caused a prolonged stimulation of 125I- efflux. Neith
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39

Thakker, Rajesh V. "Chloride channels cough up." Nature Genetics 17, no. 2 (1997): 125–27. http://dx.doi.org/10.1038/ng1097-125.

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40

Hebert, Steven C. "Crystal-clear chloride channels." Nature 379, no. 6564 (1996): 398–99. http://dx.doi.org/10.1038/379398a0.

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41

Jentsch, Thomas J. "Chloride channels are different." Nature 415, no. 6869 (2002): 276–77. http://dx.doi.org/10.1038/415276a.

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42

Zhang, Ya-ping, Hao Zhang, and Dayue Darrel Duan. "Chloride channels in stroke." Acta Pharmacologica Sinica 34, no. 1 (2012): 17–23. http://dx.doi.org/10.1038/aps.2012.140.

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43

Gögelein, Heinz. "Chloride channels in epithelia." Biochimica et Biophysica Acta (BBA) - Reviews on Biomembranes 947, no. 3 (1988): 521–47. http://dx.doi.org/10.1016/0304-4157(88)90006-8.

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44

Reeves, W. Brian, and Thomas E. Androli. "Renal Epithelial Chloride Channels." Annual Review of Physiology 54, no. 1 (1992): 29–50. http://dx.doi.org/10.1146/annurev.ph.54.030192.000333.

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45

Hartzell, Criss, Ilva Putzier, and Jorge Arreola. "CALCIUM-ACTIVATED CHLORIDE CHANNELS." Annual Review of Physiology 67, no. 1 (2005): 719–58. http://dx.doi.org/10.1146/annurev.physiol.67.032003.154341.

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46

Wolstenholme, Adrian J. "Glutamate-gated Chloride Channels." Journal of Biological Chemistry 287, no. 48 (2012): 40232–38. http://dx.doi.org/10.1074/jbc.r112.406280.

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47

WALDEGGER, SIEGFRIED, and THOMAS J. JENTSCH. "From Tonus to Tonicity." Journal of the American Society of Nephrology 11, no. 7 (2000): 1331–39. http://dx.doi.org/10.1681/asn.v1171331.

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Abstract. Chloride channels are involved in a multitude of physiologic processes ranging from basal cellular functions such as cell volume regulation and acidification of intracellular vesicles to more specialized mechanisms such as vectorial transepithelial transport and regulation of cellular excitability. This plethora of functions is accomplished by numerous functionally highly diverse chloride channels that are only partially identified at the molecular level. The CLC family of chloride channels comprises at present nine members in mammals that differ with respect to biophysical propertie
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48

BUYSE, Gunnar, Dominique TROUET, Thomas VOETS, et al. "Evidence for the intracellular location of chloride channel (ClC)-type proteins: co-localization of ClC-6a and ClC-6c with the sarco/endoplasmic-reticulum Ca2+ pump SERCA2b." Biochemical Journal 330, no. 2 (1998): 1015–21. http://dx.doi.org/10.1042/bj3301015.

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Chloride channel protein (ClC)-6a and ClC-6c, a kidney-specific splice variant with a truncated C-terminus, are proteins that belong structurally to the family of voltage-dependent chloride channels. Attempts to characterize functionally ClC-6a or ClC-6c in Xenopus oocytes have so far been negative. Similarly, expression of both ClC-6 isoforms in mammalian cells failed to provide functional information. One possible explanation of these negative results is that ClC-6 is an intracellular chloride channel rather than being located in the plasma membrane. We therefore studied the subcellular loca
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49

Schultz, B. D., A. D. DeRoos, C. J. Venglarik, A. K. Singh, R. A. Frizzell, and R. J. Bridges. "Glibenclamide blockade of CFTR chloride channels." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 2 (1996): L192—L200. http://dx.doi.org/10.1152/ajplung.1996.271.2.l192.

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The cystic fibrosis transmembrane conductance regulator (CFTR) is a protein kinase A- and ATP-regulated Cl- channel located in the apical membranes of epithelial cells. Previously Sheppard and Welsh (J. Gen. Physiol. 100: 573-591, 1992) showed that glibenclamide, a compound which binds to the sulfonylurea receptor and thus blocks nucleotide-dependent K+ channels, reduced CFTR whole cell current. The aim of this study was to identify the mechanism underlying this inhibition in cell-free membrane patches containing CFTR Cl- channels. Exposure to gliben-clamide caused a reversible reduction in cu
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50

Narahashi, T., X. Zhao, T. Ikeda, K. Nagata, and JZ Yeh. "Differential actions of insecticides on target sites: basis for selective toxicity." Human & Experimental Toxicology 26, no. 4 (2007): 361–66. http://dx.doi.org/10.1177/0960327106078408.

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Whereas the selective toxicity of insecticides between insects and mammals has a long history of studies, it is now becoming abundantly clear that, in many cases, the differential action of insecticides on insects and mammalian target receptor sites is an important factor. In this paper, we first introduce the mechanism of action and the selective toxicity of pyrethroids as a prototype of study. Then, a more detailed account is given for fipronil, based primarily on our recent studies. Pyrethroids keep the sodium channels open for a prolonged period of time, causing elevation of the depolarizi
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