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Journal articles on the topic 'Kv7.2/3'

Author: Grafiati
Published: 7 July 2024
Last updated: 19 July 2025

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1

Hernandez, Ciria C., Björn Falkenburger, and Mark S. Shapiro. "Affinity for phosphatidylinositol 4,5-bisphosphate determines muscarinic agonist sensitivity of Kv7 K+ channels." Journal of General Physiology 134, no. 5 (2009): 437–48. http://dx.doi.org/10.1085/jgp.200910313.

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Kv7 K+-channel subunits differ in their apparent affinity for PIP2 and are differentially expressed in nerve, muscle, and epithelia in accord with their physiological roles in those tissues. To investigate how PIP2 affinity affects the response to physiological stimuli such as receptor stimulation, we exposed homomeric and heteromeric Kv7.2, 7.3, and 7.4 channels to a range of concentrations of the muscarinic receptor agonist oxotremorine-M (oxo-M) in a heterologous expression system. Activation of M1 receptors by oxo-M leads to PIP2 depletion through Gq and phospholipase C (PLC). Chinese hams
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2

Miceli, Francesco, Maria V. Soldovieri, Paolo Ambrosino, Laura Manocchio, Ilaria Mosca, and Maurizio Taglialatela. "Pharmacological Targeting of Neuronal Kv7.2/3 Channels: A Focus on Chemotypes and Receptor Sites." Current Medicinal Chemistry 25, no. 23 (2018): 2637–60. http://dx.doi.org/10.2174/0929867324666171012122852.

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Background: The Kv7 (KCNQ) subfamily of voltage-gated potassium channels consists of 5 members (Kv7.1-5) each showing characteristic tissue distribution and physiological roles. Given their functional heterogeneity, Kv7 channels represent important pharmacological targets for the development of new drugs for neuronal, cardiovascular and metabolic diseases. <p> Objective: In the present manuscript, we focus on describing the pharmacological relevance and potential therapeutic applications of drugs acting on neuronally-expressed Kv7.2/3 channels, placing particular emphasis on the differen
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3

Peretz, Asher, Anton Sheinin, Cuiyong Yue, et al. "Pre- and Postsynaptic Activation of M-Channels By a Novel Opener Dampens Neuronal Firing and Transmitter Release." Journal of Neurophysiology 97, no. 1 (2007): 283–95. http://dx.doi.org/10.1152/jn.00634.2006.

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The M-type K+ current (M-current), encoded by Kv7.2/3 (KCNQ2/3) K+ channels, plays a critical role in regulating neuronal excitability because it counteracts subthreshold depolarizations. Here we have characterized the functions of pre- and postsynaptic M-channels using a novel Kv7.2/3 channel opener, NH6, which we synthesized as a new derivative of N-phenylanthranilic acid. NH6 exhibits a good selectivity as it does not affect Kv7.1 and IKS K+ currents as well as NR1/NR2B, AMPA, and GABAA receptor-mediated currents. Superfusion of NH6 increased recombinant Kv7.2/3 current amplitude (EC50 = 18
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4

Wright, Andrew B., Khrystyna Yu Sukhanova, and Keith S. Elmslie. "KV7 channels are potential regulators of the exercise pressor reflex." Journal of Neurophysiology 126, no. 1 (2021): 1–10. http://dx.doi.org/10.1152/jn.00700.2020.

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KV7 channels control neuronal excitability. We show that these channels are expressed in muscle afferents and generate currents that are blocked by XE991 and bradykinin (BK). The XE991 block suggests that KV7 current comprises KV7.2/3 and KV7.5 channels. The BK inhibition of KV7 channels may explain how BK activates the exercise pressor reflex (EPR). Retigabine can enhance KV7 current, which could help control the inappropriately activated EPR in patients with cardiovascular disease.
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5

Barro-Soria, Rene. "Effects of small molecules on neurodevelopmental disorder-associated Kv7.2/3 mutations." Biophysical Journal 123, no. 3 (2024): 528a. http://dx.doi.org/10.1016/j.bpj.2023.11.3192.

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6

Peretz, Asher S., Eti Patrich, Polina Kornilov, Nataly Menaker, and Bernard Attali. "A Novel Compound Targeting Kv7.2/3 Channels Relieves Inflammatory and Neuropathic Pain." Biophysical Journal 106, no. 2 (2014): 141a. http://dx.doi.org/10.1016/j.bpj.2013.11.820.

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7

Liu, Wenjing, and Jérôme J. Devaux. "Calmodulin orchestrates the heteromeric assembly and the trafficking of KCNQ2/3 (Kv7.2/3) channels in neurons." Molecular and Cellular Neuroscience 58 (January 2014): 40–52. http://dx.doi.org/10.1016/j.mcn.2013.12.005.

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8

Surur, Abdrrahman S., Christian Bock, Kristin Beirow, et al. "Flupirtine and retigabine as templates for ligand-based drug design of KV7.2/3 activators." Organic & Biomolecular Chemistry 17, no. 18 (2019): 4512–22. http://dx.doi.org/10.1039/c9ob00511k.

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Puzzling stability: molecular jigsaw pieces of residues characterized in light of activity, lipophilicity, stability against oxidation, and hepatotoxicity were combined to yield flupirtine analogue 25b.
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9

Li, S., V. Choi, and T. Tzounopoulos. "Pathogenic plasticity of Kv7.2/3 channel activity is essential for the induction of tinnitus." Proceedings of the National Academy of Sciences 110, no. 24 (2013): 9980–85. http://dx.doi.org/10.1073/pnas.1302770110.

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10

Miranda, Pablo, Alba Cadaveira-Mosquera, Rafaela Gonzalez-Montelongo, et al. "Regulation of the Kv7.2/3 Channels by the Neuronal Serum-and Gluococorticoids-Regulated Kinase 1.1." Biophysical Journal 104, no. 2 (2013): 268a. http://dx.doi.org/10.1016/j.bpj.2012.11.1505.

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11

Sander, Svenja E., Catherine Lambrecht, and Angelika Richter. "The KV7.2/3 preferring channel opener ICA 27243 attenuates L-DOPA-induced dyskinesia in hemiparkinsonian rats." Neuroscience Letters 545 (June 2013): 59–63. http://dx.doi.org/10.1016/j.neulet.2013.04.017.

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12

Pablo, Juan Lorenzo, and Geoffrey S. Pitt. "FGF14 is a regulator of KCNQ2/3 channels." Proceedings of the National Academy of Sciences 114, no. 1 (2016): 154–59. http://dx.doi.org/10.1073/pnas.1610158114.

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KCNQ2/3 (Kv7.2/7.3) channels and voltage-gated sodium channels (VGSCs) are enriched in the axon initial segment (AIS) where they bind to ankyrin-G and coregulate membrane potential in central nervous system neurons. The molecular mechanisms supporting coordinated regulation of KCNQ and VGSCs and the cellular mechanisms governing KCNQ trafficking to the AIS are incompletely understood. Here, we show that fibroblast growth factor 14 (FGF14), previously described as a VGSC regulator, also affects KCNQ function and localization. FGF14 knockdown leads to a reduction of KCNQ2 in the AIS and a reduct
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13

Lee, Inn-Chi, Jiann-Jou Yang, Ying-Ming Liou, and Swee-Hee Wong. "KCNQ2 Selectivity Filter Mutations Cause Kv7.2 M-Current Dysfunction and Configuration Changes Manifesting as Epileptic Encephalopathies and Autistic Spectrum Disorders." Cells 11, no. 5 (2022): 894. http://dx.doi.org/10.3390/cells11050894.

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KCNQ2 mutations can cause benign familial neonatal convulsions (BFNCs), epileptic encephalopathy (EE), and mild-to-profound neurodevelopmental disabilities. Mutations in the KCNQ2 selectivity filter (SF) are critical to neurodevelopmental outcomes. Three patients with neonatal EE carry de novo heterozygous KCNQ2 p.Thr287Ile, p.Gly281Glu and p.Pro285Thr, and all are followed-up in our clinics. Whole-cell patch-clamp analysis with transfected mutations was performed. The Kv7.2 in three mutations demonstrated significant current changes in the homomeric-transfected cells. The conduction curves fo
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14

Roeloffs, Rosemarie, Alan D. Wickenden, Christopher Crean, et al. "In Vivo Profile of ICA-27243 [N-(6-Chloro-pyridin-3-yl)-3,4-difluoro-benzamide], a Potent and Selective KCNQ2/Q3 (Kv7.2/Kv7.3) Activator in Rodent Anticonvulsant Models." Journal of Pharmacology and Experimental Therapeutics 326, no. 3 (2008): 818–28. http://dx.doi.org/10.1124/jpet.108.137794.

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15

El-Chemali, Léa El, Suzan Boutary, Song Liu, et al. "GRT-X Stimulates Dorsal Root Ganglia Axonal Growth in Culture via TSPO and Kv7.2/3 Potassium Channel Activation." International Journal of Molecular Sciences 25, no. 13 (2024): 7327. http://dx.doi.org/10.3390/ijms25137327.

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GRT-X, which targets both the mitochondrial translocator protein (TSPO) and the Kv7.2/3 (KCNQ2/3) potassium channels, has been shown to efficiently promote recovery from cervical spine injury. In the present work, we investigate the role of GRT-X and its two targets in the axonal growth of dorsal root ganglion (DRG) neurons. Neurite outgrowth was quantified in DRG explant cultures prepared from wild-type C57BL6/J and TSPO-KO mice. TSPO was pharmacologically targeted with the agonist XBD173 and the Kv7 channels with the activator ICA-27243 and the inhibitor XE991. GRT-X efficiently stimulated D
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16

Sedivy, Vojtech, Shreena Joshi, Youssef Ghaly, et al. "Role of Kv7 channels in responses of the pulmonary circulation to hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 308, no. 1 (2015): L48—L57. http://dx.doi.org/10.1152/ajplung.00362.2013.

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Hypoxic pulmonary vasoconstriction (HPV) is a beneficial mechanism that diverts blood from hypoxic alveoli to better ventilated areas of the lung, but breathing hypoxic air causes the pulmonary circulation to become hypertensive. Responses to airway hypoxia are associated with depolarization of smooth muscle cells in the pulmonary arteries and reduced activity of K+channels. As Kv7 channels have been proposed to play a key role in regulating the smooth muscle membrane potential, we investigated their involvement in the development of HPV and hypoxia-induced pulmonary hypertension. Vascular eff
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17

Wu, Yong-Jin, Charles M. Conway, Li-Qiang Sun, et al. "Discovery of (S,E)-3-(2-fluorophenyl)-N-(1-(3-(pyridin-3-yloxy)phenyl)ethyl)-acrylamide as a potent and efficacious KCNQ2 (Kv7.2) opener for the treatment of neuropathic pain." Bioorganic & Medicinal Chemistry Letters 23, no. 22 (2013): 6188–91. http://dx.doi.org/10.1016/j.bmcl.2013.08.092.

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18

Dickson, Eamonn J., Björn H. Falkenburger, and Bertil Hille. "Quantitative properties and receptor reserve of the IP3 and calcium branch of Gq-coupled receptor signaling." Journal of General Physiology 141, no. 5 (2013): 521–35. http://dx.doi.org/10.1085/jgp.201210886.

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Gq-coupled plasma membrane receptors activate phospholipase C (PLC), which hydrolyzes membrane phosphatidylinositol 4,5-bisphosphate (PIP2) into the second messengers inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). This leads to calcium release, protein kinase C (PKC) activation, and sometimes PIP2 depletion. To understand mechanisms governing these diverging signals and to determine which of these signals is responsible for the inhibition of KCNQ2/3 (KV7.2/7.3) potassium channels, we monitored levels of PIP2, IP3, and calcium in single living cells. DAG and PKC are monitored in o
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19

Falkenburger, Björn H., Eamonn J. Dickson, and Bertil Hille. "Quantitative properties and receptor reserve of the DAG and PKC branch of Gq-coupled receptor signaling." Journal of General Physiology 141, no. 5 (2013): 537–55. http://dx.doi.org/10.1085/jgp.201210887.

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Gq protein–coupled receptors (GqPCRs) of the plasma membrane activate the phospholipase C (PLC) signaling cascade. PLC cleaves the membrane lipid phosphatidylinositol 4,5-bisphosphate (PIP2) into the second messengers diacylgycerol (DAG) and inositol 1,4,5-trisphosphate (IP3), leading to calcium release, protein kinase C (PKC) activation, and in some cases, PIP2 depletion. We determine the kinetics of each of these downstream endpoints and also ask which is responsible for the inhibition of KCNQ2/3 (KV7.2/7.3) potassium channels in single living tsA-201 cells. We measure DAG production and PKC
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20

Anta, Begoña, Carlos Martín-Rodríguez, Carolina Gomis-Perez, et al. "Ubiquitin-specific Protease 36 (USP36) Controls Neuronal Precursor Cell-expressed Developmentally Down-regulated 4-2 (Nedd4-2) Actions over the Neurotrophin Receptor TrkA and Potassium Voltage-gated Channels 7.2/3 (Kv7.2/3)." Journal of Biological Chemistry 291, no. 36 (2016): 19132–45. http://dx.doi.org/10.1074/jbc.m116.722637.

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21

Erdem, Fatma A. "Phosphorylation of KV7.2 regulates its PIP2 sensitivity." Intrinsic Activity 3, Suppl. 2 (2015): A2.21. http://dx.doi.org/10.25006/ia.3.s2-a2.21.

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22

Andersen, Martin N., Søren-Peter Olesen, and Hanne B. Rasmussen. "Kv7.1 surface expression is regulated by epithelial cell polarization." American Journal of Physiology-Cell Physiology 300, no. 4 (2011): C814—C824. http://dx.doi.org/10.1152/ajpcell.00390.2010.

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The potassium channel KV7.1 is expressed in the heart where it contributes to the repolarization of the cardiac action potential. In addition, KV7.1 is expressed in epithelial tissues where it plays a role in salt and water transport. Mutations in the kcnq1 gene can lead to long QT syndrome and deafness, and several mutations have been described as trafficking mutations. To learn more about the basic mechanisms that regulate KV7.1 surface expression, we have investigated the trafficking of KV7.1 during the polarization process of the epithelial cell line Madin-Darby Canine Kidney (MDCK) using
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23

Telezhkin, Vsevolod, Alison M. Thomas, Stephen C. Harmer, Andrew Tinker, and David A. Brown. "A basic residue in the proximal C-terminus is necessary for efficient activation of the M-channel subunit Kv7.2 by PI(4,5)P2." Pflügers Archiv - European Journal of Physiology 465, no. 7 (2013): 945–53. http://dx.doi.org/10.1007/s00424-012-1199-3.

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24

Andersen, Martin Nybo, Katarzyna Krzystanek, Frederic Petersen, et al. "A Phosphoinositide 3-Kinase (PI3K)-serum- and glucocorticoid-inducible Kinase 1 (SGK1) Pathway Promotes Kv7.1 Channel Surface Expression by Inhibiting Nedd4-2 Protein." Journal of Biological Chemistry 288, no. 52 (2013): 36841–54. http://dx.doi.org/10.1074/jbc.m113.525931.

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25

Dai, Shuiping, Duane D. Hall, and Johannes W. Hell. "Supramolecular Assemblies and Localized Regulation of Voltage-Gated Ion Channels." Physiological Reviews 89, no. 2 (2009): 411–52. http://dx.doi.org/10.1152/physrev.00029.2007.

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This review addresses the localized regulation of voltage-gated ion channels by phosphorylation. Comprehensive data on channel regulation by associated protein kinases, phosphatases, and related regulatory proteins are mainly available for voltage-gated Ca2+ channels, which form the main focus of this review. Other voltage-gated ion channels and especially Kv7.1-3 (KCNQ1-3), the large- and small-conductance Ca2+-activated K+ channels BK and SK2, and the inward-rectifying K+ channels Kir3 have also been studied to quite some extent and will be included. Regulation of the L-type Ca2+ channel Cav
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26

Amin, Ahmad S., John R. Giudicessi, Anke J. Tijsen, et al. "Variants in the 3′ untranslated region of the KCNQ1-encoded Kv7.1 potassium channel modify disease severity in patients with type 1 long QT syndrome in an allele-specific manner." European Heart Journal 33, no. 6 (2011): 714–23. http://dx.doi.org/10.1093/eurheartj/ehr473.

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27

Giudicessi, J. R., A. S. Amin, A. J. Tjisen, et al. "Modification of Disease Severity by Functional Variants in the 3′ Untranslated Region of the KCNQ1-Encoded Kv7.1 Channel is Most Pronounced in Patients Harboring Dominant-Negative LQT1-Causative Mutations." Heart Rhythm 8, no. 11 (2011): 1827. http://dx.doi.org/10.1016/j.hrthm.2011.09.050.

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28

Haick, Jennifer M., Lioubov I. Brueggemann, Leanne L. Cribbs, Mitchell F. Denning, Jeffrey Schwartz, and Kenneth L. Byron. "PKC-dependent regulation of Kv7.5 channels by the bronchoconstrictor histamine in human airway smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 6 (2017): L822—L834. http://dx.doi.org/10.1152/ajplung.00567.2016.

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Kv7 potassium channels have recently been found to be expressed and functionally important for relaxation of airway smooth muscle. Previous research suggests that native Kv7 currents are inhibited following treatment of freshly isolated airway smooth muscle cells with bronchoconstrictor agonists, and in intact airways inhibition of Kv7 channels is sufficient to induce bronchiolar constriction. However, the mechanism by which Kv7 currents are inhibited by bronchoconstrictor agonists has yet to be elucidated. In the present study, native Kv7 currents in cultured human trachealis smooth muscle ce
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29

Abbott, Geoffrey W., and Rían W. Manville. "Discovery of a potent, Kv7.3-selective potassium channel opener from a Polynesian traditional botanical anticonvulsant." Communications Chemistry 7, no. 1 (2024). http://dx.doi.org/10.1038/s42004-024-01318-9.

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AbstractPlants remain an important source of biologically active small molecules with high therapeutic potential. The voltage-gated potassium (Kv) channel formed by Kv7.2/3 (KCNQ2/3) heteromers is a major target for anticonvulsant drug development. Here, we screened 1444 extracts primarily from plants collected in California and the US Virgin Islands, for their ability to activate Kv7.2/3 but not inhibit Kv1.3, to select against tannic acid being the active component. We validated the 7 strongest hits, identified Thespesia populnea (miro, milo, portia tree) as the most promising, then discover
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30

Gaspar, Ingride Luzio, Gaetano Terrone, Giusy Carleo, et al. "Potassium current inactivation as a novel pathomechanism for KCNQ2 developmental and epileptic encephalopathy." Epilepsia, April 28, 2025. https://doi.org/10.1111/epi.18427.

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AbstractDe novo variants in KCNQ2 cause neonatal onset developmental and epileptic encephalopathy (KCNQ2‐DEE; Online Mendelian Inheritance in Man #613720), most often by loss‐of‐function in vitro effects. In this study, we describe a neonatal onset DEE proband carrying a recurrent de novo KCNQ2 variant (c.794C>T; p.A265V) affecting the pore domain of KCNQ2‐encoded Kv7.2 subunits. Whole‐cell patch‐clamp measurement in a mammalian heterologous expression system revealed that, when compared to wild‐type Kv7.2 channels, channels containing Kv7.2 A265V subunits displayed (1) reduced maximal curr
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31

Filareto, Ilaria, Ilaria Mosca, Elena Freri, et al. "Pharmacological approaches in drug-resistant pediatric epilepsies caused by pathogenic variants in potassium channel genes." Frontiers in Cellular Neuroscience 18 (January 24, 2025). https://doi.org/10.3389/fncel.2024.1512365.

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Variants in genes encoding for voltage-gated K+ (Kv) channels are frequent cause of drug-resistant pediatric epilepsies. Obtaining a molecular diagnosis gives the opportunity to assess the efficacy of pharmacological strategies based on in vitro features of mutant channels. In this retrospective observational study, we selected patients with drug-resistant pediatric epilepsies caused by variants in potassium channel encoding genes, followed at the Fondazione IRCCS Istituto Neurologico Carlo Besta of Milan, Italy. After the experimental characterization of variants’ functional properties in tra
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32

Raveh, Adi, Yefim Pen, Alon Silberman, et al. "Dual Kv7.2/3-TRPV1 modulators inhibit nociceptor hyperexcitability and alleviate pain without target-related side effects." Pain, September 24, 2024. http://dx.doi.org/10.1097/j.pain.0000000000003390.

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Abstract Persistent or chronic pain is the primary reason people seek medical care, yet current therapies are either limited in efficacy or cause intolerable side effects. Diverse mechanisms contribute to the basic phenomena of nociceptor hyperexcitability that initiates and maintains pain. Two prominent players in the modulation of nociceptor hyperexcitability are the transient receptor potential vanilloid type 1 (TRPV1) ligand-gated ion channel and the voltage-gated potassium channel, Kv7.2/3, that reciprocally regulate neuronal excitability. Across many drug development programs targeting e
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Sheng, Zhao-Fu, Hua Zhang, PeiRu Zheng, et al. "Impaired Kv7 channel activity in the central amygdala contributes to elevated sympathetic outflow in hypertension." Cardiovascular Research, February 14, 2021. http://dx.doi.org/10.1093/cvr/cvab031.

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Abstract Aims Elevated sympathetic outflow is associated with primary hypertension. However, the mechanisms involved in heightened sympathetic outflow in hypertension are unclear. The central amygdala (CeA) regulates autonomic components of emotions through projections to the brainstem. The neuronal Kv7 channel is a non-inactivating voltage-dependent K+ channel encoded by KCNQ2/3 genes involved in stabilizing the neuronal membrane potential and regulating neuronal excitability. In this study, we investigated if altered Kv7 channel activity in the CeA contributes to heightened sympathetic outfl
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Celentano, Camilla, Lidia Carotenuto, Francesco Miceli, et al. "Kv7 CHANNELS ACTIVATION REDUCES BRAIN ENDOTHELIAL CELLS PERMEABILITY AND PREVENTS KAINIC ACID INDUCED BLOOD BRAIN BARRIER DAMAGE." American Journal of Physiology-Cell Physiology, January 29, 2024. http://dx.doi.org/10.1152/ajpcell.00709.2023.

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Ion channels in the blood brain barrier (BBB) play a main role in controlling interstitial fluid composition and cerebral blood flow, and their dysfunction contributes to the disruption of the BBB occurring in many neurological diseases such as epilepsy. In this study, using morphological and functional approaches, we evaluated the expression and role in the BBB of Kv7 channels, a family of voltage-gated potassium channels including five members (Kv7.1-5) that play a major role in the regulation of cell excitability and transmembrane flux of potassium ions. Immunofluorescence experiments showe
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35

Varghese, Nissi, Bruno Moscoso, Ana Chavez, et al. "KCNQ2/3 Gain-of-Function Variants and Cell Excitability: Differential Effects in CA1 vs. L2/3 pyramidal neurons." Journal of Neuroscience, August 22, 2023, JN—RM—0980–23. http://dx.doi.org/10.1523/jneurosci.0980-23.2023.

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Gain-of-function pathogenic variants in the potassium channels KCNQ2 (KV7.2) and KCNQ3 (KV7.3) lead to hyperexcitability disorders such as epilepsy and autism spectrum disorders. However, the underlying cellular mechanisms of how these variants impair forebrain function are unclear. Here, we show that the R201C variant in KCNQ2 has opposite effects on the excitability of two types of mouse pyramidal neurons of either sex, causing hyperexcitability in layer 2/3 (L2/3) pyramidal neurons and hypoexcitability in CA1 pyramidal neurons. Similarly, the homologous R231C variant in KCNQ3 leads to hyper
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36

Li, Shuang, Bopanna I. Kalappa, and Thanos Tzounopoulos. "Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus." eLife 4 (August 27, 2015). http://dx.doi.org/10.7554/elife.07242.

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Vulnerability to noise-induced tinnitus is associated with increased spontaneous firing rate in dorsal cochlear nucleus principal neurons, fusiform cells. This hyperactivity is caused, at least in part, by decreased Kv7.2/3 (KCNQ2/3) potassium currents. However, the biophysical mechanisms underlying resilience to tinnitus, which is observed in noise-exposed mice that do not develop tinnitus (non-tinnitus mice), remain unknown. Our results show that noise exposure induces, on average, a reduction in KCNQ2/3 channel activity in fusiform cells in noise-exposed mice by 4 days after exposure. Tinni
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37

Perez-Vizcaino, Francisco, Angel Cogolludo, and Gema Mondejar-Parreño. "Transcriptomic profile of cationic channels in human pulmonary arterial hypertension." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-95196-z.

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AbstractThe dysregulation of K+ channels is a hallmark of pulmonary arterial hypertension (PAH). Herein, the channelome was analyzed in lungs of patients with PAH in a public transcriptomic database. Sixty six (46%) mRNA encoding cationic channels were dysregulated in PAH with most of them downregulated (83%). The principal component analysis indicated that dysregulated cationic channel expression is a signature of the disease. Changes were very similar in idiopathic, connective tissue disease and congenital heart disease associated PAH. This analysis 1) is in agreement with the widely recogni
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38

Tracy, Gregory C., Angelina R. Wilton, Justin S. Rhodes, and Hee Jung Chung. "Heterozygous Deletion of Epilepsy Gene KCNQ2 Has Negligible Effects on Learning and Memory." Frontiers in Behavioral Neuroscience 16 (July 19, 2022). http://dx.doi.org/10.3389/fnbeh.2022.930216.

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Neuronal Kv7/Potassium Voltage-Gated Channel Subfamily Q (KCNQ) potassium channels underlie M-current that potently suppresses repetitive and burst firing of action potentials (APs). They are mostly heterotetramers of Kv7.2 and Kv7.3 subunits in the hippocampus and cortex, the brain regions important for cognition and behavior. Underscoring their critical roles in inhibiting neuronal excitability, autosomal dominantly inherited mutations in Potassium Voltage-Gated Channel Subfamily Q Member 2 (KCNQ2) and Potassium Voltage-Gated Channel Subfamily Q Member 3 (KCNQ3) genes are associated with ben
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39

Li, De-Pei, Zhao-Fu Sheng, Hua Zhang, and Peiru Zheng. "Dysfunction of M channels in the insular cortex is involved in pathogenesis of primary hypertension." Physiology 39, S1 (2024). http://dx.doi.org/10.1152/physiol.2024.39.s1.1993.

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Heightened sympathetic nerve activity is critically involved in the pathogenesis of primary hypertension. However, the sources driving increased sympathetic vasomotor tone remain unclear. The posterior insular cortex (PIC) is a brain region involved in regulating blood pressure and sympathetic tone. Neurons in the PIC project to the rostral ventrolateral medulla (RVLM), a key brain stem region in regulating sympathetic nerve activity and blood pressure. The non-inactivating voltage-dependent K+ channels, M channels (Kv7/KCNQ channel family) encoded by KCNQ2/3 genes, play a unique role in stabi
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40

French, Jacqueline A., Roger J. Porter, Emilio Perucca, et al. "Efficacy and Safety of XEN1101, a Novel Potassium Channel Opener, in Adults With Focal Epilepsy." JAMA Neurology, October 9, 2023. http://dx.doi.org/10.1001/jamaneurol.2023.3542.

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ImportanceMany patients with focal epilepsy experience seizures despite treatment with currently available antiseizure medications (ASMs) and may benefit from novel therapeutics.ObjectiveTo evaluate the efficacy and safety of XEN1101, a novel small-molecule selective Kv7.2/Kv7.3 potassium channel opener, in the treatment of focal-onset seizures (FOSs).Design, Setting, and ParticipantsThis phase 2b, randomized, double-blind, placebo-controlled, parallel-group, dose-ranging adjunctive trial investigated XEN1101 over an 8-week treatment period from January 30, 2019, to September 2, 2021, and incl
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41

Pant, Shashank, Jiaren Zhang, Eung Chang Kim, Kin Lam, Hee Jung Chung, and Emad Tajkhorshid. "PIP2-dependent coupling of voltage sensor and pore domains in Kv7.2 channel." Communications Biology 4, no. 1 (2021). http://dx.doi.org/10.1038/s42003-021-02729-3.

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AbstractPhosphatidylinositol-4,5-bisphosphate (PIP2) is a signaling lipid which regulates voltage-gated Kv7/KCNQ potassium channels. Altered PIP2 sensitivity of neuronal Kv7.2 channel is involved in KCNQ2 epileptic encephalopathy. However, the molecular action of PIP2 on Kv7.2 gating remains largely elusive. Here, we use molecular dynamics simulations and electrophysiology to characterize PIP2 binding sites in a human Kv7.2 channel. In the closed state, PIP2 localizes to the periphery of the voltage-sensing domain (VSD). In the open state, PIP2 binds to 4 distinct interfaces formed by the cyto
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42

Pant, Shashank, Jiaren Zhang, Eung Chang Kim, Kin Lam, Hee Jung Chung, and Emad Tajkhorshid. "PIP2-dependent coupling of voltage sensor and pore domains in Kv7.2 channel." Communications Biology 4, no. 1 (2021). http://dx.doi.org/10.1038/s42003-021-02729-3.

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AbstractPhosphatidylinositol-4,5-bisphosphate (PIP2) is a signaling lipid which regulates voltage-gated Kv7/KCNQ potassium channels. Altered PIP2 sensitivity of neuronal Kv7.2 channel is involved in KCNQ2 epileptic encephalopathy. However, the molecular action of PIP2 on Kv7.2 gating remains largely elusive. Here, we use molecular dynamics simulations and electrophysiology to characterize PIP2 binding sites in a human Kv7.2 channel. In the closed state, PIP2 localizes to the periphery of the voltage-sensing domain (VSD). In the open state, PIP2 binds to 4 distinct interfaces formed by the cyto
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43

Klemz, Alexander, Florian Wildner, Ecem Tütüncü, and Zoltan Gerevich. "Regulation of Hippocampal Gamma Oscillations by Modulation of Intrinsic Neuronal Excitability." Frontiers in Neural Circuits 15 (January 26, 2022). http://dx.doi.org/10.3389/fncir.2021.778022.

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Ion channels activated around the subthreshold membrane potential determine the likelihood of neuronal firing in response to synaptic inputs, a process described as intrinsic neuronal excitability. Long-term plasticity of chemical synaptic transmission is traditionally considered the main cellular mechanism of information storage in the brain; however, voltage- and calcium-activated channels modulating the inputs or outputs of neurons are also subjects of plastic changes and play a major role in learning and memory formation. Gamma oscillations are associated with numerous higher cognitive fun
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44

Yang, Gui-mei, Fu-yun Tian, Yan-wen Shen, et al. "Functional characterization and in vitro pharmacological rescue of KCNQ2 pore mutations associated with epileptic encephalopathy." Acta Pharmacologica Sinica, March 17, 2023. http://dx.doi.org/10.1038/s41401-023-01073-y.

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AbstractMutations in the KCNQ2 gene encoding KV7.2 subunit that mediates neuronal M-current cause a severe form of developmental and epileptic encephalopathy (DEE). Electrophysiological evaluation of KCNQ2 mutations has been proved clinically useful in improving outcome prediction and choosing rational anti-seizure medications (ASMs). In this study we described the clinical characteristics, electrophysiological phenotypes and the in vitro response to KCNQ openers of five KCNQ2 pore mutations (V250A, N258Y, H260P, A265T and G290S) from seven patients diagnosed with KCNQ2-DEE. The KCNQ2 variants
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45

Bialer, Meir, Svein I. Johannessen, Matthias J. Koepp, et al. "Progress report on new medications for seizures and epilepsy: A summary of the 17th Eilat Conference on New Antiepileptic Drugs and Devices (EILAT XVII). I. Drugs in preclinical and early clinical development." Epilepsia, July 15, 2024. http://dx.doi.org/10.1111/epi.18056.

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AbstractFor >30 years, the Eilat Conference on New Antiepileptic Drugs and Devices has provided a forum for the discussion of advances in the development of new therapies for seizures and epilepsy. The EILAT XVII conference took place in Madrid, Spain, on May 5–8, 2024. Participants included basic scientists and clinical investigators from industry and academia, other health care professionals, and representatives from lay organizations. We summarize in this article information on treatments in preclinical and in early clinical development discussed at the conference. These include AMT‐260,
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46

JULIANA, CHRISTINE, and DIVA DE LEON. "1745-P: Voltage-Gated K+ Channel Kv7.1 Is an Important Regulator of Insulin Secretion in Normal and Hyperinsulinemic Islets." Diabetes 72, Supplement_1 (2023). http://dx.doi.org/10.2337/db23-1745-p.

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Fifty percent of infants with Beckwith-Wiedemann syndrome (BWS), an overgrowth syndrome caused by genetic / epigenetic abnormalities in imprinted genes on chromosome 11p15, have persistent hypoglycemia due to hyperinsulinism (BWS-HI). BWS-HI islets exhibit increased baseline and glucose-stimulated insulin secretion (GSIS) and are responsive to the KATP channel inhibitor glyburide, suggesting it is not caused by impaired KATP channels. KCNQ1 expression, encoding the pore-forming α subunit of voltage-gated K+ channel Kv7.1, is reduced in BWS-HI islets compared to normal islets (3-fold; p = 4.5×1
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47

De Wachter, Matthias, Charissa Millevert, Joost Nicolai, et al. "Amitriptyline use in individuals with KCNQ2/3 gain‐of‐function variants: A retrospective cohort study." Epilepsia, February 17, 2025. https://doi.org/10.1111/epi.18310.

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AbstractObjectiveHeterozygous gain‐of‐function (GOF) variants in KCNQ2 and KCNQ3, encoding the voltage‐gated potassium channel subunits Kv7.2 and Kv7.3, lead to neurodevelopmental disorders for which no established treatments are available. Amitriptyline, an antidepressant, blocks Kv7.2/Kv7.3 and has previously been reported to be effective in a single individual with a KCNQ2 GOF variant. We designed a retrospective, single‐arm, multicenter study to investigate the effects of amitriptyline in a real‐world setting.MethodsWe used a 7‐point Likert scale to measure seizure frequency, clinical exam
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48

Trancuccio, A., A. Mazzanti, D. Kukavica, et al. "Mutation site-specific risk profile in patients with Type 1 Long QT Syndrome." European Heart Journal 41, Supplement_2 (2020). http://dx.doi.org/10.1093/ehjci/ehaa946.0743.

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Abstract Background Type 1 Long QT Syndrome (LQT1) is an arrhythmogenic disorder, caused by loss-of-function mutations on KCNQ1 gene, coding for Kv7.1 potassium channel. Although LQT1 is described as the most benign form of LQTS, patients still experience arrhythmic events and there is an unmet need for personalized risk stratification. Attempts have been made to correlate the location of mutations with outcome, but the results are unequivocal. Purpose We provide in the present study a new mutation site-specific risk profile obtained from a large cohort of LQT1 patients. Methods We gathered da
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Liao, Qian-Qian, Qing-Qing Dong, Hui Zhang, Hua-Pan Shu, Yu-Chi Tu, and Li-Jun Yao. "Contributions of SGK3 to transporter-related diseases." Frontiers in Cell and Developmental Biology 10 (December 1, 2022). http://dx.doi.org/10.3389/fcell.2022.1007924.

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Serum- and glucocorticoid-induced kinase 3 (SGK3), which is ubiquitously expressed in mammals, is regulated by estrogens and androgens. SGK3 is activated by insulin and growth factors through signaling pathways involving phosphatidylinositol-3-kinase (PI3K), 3-phosphoinositide-dependent kinase-1 (PDK-1), and mammalian target of rapamycin complex 2 (mTORC2). Activated SGK3 can activate ion channels (TRPV5/6, SOC, Kv1.3, Kv1.5, Kv7.1, BKCa, Kir2.1, Kir2.2, ENaC, Nav1.5, ClC-2, and ClC Ka), carriers and receptors (Npt2a, Npt2b, NHE3, GluR1, GluR6, SN1, EAAT1, EAAT2, EAAT4, EAAT5, SGLT1, SLC1A5, S
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50

Svecova, O., R. Kula, L. Chmelikova, et al. "Clinical, genetic and functional analysis of R562S-Kv7.1 mutation associated with long QT syndrome type 1." EP Europace 23, Supplement_3 (2021). http://dx.doi.org/10.1093/europace/euab116.560.

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Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): Ministry of Education, Youth and Sports of the Czech Republic Introduction Loss-of-function variants of the KCNQ1 gene are associated with life-threatening arrhythmogenic long QT syndrome type 1 (LQT1). This gene encodes structure of the slow delayed rectifier potassium channel (IKs). Some functional characteristics of the C-terminal KCNQ1 variant c.1686G > C (p.R562S) have been recently described [1]. However, accumulation of the current under beta-adrenergic stimulation, essential
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