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Journal articles on the topic 'Kv11.1 channel'

Author: Grafiati

Published: 14 March 2023

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1

Al-Sabi, Ahmed, Oleg Shamotienko, Sorcha Ni Dhochartaigh та ін. "Arrangement of Kv1 α subunits dictates sensitivity to tetraethylammonium". Journal of General Physiology 136, № 3 (2010): 273–82. http://dx.doi.org/10.1085/jgp.200910398.

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Shaker-related Kv1 channels contain four channel-forming α subunits. Subfamily member Kv1.1 often occurs oligomerized with Kv1.2 α subunits in synaptic membranes, and so information was sought on the influence of their positions within tetramers on the channels’ properties. Kv1.1 and 1.2 α genes were tandem linked in various arrangements, followed by expression as single-chain proteins in mammalian cells. As some concatenations reported previously seemed not to reliably position Kv1 subunits in their assemblies, the identity of expressed channels was methodically evaluated. Surface protein, is

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2

Denisova, Kristina R., Nikita A. Orlov, Sergey A. Yakimov, Mikhail P. Kirpichnikov, Alexey V. Feofanov, and Oksana V. Nekrasova. "Atto488-Agitoxin 2—A Fluorescent Ligand with Increased Selectivity for Kv1.3 Channel Binding Site." Bioengineering 9, no. 7 (2022): 295. http://dx.doi.org/10.3390/bioengineering9070295.

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Fluorescently labeled peptide blockers of ion channels are useful probes in studying the localization and functioning of the channels and in the performance of a search for new channel ligands with bioengineering screening systems. Here, we report on the properties of Atto488-agitoxin 2 (A-AgTx2), a derivative of the Kv1 channel blocker agitoxin 2 (AgTx2), which was N-terminally labeled with Atto 488 fluorophore. The interactions of A-AgTx2 with the outer binding sites of the potassium voltage-gated Kv1.x (x = 1, 3, 6) channels were studied using bioengineered hybrid KcsA–Kv1.x (x = 1, 3, 6) c

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3

Large, R. J., M. A. Hollywood, G. P. Sergeant, et al. "Ionic currents in intimal cultured synoviocytes from the rabbit." American Journal of Physiology-Cell Physiology 299, no. 5 (2010): C1180—C1194. http://dx.doi.org/10.1152/ajpcell.00028.2010.

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Hyaluronan, a joint lubricant and regulator of synovial fluid content, is secreted by fibroblast-like synoviocytes lining the joint cavity, and secretion is greatly stimulated by Ca2+-dependent protein kinase C. This study aimed to define synoviocyte membrane currents and channels that may influence synoviocyte Ca2+ dynamics. Resting membrane potential ranged from −30 mV to −66 mV (mean −45 ± 8.60 mV, n = 40). Input resistance ranged from 0.54 GΩ to 2.6 GΩ (mean 1.28 ± 0.57 GΩ; ν = 33). Cell capacitance averaged 97.97 ± 5.93 pF. Voltage clamp using Cs+ pipette solution yielded a transient inwa

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4

D’Adamo, Maria Cristina, Antonella Liantonio, Jean-Francois Rolland, Mauro Pessia, and Paola Imbrici. "Kv1.1 Channelopathies: Pathophysiological Mechanisms and Therapeutic Approaches." International Journal of Molecular Sciences 21, no. 8 (2020): 2935. http://dx.doi.org/10.3390/ijms21082935.

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Kv1.1 belongs to the Shaker subfamily of voltage-gated potassium channels and acts as a critical regulator of neuronal excitability in the central and peripheral nervous systems. KCNA1 is the only gene that has been associated with episodic ataxia type 1 (EA1), an autosomal dominant disorder characterized by ataxia and myokymia and for which different and variable phenotypes have now been reported. The iterative characterization of channel defects at the molecular, network, and organismal levels contributed to elucidating the functional consequences of KCNA1 mutations and to demonstrate that a

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5

Yuan, Xiao-Jian, Jian Wang, Magdalena Juhaszova, Vera A. Golovina, and Lewis J. Rubin. "Molecular basis and function of voltage-gated K+ channels in pulmonary arterial smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 4 (1998): L621—L635. http://dx.doi.org/10.1152/ajplung.1998.274.4.l621.

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K+-channel activity-mediated alteration of the membrane potential and cytoplasmic free Ca2+ concentration ([Ca2+]cyt) is a pivotal mechanism in controlling pulmonary vasomotor tone. By using combined approaches of patch clamp, imaging fluorescent microscopy, and molecular biology, we examined the electrophysiological properties of K+ channels and the role of different K+ currents in regulating [Ca2+]cytand explored the molecular identification of voltage-gated K+(KV)- and Ca2+-activated K+(KCa)-channel genes expressed in pulmonary arterial smooth muscle cells (PASMC). Two kinetically distinct

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6

Rash, John E., Kimberly G. Vanderpool, Thomas Yasumura, Jordan Hickman, Jonathan T. Beatty, and James I. Nagy. "KV1 channels identified in rodent myelinated axons, linked to Cx29 in innermost myelin: support for electrically active myelin in mammalian saltatory conduction." Journal of Neurophysiology 115, no. 4 (2016): 1836–59. http://dx.doi.org/10.1152/jn.01077.2015.

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Saltatory conduction in mammalian myelinated axons was thought to be well understood before recent discoveries revealed unexpected subcellular distributions and molecular identities of the K+-conductance pathways that provide for rapid axonal repolarization. In this study, we visualize, identify, localize, quantify, and ultrastructurally characterize axonal KV1.1/KV1.2 channels in sciatic nerves of rodents. With the use of light microscopic immunocytochemistry and freeze-fracture replica immunogold labeling electron microscopy, KV1.1/KV1.2 channels are localized to three anatomically and compo

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7

Gladkikh, Irina, Steve Peigneur, Oksana Sintsova, et al. "Kunitz-Type Peptides from the Sea Anemone Heteractis crispa Demonstrate Potassium Channel Blocking and Anti-Inflammatory Activities." Biomedicines 8, no. 11 (2020): 473. http://dx.doi.org/10.3390/biomedicines8110473.

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The Kunitz/BPTI peptide family includes unique representatives demonstrating various biological activities. Electrophysiological screening of peptides HCRG1 and HCRG2 from the sea anemone Heteractis crispa on six Kv1.x channel isoforms and insect Shaker IR channel expressed in Xenopus laevis oocytes revealed their potassium channels blocking activity. HCRG1 and HCRG2 appear to be the first Kunitz-type peptides from sea anemones blocking Kv1.3 with IC50 of 40.7 and 29.7 nM, respectively. In addition, peptides mainly vary in binding affinity to the Kv1.2 channels. It was established that the sin

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8

Imbrici, Paola, Maria Cristina D'Adamo, Antonella Cusimano та Mauro Pessia. "Episodic ataxia type 1 mutation F184C alters Zn2+-induced modulation of the human K+ channel Kv1.4-Kv1.1/Kvβ1.1". American Journal of Physiology-Cell Physiology 292, № 2 (2007): C778—C787. http://dx.doi.org/10.1152/ajpcell.00259.2006.

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Episodic ataxia type 1 (EA1) is a Shaker-like channelopathy characterized by continuous myokymia and attacks of imbalance with jerking movements of the head, arms, and legs. Although altered expression and gating properties of Kv1.1 channels underlie EA1, several disease-causing mechanisms remain poorly understood. It is likely that Kv1.1, Kv1.4, and Kvβ1.1 subunits form heteromeric channels at hippocampal mossy fiber boutons from which Zn2+ ions are released into the synaptic cleft in a Ca2+-dependent fashion. The sensitivity of this macromolecular channel complex to Zn2+ is unknown. Here, we

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9

Brock, Mathew W., Chris Mathes, and William F. Gilly. "Selective Open-Channel Block of Shaker (Kv1) Potassium Channels by S-Nitrosodithiothreitol (Sndtt)." Journal of General Physiology 118, no. 1 (2001): 113–34. http://dx.doi.org/10.1085/jgp.118.1.113.

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Large quaternary ammonium (QA) ions block voltage-gated K+ (Kv) channels by binding with a 1:1 stoichiometry in an aqueous cavity that is exposed to the cytoplasm only when channels are open. S-nitrosodithiothreitol (SNDTT; ONSCH2CH(OH)CH(OH)CH2SNO) produces qualitatively similar “open-channel block” in Kv channels despite a radically different structure. SNDTT is small, electrically neutral, and not very hydrophobic. In whole-cell voltage-clamped squid giant fiber lobe neurons, bath-applied SNDTT causes reversible time-dependent block of Kv channels, but not Na+ or Ca2+ channels. Inactivation

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10

Platoshyn, Oleksandr, Carmelle V. Remillard, Ivana Fantozzi, et al. "Diversity of voltage-dependent K+ channels in human pulmonary artery smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 1 (2004): L226—L238. http://dx.doi.org/10.1152/ajplung.00438.2003.

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Electrical excitability, which plays an important role in excitation-contraction coupling in the pulmonary vasculature, is regulated by transmembrane ion flux in pulmonary artery smooth muscle cells (PASMC). This study examined the heterogeneous nature of native voltage-dependent K+ channels in human PASMC. Both voltage-gated K+ (KV) currents and Ca2+-activated K+ (KCa) currents were observed and characterized. In cell-attached patches of PASMC bathed in Ca2+-containing solutions, depolarization elicited a wide range of K+ unitary conductances (6–290 pS). When cells were dialyzed with Ca2+-fre

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11

Zhao, Juan, Dimitri Petitjean, Georges A. Haddad, Zarah Batulan, and Rikard Blunck. "A Common Kinetic Property of Mutations Linked to Episodic Ataxia Type 1 Studied in the Shaker Kv Channel." International Journal of Molecular Sciences 21, no. 20 (2020): 7602. http://dx.doi.org/10.3390/ijms21207602.

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(1) Background: Episodic ataxia type 1 is caused by mutations in the KCNA1 gene encoding for the voltage-gated potassium channel Kv1.1. There have been many mutations in Kv1.1 linked to episodic ataxia reported and typically investigated by themselves or in small groups. The aim of this article is to determine whether we can define a functional parameter common to all Kv1.1 mutants that have been linked to episodic ataxia. (2) Methods: We introduced the disease mutations linked to episodic ataxia in the drosophila analog of Kv1.1, the Shaker Kv channel, and expressed the channels in Xenopus oo

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12

Chen, Gang, Wangcai Gao, Kenneth C. Reinert, et al. "Involvement of Kv1 Potassium Channels in Spreading Acidification and Depression in the Cerebellar Cortex." Journal of Neurophysiology 94, no. 2 (2005): 1287–98. http://dx.doi.org/10.1152/jn.00224.2005.

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Spreading acidification and depression (SAD) is a form of propagated activity in the cerebellar cortex characterized by acidification and a transient depression in excitability. This study investigated the role of Kv1 potassium channels in SAD using neutral red, flavoprotein autofluorescence, and voltage-sensitive dye optical imaging in the mouse cerebellar cortex, in vivo. The probability of evoking SAD was greatly increased by blocking Kv1.1 as well as Kv1.2 potassium channels by their specific blockers dendrotoxin K (DTX-K) and tityustoxin (TsTX), respectively. DTX-K not only greatly lowere

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13

Dinoi, Giorgia, Michael Morin, Elena Conte, et al. "Clinical and Functional Study of a De Novo Variant in the PVP Motif of Kv1.1 Channel Associated with Epilepsy, Developmental Delay and Ataxia." International Journal of Molecular Sciences 23, no. 15 (2022): 8079. http://dx.doi.org/10.3390/ijms23158079.

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Mutations in the KCNA1 gene, encoding the voltage-gated potassium channel Kv1.1, have been associated with a spectrum of neurological phenotypes, including episodic ataxia type 1 and developmental and epileptic encephalopathy. We have recently identified a de novo variant in KCNA1 in the highly conserved Pro-Val-Pro motif within the pore of the Kv1.1 channel in a girl affected by early onset epilepsy, ataxia and developmental delay. Other mutations causing severe epilepsy are located in Kv1.1 pore domain. The patient was initially treated with a combination of antiepileptic drugs with limited

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14

Hsiao, Chie-Fang, Gurvinder Kaur, Angela Vong, Harpreet Bawa, and Scott H. Chandler. "Participation of Kv1 Channels in Control of Membrane Excitability and Burst Generation in Mesencephalic V Neurons." Journal of Neurophysiology 101, no. 3 (2009): 1407–18. http://dx.doi.org/10.1152/jn.91053.2008.

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The function and biophysical properties of low threshold Kv1 current in control of membrane resonance, subthreshold oscillations, and bursting in mesencephalic V neurons (Mes V) were examined in rat brain stem slices (P8–P12) using whole cell current and voltage patch-clamp methods. α-dendrotoxin application, a toxin with high specificity for Kv1.1, 1.2, and 1.6 channels, showed the presence of a low-threshold K+ current that activated rapidly around −50 mV and was relatively noninactivating over a 1-s period and had a V1/2max of −36.2 mV. Other toxins, specific for individual channels contain

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15

Nekrasova, Oksana V., Alexandra L. Primak, Anastasia A. Ignatova, et al. "N-Terminal Tagging with GFP Enhances Selectivity of Agitoxin 2 to Kv1.3-Channel Binding Site." Toxins 12, no. 12 (2020): 802. http://dx.doi.org/10.3390/toxins12120802.

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Recently developed fluorescent protein-scorpion toxin chimeras (FP-Tx) show blocking activities for potassium voltage-gated channels of Kv1 family and retain almost fully pharmacological profiles of the parental peptide toxins (Kuzmenkov et al., Sci Rep. 2016, 6, 33314). Here we report on N-terminally green fluorescent protein (GFP)-tagged agitoxin 2 (GFP-L2-AgTx2) with high affinity and selectivity for the binding site of Kv1.3 channel involved in the pathogenesis of various (primarily of autoimmune origin) diseases. The basis for this selectivity relates to N-terminal location of GFP, since

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16

Vivekananda, Umesh, Pavel Novak, Oscar D. Bello, et al. "Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization." Proceedings of the National Academy of Sciences 114, no. 9 (2017): 2395–400. http://dx.doi.org/10.1073/pnas.1608763114.

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Although action potentials propagate along axons in an all-or-none manner, subthreshold membrane potential fluctuations at the soma affect neurotransmitter release from synaptic boutons. An important mechanism underlying analog–digital modulation is depolarization-mediated inactivation of presynaptic Kv1-family potassium channels, leading to action potential broadening and increased calcium influx. Previous studies have relied heavily on recordings from blebs formed after axon transection, which may exaggerate the passive propagation of somatic depolarization. We recorded instead from small bo

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17

Wang, Yuanyuan, Xiaoyi Mo, Conghui Ping та ін. "Site-specific contacts enable distinct modes of TRPV1 regulation by the potassium channel Kvβ1 subunit". Journal of Biological Chemistry 295, № 50 (2020): 17337–48. http://dx.doi.org/10.1074/jbc.ra120.015605.

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Transient receptor potential vanilloid 1 (TRPV1) channel is a multimodal receptor that is responsible for nociceptive, thermal, and mechanical sensations. However, which biomolecular partners specifically interact with TRPV1 remains to be elucidated. Here, we used cDNA library screening of genes from mouse dorsal root ganglia combined with patch-clamp electrophysiology to identify the voltage-gated potassium channel auxiliary subunit Kvβ1 physically interacting with TRPV1 channel and regulating its function. The interaction was validated in situ using endogenous dorsal root ganglia neurons, as

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18

Pineda, Ricardo H., Christopher S. Knoeckel, Alison D. Taylor, Adriana Estrada-Bernal та Angeles B. Ribera. "Kv1 Potassium Channel Complexes In Vivo Require Kvβ2 Subunits in Dorsal Spinal Neurons". Journal of Neurophysiology 100, № 4 (2008): 2125–36. http://dx.doi.org/10.1152/jn.90667.2008.

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Whereas Kvβ2 subunits modulate potassium current properties carried by Kv1 channel complexes in heterologous systems, little is known about the contributions of Kvβ2 subunits to native potassium channel function. Using antisense approaches and in situ recordings from Xenopus embryo spinal cord neurons, we tested the in vivo roles of Kvβ2 subunits in modulation of voltage-dependent potassium current ( IKv). We focused on 1) two different populations of dorsal spinal neurons that express both Kvβ2 and Kv1 α-subunit genes and 2) the 24- and 48-h developmental period, during which IKv undergoes de

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19

Jerng, Henry H., Jay M. Patel, Tamor A. Khan, Benjamin R. Arenkiel, and Paul J. Pfaffinger. "Light-regulated voltage-gated potassium channels for acute interrogation of channel function in neurons and behavior." PLOS ONE 16, no. 3 (2021): e0248688. http://dx.doi.org/10.1371/journal.pone.0248688.

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Voltage-gated potassium (Kv) channels regulate the membrane potential and conductance of excitable cells to control the firing rate and waveform of action potentials. Even though Kv channels have been intensely studied for over 70 year, surprisingly little is known about how specific channels expressed in various neurons and their functional properties impact neuronal network activity and behavior in vivo. Although many in vivo genetic manipulations of ion channels have been tried, interpretation of these results is complicated by powerful homeostatic plasticity mechanisms that act to maintain

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20

Imbrici, Paola, Maria Cristina D'Adamo, Alessandro Grottesi, Andrea Biscarini, and Mauro Pessia. "Episodic ataxia type 1 mutations affect fast inactivation of K+ channels by a reduction in either subunit surface expression or affinity for inactivation domain." American Journal of Physiology-Cell Physiology 300, no. 6 (2011): C1314—C1322. http://dx.doi.org/10.1152/ajpcell.00456.2010.

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Episodic ataxia type 1 (EA1) is an autosomal dominant disorder characterized by continuous myokymia and episodic attacks of ataxia. Mutations in the gene KCNA1 that encodes the voltage-gated potassium channel Kv1.1 are responsible for EA1. In several brain areas, Kv1.1 coassembles with Kv1.4, which confers N-type inactivating properties to heteromeric channels. It is therefore likely that the rate of inactivation will be determined by the number of Kv1.4 inactivation particles, as set by the precise subunit stoichiometry. We propose that EA1 mutations affect the rate of N-type inactivation eit

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Silverå Ejneby, Malin, Björn Wallner, and Fredrik Elinder. "Coupling stabilizers open KV1-type potassium channels." Proceedings of the National Academy of Sciences 117, no. 43 (2020): 27016–21. http://dx.doi.org/10.1073/pnas.2007965117.

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The opening and closing of voltage-gated ion channels are regulated by voltage sensors coupled to a gate that controls the ion flux across the cellular membrane. Modulation of any part of gating constitutes an entry point for pharmacologically regulating channel function. Here, we report on the discovery of a large family of warfarin-like compounds that open the two voltage-gated type 1 potassium (KV1) channels KV1.5 and Shaker, but not the related KV2-, KV4-, or KV7-type channels. These negatively charged compounds bind in the open state to positively charged arginines and lysines between the

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Wang, Jian-Ying, Jian Wang, Vera A. Golovina, Li Li, Oleksandr Platoshyn, and Jason Xiao-Jian Yuan. "Role of K+ channel expression in polyamine-dependent intestinal epithelial cell migration." American Journal of Physiology-Cell Physiology 278, no. 2 (2000): C303—C314. http://dx.doi.org/10.1152/ajpcell.2000.278.2.c303.

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Polyamines are essential for cell migration during early mucosal restitution after wounding in the gastrointestinal tract. Activity of voltage-gated K+ channels (Kv) controls membrane potential ( E m) that regulates cytoplasmic free Ca2+ concentration ([Ca2+]cyt) by governing the driving force for Ca2+ influx. This study determined whether polyamines are required for the stimulation of cell migration by altering K+ channel gene expression, E m, and [Ca2+]cyt in intestinal epithelial cells (IEC-6). The specific inhibitor of polyamine synthesis, α-difluoromethylornithine (DFMO, 5 mM), depleted c

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23

Friederich, Patrick, Dietmar Benzenberg, Sokratis Trellakis, and Bernd W. Urban. "Interaction of Volatile Anesthetics with Human Kv Channels in Relation to Clinical Concentrations." Anesthesiology 95, no. 4 (2001): 954–58. http://dx.doi.org/10.1097/00000542-200110000-00026.

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Background Recent evidence shows that inhibition of human Kv3 channels by intravenous anesthetics occurs at clinical concentrations. The effects of volatile anesthetics on these human ion channels are unknown. This study was designed to establish whether minimum alveolar concentrations (MAC) of halothane, enflurane, isoflurane, and desflurane exhibit effects on Kv3 channeLs. To obtain an indication whether these findings may be specific to Kv3 channels, the effects of enflurane and isoflurane on human Kv1.1 channels were also investigated. Methods Kv3 channels natively expressed in SH-SY5Y cel

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Extrémet, Johanna, Oussama El Far, Norbert Ankri, Sarosh R. Irani, Dominique Debanne, and Michaël Russier. "An Epitope-Specific LGI1-Autoantibody Enhances Neuronal Excitability by Modulating Kv1.1 Channel." Cells 11, no. 17 (2022): 2713. http://dx.doi.org/10.3390/cells11172713.

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Leucine-rich Glioma-Inactivated protein 1 (LGI1) is expressed in the central nervous system and its genetic loss of function is associated with epileptic disorders. Additionally, patients with LGI1-directed autoantibodies have frequent focal seizures as a key feature of their disease. LGI1 is composed of a Leucine-Rich Repeat (LRR) and an Epitempin (EPTP) domain. These domains are reported to interact with different members of the transsynaptic complex formed by LGI1 at excitatory synapses, including presynaptic Kv1 potassium channels. Patient-derived recombinant monoclonal antibodies (mAbs) a

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Speake, Tracey, Jonathan D. Kibble, and Peter D. Brown. "Kv1.1 and Kv1.3 channels contribute to the delayed-rectifying K+ conductance in rat choroid plexus epithelial cells." American Journal of Physiology-Cell Physiology 286, no. 3 (2004): C611—C620. http://dx.doi.org/10.1152/ajpcell.00292.2003.

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The choroid plexuses secrete, and maintain the composition of, the cerebrospinal fluid. K+ channels play an important role in these processes. In this study the molecular identity and properties of the delayed-rectifying K+ (Kv) conductance in rat choroid plexus epithelial cells were investigated. Whole cell K+ currents were significantly reduced by 10 nM dendrotoxin-K and 1 nM margatoxin, which are specific inhibitors of Kv1.1 and Kv1.3 channels, respectively. A combination of dendrotoxin-K and margatoxin caused a depolarization of the membrane potential in current-clamp experiments. Western

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Tobin, Ann A., Biny K. Joseph, Hamood N. Al-Kindi, et al. "Loss of cerebrovascular Shaker-type K+ channels: a shared vasodilator defect of genetic and renal hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 1 (2009): H293—H303. http://dx.doi.org/10.1152/ajpheart.00991.2008.

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The cerebral arteries of hypertensive rats are depolarized and highly myogenic, suggesting a loss of K+ channels in the vascular smooth muscle cells (VSMCs). The present study evaluated whether the dilator function of the prominent Shaker-type voltage-gated K+ (KV1) channels is attenuated in middle cerebral arteries from two rat models of hypertension. Block of KV1 channels by correolide (1 μmol/l) or psora-4 (100 nmol/l) reduced the resting diameter of pressurized (80 mmHg) cerebral arteries from normotensive rats by an average of 28 ± 3% or 26 ± 3%, respectively. In contrast, arteries from s

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Ohanyan, Vahagn, Sean M. Raph, Marc M. Dwenger та ін. "Myocardial Blood Flow Control by Oxygen Sensing Vascular Kvβ Proteins". Circulation Research 128, № 6 (2021): 738–51. http://dx.doi.org/10.1161/circresaha.120.317715.

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Rationale: Voltage-gated potassium (Kv) channels in vascular smooth muscle are essential for coupling myocardial blood flow (MBF) with the metabolic demand of the heart. These channels consist of a transmembrane pore domain that associates with auxiliary Kvβ (voltage-gated potassium channel β)1 and Kvβ2 proteins, which differentially regulate Kv function in excitable cells. Nonetheless, the physiological role of Kvβ proteins in regulating vascular tone and metabolic hyperemia in the heart remains unknown. Objective: To test the hypothesis that Kvβ proteins confer oxygen sensitivity to vascular

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Shvetsova, Anastasia A., Dina K. Gaynullina, Olga S. Tarasova, and Rudolf Schubert. "Remodeling of Arterial Tone Regulation in Postnatal Development: Focus on Smooth Muscle Cell Potassium Channels." International Journal of Molecular Sciences 22, no. 11 (2021): 5413. http://dx.doi.org/10.3390/ijms22115413.

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Maturation of the cardiovascular system is associated with crucial structural and functional remodeling. Thickening of the arterial wall, maturation of the sympathetic innervation, and switching of the mechanisms of arterial contraction from calcium-independent to calcium-dependent occur during postnatal development. All these processes promote an almost doubling of blood pressure from the moment of birth to reaching adulthood. This review focuses on the developmental alterations of potassium channels functioning as key smooth muscle membrane potential determinants and, consequently, vascular

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Imbrici, Paola, Andrea Accogli, Rikard Blunck, et al. "Musculoskeletal Features without Ataxia Associated with a Novel de novo Mutation in KCNA1 Impairing the Voltage Sensitivity of Kv1.1 Channel." Biomedicines 9, no. 1 (2021): 75. http://dx.doi.org/10.3390/biomedicines9010075.

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The KCNA1 gene encodes the α subunit of the voltage-gated Kv1.1 potassium channel that critically regulates neuronal excitability in the central and peripheral nervous systems. Mutations in KCNA1 have been classically associated with episodic ataxia type 1 (EA1), a movement disorder triggered by physical and emotional stress. Additional features variably reported in recent years include epilepsy, myokymia, migraine, paroxysmal dyskinesia, hyperthermia, hypomagnesemia, and cataplexy. Interestingly, a few individuals with neuromyotonia, either isolated or associated with skeletal deformities, ha

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SRAIRI-ABID, Najet, Joseba Iñaki GUIJARRO, Rym BENKHALIFA, et al. "A new type of scorpion Na+-channel-toxin-like polypeptide active on K+ channels." Biochemical Journal 388, no. 2 (2005): 455–64. http://dx.doi.org/10.1042/bj20041407.

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We have purified and characterized two peptides, named KAaH1 and KAaH2 (AaH polypeptides 1 and 2 active on K+ channels, where AaH stands for Androctonus australis Hector), from the venom of A. australis Hector scorpions. Their sequences contain 58 amino acids including six half-cysteines and differ only at positions 26 (Phe/Ser) and 29 (Lys/Gln). Although KAaH1 and KAaH2 show important sequence similarity with anti-mammal β toxins specific for voltage-gated Na+ channels, only weak β-like effects were observed when KAaH1 or KAaH2 (1 μM) were tested on brain Nav1.2 channels. In contrast, KAaH1 b

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MacDonald, Patrick E., Xiao Fang Ha, Jing Wang, et al. "Members of the Kv1 and Kv2 Voltage-Dependent K+ Channel Families Regulate Insulin Secretion." Molecular Endocrinology 15, no. 8 (2001): 1423–35. http://dx.doi.org/10.1210/mend.15.8.0685.

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Abstract In pancreatic β-cells, voltage-dependent K+ (Kv) channels are potential mediators of repolarization, closure of Ca2+ channels, and limitation of insulin secretion. The specific Kv channels expressed in β-cells and their contribution to the delayed rectifier current and regulation of insulin secretion in these cells are unclear. High-level protein expression and mRNA transcripts for Kv1.4, 1.6, and 2.1 were detected in rat islets and insulinoma cells. Inhibition of these channels with tetraethylammonium decreased IDR by approximately 85% and enhanced glucose-stimulated insulin secretio

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Hsu, Hsin-Te, You-Lan Yang, Wan-Chen Chen, Chi-Ming Chen, and Wun-Chang Ko. "Butylidenephthalide Blocks Potassium Channels and Enhances Basal Tension in Isolated Guinea-Pig Trachea." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/875230.

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Butylidenephthalide (Bdph, 30~300 μM), a constituent ofLigusticum chuanxiongHort., significantly enhanced tension in isolated guinea-pig trachea. In this study, we investigate the mechanism(s) of Bdph-induced contraction in the tissue. Isolated trachea was bathed in 5 mL of Krebs solution containing indomethacin (3 μM), and its tension changes were isometrically recorded. Cromakalim (3 μM), an ATP-dependent K+channel opener, significantly antagonized the Bdph-induced enhancement of baseline tension. Bdph (300 μM) also significantly antagonized cromakalim-induced relaxation. Bdph (300 μM) did n

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Finnegan, Thomas F., Shao-Rui Chen та Hui-Lin Pan. "μ Opioid Receptor Activation Inhibits GABAergic Inputs to Basolateral Amygdala Neurons Through Kv1.1/1.2 Channels". Journal of Neurophysiology 95, № 4 (2006): 2032–41. http://dx.doi.org/10.1152/jn.01004.2005.

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The basolateral amygdala (BLA) is the major amygdaloid nucleus distributed with μ opioid receptors. The afferent input from the BLA to the central nucleus of the amygdala (CeA) is considered important for opioid analgesia. However, little is known about the effect of μ opioids on synaptic transmission in the BLA. In this study, we examined the effect of μ opioid receptor stimulation on the inhibitory and excitatory synaptic inputs to CeA-projecting BLA neurons. BLA neurons were retrogradely labeled with a fluorescent tracer injected into the CeA of rats. Whole cell voltage-clamp recordings wer

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34

Yuan, Li-Lian, Xixi Chen, Kumud Kunjilwar, Paul Pfaffinger, and Daniel Johnston. "Acceleration of K+ channel inactivation by MEK inhibitor U0126." American Journal of Physiology-Cell Physiology 290, no. 1 (2006): C165—C171. http://dx.doi.org/10.1152/ajpcell.00206.2005.

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Voltage-dependent (Kv)4.2-encoded A-type K+ channels play an important role in controlling neuronal excitability and are subject to modulation by various protein kinases, including ERK. In studies of ERK modulation, the organic compound U0126 is often used to suppress the activity of MEK, which is a kinase immediately upstream from ERK. We have observed that the inactivation time constant of heterologously expressed Kv4.2 channels was accelerated by U0126 at 1–20 μM. This effect, however, was not Kv4 family specific, because U0126 also converted noninactivating K+ currents mediated by Kv1.1 su

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Yin, Shi-Jin, Ling Jiang, Hong Yi, et al. "Different Residues in Channel Turret Determining the Selectivity of ADWX-1 Inhibitor Peptide between Kv1.1 and Kv1.3 Channels." Journal of Proteome Research 7, no. 11 (2008): 4890–97. http://dx.doi.org/10.1021/pr800494a.

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36

Orlov, Nikita A., Anastasia A. Ignatova, Elena V. Kryukova, et al. "Combining mKate2-Kv1.3 Channel and Atto488-Hongotoxin for the Studies of Peptide Pore Blockers on Living Eukaryotic Cells." Toxins 14, no. 12 (2022): 858. http://dx.doi.org/10.3390/toxins14120858.

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The voltage-gated potassium Kv1.3 channel is an essential component of vital cellular processes which is also involved in the pathogenesis of some autoimmune, neuroinflammatory and oncological diseases. Pore blockers of the Kv1.3 channel are considered as potential drugs and are used to study Kv1 channels’ structure and functions. Screening and study of the blockers require the assessment of their ability to bind the channel. Expanding the variety of methods used for this, we report on the development of the fluorescent competitive binding assay for measuring affinities of pore blockers to Kv1

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Sciamanna, Giuseppe, and Charles J. Wilson. "The ionic mechanism of gamma resonance in rat striatal fast-spiking neurons." Journal of Neurophysiology 106, no. 6 (2011): 2936–49. http://dx.doi.org/10.1152/jn.00280.2011.

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Striatal fast-spiking (FS) cells in slices fire in the gamma frequency range and in vivo are often phase-locked to gamma oscillations in the field potential. We studied the firing patterns of these cells in slices from rats ages 16–23 days to determine the mechanism of their gamma resonance. The resonance of striatal FS cells was manifested as a minimum frequency for repetitive firing. At rheobase, cells fired a doublet of action potentials or doublets separated by pauses, with an instantaneous firing rate averaging 44 spikes/s. The minimum rate for sustained firing was also responsible for th

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Dick, Gregory M., Ian N. Bratz, Léna Borbouse, et al. "Voltage-dependent K+ channels regulate the duration of reactive hyperemia in the canine coronary circulation." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 5 (2008): H2371—H2381. http://dx.doi.org/10.1152/ajpheart.01279.2007.

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We previously demonstrated a role for voltage-dependent K+ (KV) channels in coronary vasodilation elicited by myocardial metabolism and exogenous H2O2, as responses were attenuated by the KV channel blocker 4-aminopyridine (4-AP). Here we tested the hypothesis that KV channels participate in coronary reactive hyperemia and examined the role of KV channels in responses to nitric oxide (NO) and adenosine, two putative mediators. Reactive hyperemia (30-s occlusion) was measured in open-chest dogs before and during 4-AP treatment [intracoronary (ic), plasma concentration 0.3 mM]. 4-AP reduced base

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Smart, Sharon L., Valeri Lopantsev, C. L. Zhang, et al. "Deletion of the KV1.1 Potassium Channel Causes Epilepsy in Mice." Neuron 20, no. 4 (1998): 809–19. http://dx.doi.org/10.1016/s0896-6273(00)81018-1.

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Erisir, A., D. Lau, B. Rudy, and C. S. Leonard. "Function of Specific K+ Channels in Sustained High-Frequency Firing of Fast-Spiking Neocortical Interneurons." Journal of Neurophysiology 82, no. 5 (1999): 2476–89. http://dx.doi.org/10.1152/jn.1999.82.5.2476.

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Fast-spiking GABAergic interneurons of the neocortex and hippocampus fire high-frequency trains of brief action potentials with little spike-frequency adaptation. How these striking properties arise is unclear, although recent evidence suggests K+ channels containing Kv3.1-Kv3.2 proteins play an important role. We investigated the role of these channels in the firing properties of fast-spiking neocortical interneurons from mouse somatosensory cortex using a pharmacological and modeling approach. Low tetraethylammonium (TEA) concentrations (≤1 mM), which block only a few known K+channels includ

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Poveda, Clara, Maria Valero, Marianny Pernia, et al. "Expression and Localization of Kv1.1 and Kv3.1b Potassium Channels in the Cochlear Nucleus and Inferior Colliculus after Long-Term Auditory Deafferentation." Brain Sciences 10, no. 1 (2020): 35. http://dx.doi.org/10.3390/brainsci10010035.

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Deafness affects the expression and distribution of voltage-dependent potassium channels (Kvs) of central auditory neurons in the short-term, i.e., hours to days, but the consequences in the expression of Kvs after long-term deafness remain unknown. We tested expression and distribution of Kv1.1 and Kv3.1b, key for auditory processing, in the rat cochlear nucleus (CN), and in the inferior colliculus (IC), at 1, 15 and 90 days after mechanical lesion of the cochlea, using a combination of qRT-PCR and Western blot in the whole CN, along with semi-quantitative immunocytochemistry in the AVCN, whe

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Johnson, Rosalyn P., Ahmed F. El-Yazbi, Morgan F. Hughes, et al. "Identification and Functional Characterization of Protein Kinase A-catalyzed Phosphorylation of Potassium Channel Kv1.2 at Serine 449." Journal of Biological Chemistry 284, no. 24 (2009): 16562–74. http://dx.doi.org/10.1074/jbc.m109.010918.

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Vascular smooth muscle Kv1 delayed rectifier K+ channels (KDR) containing Kv1.2 control membrane potential and thereby regulate contractility. Vasodilatory agonists acting via protein kinase A (PKA) enhance vascule smooth muscle Kv1 activity, but the molecular basis of this regulation is uncertain. We characterized the role of a C-terminal phosphorylation site, Ser-449, in Kv1.2 expressed in HEK 293 cells by biochemical and electrophysiological methods. We found that 1) in vitro phosphorylation of Kv1.2 occurred exclusively at serine residues, 2) one major phosphopeptide that co-migrated with

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Gittelman, Joshua X., and Bruce L. Tempel. "Kv1.1-Containing Channels Are Critical for Temporal Precision During Spike Initiation." Journal of Neurophysiology 96, no. 3 (2006): 1203–14. http://dx.doi.org/10.1152/jn.00092.2005.

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Low threshold, voltage-gated potassium currents ( Ikl) are widely expressed in auditory neurons that can fire temporally precise action potentials (APs). In the medial nucleus of the trapezoid body (MNTB), channels containing the Kv1.1 subunit (encoded by the Kcna1 gene) underlie Ikl. Using pharmacology, genetics and whole cell patch-clamp recordings in mouse brain slices, we tested the role of Ikl in limiting AP latency-variability (jitter) in response to trains of single inputs at moderate to high stimulation rates. With dendrotoxin-K (DTX-K, a selective blocker of Kv1.1-containing channels)

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Skutel, Mikhail, Aleksandra Primak, Mikhail Kirpichnikov, Alexander Arseniev, Alexey Feofanov, and Oksana Nekrasova. "RFP-tagged Hongotoxin 1 and Its Interactions with KscA-Kv1.1 Hybrid Channels." Microscopy and Microanalysis 26, S2 (2020): 1378–80. http://dx.doi.org/10.1017/s1431927620017900.

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Xiong, Weichen, Huizhen Fan, Qingye Zeng, et al. "The in vitro anticancer effects of FS48 from salivary glands of Xenopsylla cheopis on NCI-H460 cells via its blockage of voltage-gated K⁺ channels." Acta Pharmaceutica 73, no. 1 (2023): 145–55. http://dx.doi.org/10.2478/acph-2023-0010.

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Abstract Voltage-gated K+ (Kv) channels play a role in the cellular processes of various cancer cells, including lung cancer cells. We previously identified and reported a salivary protein from the Xenopsylla cheopis, FS48, which exhibited inhibitory activity against Kv1.1-1.3 channels when assayed in HEK 293T cells. However, whether FS48 has an inhibitory effect on cancer cells expressing Kv channels is unclear. The present study aims to reveal the effects of FS48 on the Kv channels and the NCI-H460 human lung cancer cells through patch clamp, MTT, wound healing, transwell, gelatinase zymogra

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Primak, A. L., M. A. Skutel, O. V. Nekrasova, A. S. Arseniev, M. P. Kirpichnikov, and A. V. Feofanov. "Kv1 Potassium Channel Ligands Based on Hongotoxin 1 and Red Fluorescent Protein." Russian Journal of Bioorganic Chemistry 46, no. 6 (2020): 1011–17. http://dx.doi.org/10.1134/s1068162020060266.

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Kanemasa, T., L. Gan, T. M. Perney, L. Y. Wang, and L. K. Kaczmarek. "Electrophysiological and pharmacological characterization of a mammalian Shaw channel expressed in NIH 3T3 fibroblasts." Journal of Neurophysiology 74, no. 1 (1995): 207–17. http://dx.doi.org/10.1152/jn.1995.74.1.207.

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1. The Shaw-like voltage-activated potassium channel Kv3.1 is expressed in neurons that generate rapid trains of action potentials. By expressing this channel in a mammalian cell line and by simulating its activation, we tested the potential role of this channel in action potential repolarization. 2. NIH 3T3 fibroblasts were stably transfected with Kv3.1 DNA. Currents recorded in these cells had a threshold of activation at approximately -10 mV, showed little inactivation, and were very sensitive to blockade by 4-aminopyridine and tetraethylammonium. 3. Kv3.1 currents activated rapidly at the

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Verdura, Edgard, Carme Fons, Agatha Schlüter, et al. "Complete loss of KCNA1 activity causes neonatal epileptic encephalopathy and dyskinesia." Journal of Medical Genetics 57, no. 2 (2019): 132–37. http://dx.doi.org/10.1136/jmedgenet-2019-106373.

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BackgroundSince 1994, over 50 families affected by the episodic ataxia type 1 disease spectrum have been described with mutations in KCNA1, encoding the voltage-gated K+ channel subunit Kv1.1. All of these mutations are either transmitted in an autosomal-dominant mode or found as de novo events.MethodsA patient presenting with a severe combination of dyskinesia and neonatal epileptic encephalopathy was sequenced by whole-exome sequencing (WES). A candidate variant was tested using cellular assays and patch-clamp recordings.ResultsWES revealed a homozygous variant (p.Val368Leu) in KCNA1, involv

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Straub, Stephen V., Sylvie M. Perez, Beijing Tan, et al. "Pharmacological inhibition of Kv1.3 fails to modulate insulin sensitivity in diabetic mice or human insulin-sensitive tissues." American Journal of Physiology-Endocrinology and Metabolism 301, no. 2 (2011): E380—E390. http://dx.doi.org/10.1152/ajpendo.00076.2011.

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Genetic ablation of the voltage-gated potassium channel Kv1.3 improves insulin sensitivity and increases metabolic rate in mice. Inhibition of Kv1.3 in mouse adipose and skeletal muscle is reported to increase glucose uptake through increased GLUT4 translocation. Since Kv1.3 represents a novel target for the treatment of diabetes, the present study investigated whether Kv1.3 is functionally expressed in human adipose and skeletal muscle and whether specific pharmacological inhibition of the channel is capable of modulating insulin sensitivity in diabetic mouse models. Voltage-gated K+ channel

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Seagar, Michael, Michael Russier, Olivier Caillard, et al. "LGI1 tunes intrinsic excitability by regulating the density of axonal Kv1 channels." Proceedings of the National Academy of Sciences 114, no. 29 (2017): 7719–24. http://dx.doi.org/10.1073/pnas.1618656114.

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Autosomal dominant epilepsy with auditory features results from mutations in leucine-rich glioma-inactivated 1 (LGI1), a soluble glycoprotein secreted by neurons. Animal models of LGI1 depletion display spontaneous seizures, however, the function of LGI1 and the mechanisms by which deficiency leads to epilepsy are unknown. We investigated the effects of pure recombinant LGI1 and genetic depletion on intrinsic excitability, in the absence of synaptic input, in hippocampal CA3 neurons, a classical focus for epileptogenesis. Our data indicate that LGI1 is expressed at the axonal initial segment a

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