Relevant bibliographies by topics / Kv7.2/3

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

Author: Grafiati
Published: 7 July 2024
Last updated: 19 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 hamster ovary cells were transiently transfected with Kv7 subunits and M1 receptors and studied under perforated-patch voltage clamp. For Kv7.2/7.3 heteromers, the EC50 for current suppression was 0.44 ± 0.08 µM, and the maximal inhibition (Inhibmax) was 74 ± 3% (n = 5–7). When tonic PIP2 abundance was increased by overexpression of PIP 5-kinase, the EC50 was shifted threefold to the right (1.2 ± 0.1 µM), but without a significant change in Inhibmax (73 ± 4%, n = 5). To investigate the muscarinic sensitivity of Kv7.3 homomers, we used the A315T pore mutant (Kv7.3T) that increases whole-cell currents by 30-fold without any change in apparent PIP2 affinity. Kv7.3T currents had a slightly right-shifted EC50 as compared with Kv7.2/7.3 heteromers (1.0 ± 0.8 µM) and a strongly reduced Inhibmax (39 ± 3%). In contrast, the dose–response curve of homomeric Kv7.4 channels was shifted considerably to the left (66 ± 8 nM), and Inhibmax was slightly increased (81 ± 6%, n = 3–4). We then studied several Kv7.2 mutants with altered apparent affinities for PIP2 by coexpressing them with Kv7.3T subunits to boost current amplitudes. For the lower affinity (Kv7.2 (R463Q)/Kv7.3T) or higher affinity (Kv7.2 (R463E)/Kv7.3T) channels, the EC50 and Inhibmax were similar to Kv7.4 or Kv7.3T homomers (0.12 ± 0.08 µM and 79 ± 6% [n = 3–4] and 0.58 ± 0.07 µM and 27 ± 3% [n = 3–4], respectively). The very low-affinity Kv7.2 (R452E, R459E, and R461E) triple mutant was also coexpressed with Kv7.3T. The resulting heteromer displayed a very low EC50 for inhibition (32 ± 8 nM) and a slightly increased Inhibmax (83 ± 3%, n = 3–4). We then constructed a cellular model that incorporates PLC activation by oxo-M, PIP2 hydrolysis, PIP2 binding to Kv7-channel subunits, and K+ current through Kv7 tetramers. We were able to fully reproduce our data and extract a consistent set of PIP2 affinities.
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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 different chemotypes, and highlighting their pharmacodynamic and, whenever possible, pharmacokinetic peculiarities. <p> Methods: The present work is based on an in-depth search of the currently available scientific literature, and on our own experience and knowledge in the field of neuronal Kv7 channel pharmacology. Space limitations impeded to describe the full pharmacological potential of Kv7 channels; thus, we have chosen to focus on neuronal channels composed of Kv7.2 and Kv7.3 subunits, and to mainly concentrate on their involvement in epilepsy. <p> Results: An astonishing heterogeneity in the molecular scaffolds exploitable to develop Kv7.2/3 modulators is evident, with important structural/functional peculiarities of distinct compound classes. <p> Conclusion: In the present work we have attempted to show the current status and growing potential of the Kv7 pharmacology field. We anticipate a bright future for the field, and express our hopes that the efforts herein reviewed will result in an improved treatment of hyperexcitability (or any other) diseases.
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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 μM) by causing a hyperpolarizing shift of the voltage activation curve and by markedly slowing the deactivation kinetics. Activation of native M-currents by NH6 robustly reduced the number of evoked and spontaneous action potentials in cultured cortical, hippocampal and dorsal root ganglion neurons. In hippocampal slices, NH6 decreased somatically evoked spike afterdepolarization of CA1 pyramidal neurons and induced regular firing in bursting neurons. Activation of M-channels by NH6, potently reduced the frequency of spontaneous excitatory and inhibitory postsynaptic currents. Activation of M-channels also decreased the frequency of miniature excitatory (mEPSC) and inhibitory (mIPSC) postsynaptic currents without affecting their amplitude and waveform, thus suggesting that M-channels presynaptically inhibit glutamate and GABA release. Our results suggest a role of presynaptic M-channels in the release of glutamate and GABA. They also indicate that M-channels act pre- and postsynaptically to dampen neuronal excitability.
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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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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 chronicisation des douleurs neuropathiques. Récemment, une nouvelle classe de molécules, GRT-X, ciblant à la fois la TSPO et les Kv7.2/3, a été développée par la compagnie pharmaceutique Grünenthal. Le but de cette thèse est d'étudier le rôle du GRT-X dans la poussée axonale. Cette preuve de concept a été effectuée sur des cultures d'explants et des cultures dissociées de ganglions spinaux embryonnaires (ou Dorsal Root Ganglia, DRG) à E13.5 provenant soit de souris C57BL6/J, soit de souris TSPO-KO. Des études microscopiques, moléculaires et cinétiques ont été réalisées, et les effets du GRT-X ont été comparés à ceux d'autres molécules : étifoxine (agoniste de la TSPO), XBD173 (agoniste de la TSPO), ICA-27243 (agoniste des Kv7.2/3) et XE991 (antagoniste des Kv7.2/3) dans les deux modèles expérimentaux. Les résultats montrent que le GRT-X a un effet positif sur la poussée axonale. Cet effet est plus important que celui des autres groupes et est maintenu aux différents moments et aux différentes doses testées. De plus, le GRT-X induit une augmentation de l'expression des gènes impliqués dans le développement, la myélinisation et la poussée axonale par rapport aux autres groupes. Les mêmes expériences réalisées sur les DRG embryonnaires TSPO-KO montrent une diminution de l'efficacité du GRT-X. Ces résultats montrent l'implication du GRT-X dans la poussée axonale qui est liée à son double mode d'action (TSPO et Kv7.2/3). Ainsi, le GRT-X serait une cible prometteuse pour le traitement de lésions du système nerveux périphérique en favorisant la poussée axonale par liaison à la TSPO, mais aussi en diminuant la douleur en se liant aux Kv7.2/3 qui régulent l'hyperexcitabilité neuronale<br>While adult peripheral nerves retain the ability to regenerate, functional restoration is often unsatisfactory in cases of traumatic injury or peripheral neuropathy. Furthermore, poor recovery is frequently associated with the development of chronic neuropathic pain. The mitochondrial translocator protein (TSPO, 18 kDa) and the voltage-dependent Kv7.2/3 potassium channels (KCQN2/3) represent two promising targets for enhancing peripheral nerve regeneration, promoting functional recovery, and preventing the chronicization of neuropathic pain. Recently, a novel class of molecules, GRT-X, that targets both TSPO and Kv7.2/3 has been developed by the pharmaceutical company Grünenthal. The objective of this thesis is to investigate the role of GRT-X in axonal growth. This proof-of-concept study was conducted using explant and dissociated cultures of embryonic dorsal root ganglia (DRG) at E13.5 from either C57BL6/J or TSPO-KO mice. Microscopic, molecular, and kinetic studies were performed, and the effects of GRT-X were compared with those of other molecules: etifoxine (a TSPO agonist), XBD173 (a TSPO agonist), ICA-27243 (a Kv7.2/3 agonist), and XE991 (a Kv7.2/3 antagonist) in both experimental models. Our data demonstrates that GRT-X exerts a positive influence on axonal growth. This effect surpasses that of the other molecules and is sustained at various tested time points and doses. Furthermore, GRT-X elevates the expression levels of genes involved in development, myelination, and axonal growth in comparison to the other groups. In parallel, the same experiments conducted on TSPO-KO embryonic DRGs reveal a reduced efficacy of GRT-X. These findings highlight the involvement of GRT-X in axonal growth, attributed to its dual mode of action (TSPO and Kv7.2/3). Therefore, GRT-X holds promise as a potential target for the treatment of lesions affecting the peripheral nervous system by promoting axonal growth via TSPO binding and concurrently reducing pain through its interaction with Kv7.2/3, which regulate neuronal hyperexcitability
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