Relevant bibliographies by topics / Kv7.2/3

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Kv7.2/3'

Author: Grafiati
Published: 7 July 2024
Last updated: 31 July 2025

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

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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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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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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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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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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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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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Dissertations / Theses on the topic "Kv7.2/3"

1

El, Chemali Léa. "Effets neuroprotecteurs et neurorégénérateurs d'un nouveau ligand de TSPO et des canaux potassiques Kv7.2/3 dans le système nerveux périphérique." Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL141.

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Bien que les nerfs périphériques adultes conservent la capacité de se régénérer, la restauration fonctionnelle reste souvent décevante en cas de lésions traumatiques ou de neuropathies périphériques. De plus, une mauvaise récupération est souvent associée au développement de douleurs neuropathiques chroniques. La protéine translocatrice mitochondriale (protéine de translocation, TSPO, 18 kDa) et les canaux potassiques Kv7.2/3 (KCQN2/3) voltage-dépendants sont deux cibles prometteuses pour favoriser la régénération des nerfs périphériques et la récupération fonctionnelle, et pour prévenir la ch
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Journal articles
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