Literatura científica selecionada sobre o tema "Kv7.2/3"
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Artigos de revistas sobre o assunto "Kv7.2/3"
Hernandez, Ciria C., Björn Falkenburger e Mark S. Shapiro. "Affinity for phosphatidylinositol 4,5-bisphosphate determines muscarinic agonist sensitivity of Kv7 K+ channels". Journal of General Physiology 134, n.º 5 (26 de outubro de 2009): 437–48. http://dx.doi.org/10.1085/jgp.200910313.
Texto completo da fonteMiceli, Francesco, Maria V. Soldovieri, Paolo Ambrosino, Laura Manocchio, Ilaria Mosca e Maurizio Taglialatela. "Pharmacological Targeting of Neuronal Kv7.2/3 Channels: A Focus on Chemotypes and Receptor Sites". Current Medicinal Chemistry 25, n.º 23 (4 de julho de 2018): 2637–60. http://dx.doi.org/10.2174/0929867324666171012122852.
Texto completo da fontePeretz, Asher, Anton Sheinin, Cuiyong Yue, Nurit Degani-Katzav, Gilad Gibor, Rachel Nachman, Anna Gopin et al. "Pre- and Postsynaptic Activation of M-Channels By a Novel Opener Dampens Neuronal Firing and Transmitter Release". Journal of Neurophysiology 97, n.º 1 (janeiro de 2007): 283–95. http://dx.doi.org/10.1152/jn.00634.2006.
Texto completo da fonteWright, Andrew B., Khrystyna Yu Sukhanova e Keith S. Elmslie. "KV7 channels are potential regulators of the exercise pressor reflex". Journal of Neurophysiology 126, n.º 1 (1 de julho de 2021): 1–10. http://dx.doi.org/10.1152/jn.00700.2020.
Texto completo da fonteBarro-Soria, Rene. "Effects of small molecules on neurodevelopmental disorder-associated Kv7.2/3 mutations". Biophysical Journal 123, n.º 3 (fevereiro de 2024): 528a. http://dx.doi.org/10.1016/j.bpj.2023.11.3192.
Texto completo da fontePeretz, Asher S., Eti Patrich, Polina Kornilov, Nataly Menaker e Bernard Attali. "A Novel Compound Targeting Kv7.2/3 Channels Relieves Inflammatory and Neuropathic Pain". Biophysical Journal 106, n.º 2 (janeiro de 2014): 141a. http://dx.doi.org/10.1016/j.bpj.2013.11.820.
Texto completo da fonteLiu, Wenjing, e 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 (janeiro de 2014): 40–52. http://dx.doi.org/10.1016/j.mcn.2013.12.005.
Texto completo da fonteSurur, Abdrrahman S., Christian Bock, Kristin Beirow, Konrad Wurm, Lukas Schulig, Markus K. Kindermann, Werner Siegmund, Patrick J. Bednarski e Andreas Link. "Flupirtine and retigabine as templates for ligand-based drug design of KV7.2/3 activators". Organic & Biomolecular Chemistry 17, n.º 18 (2019): 4512–22. http://dx.doi.org/10.1039/c9ob00511k.
Texto completo da fonteLi, S., V. Choi e 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, n.º 24 (28 de maio de 2013): 9980–85. http://dx.doi.org/10.1073/pnas.1302770110.
Texto completo da fonteMiranda, Pablo, Alba Cadaveira-Mosquera, Rafaela Gonzalez-Montelongo, Alvaro Villarroel, Jose Antonio Lamas, Diego Alvarez de la Rosa e Teresa Giraldez. "Regulation of the Kv7.2/3 Channels by the Neuronal Serum-and Gluococorticoids-Regulated Kinase 1.1". Biophysical Journal 104, n.º 2 (janeiro de 2013): 268a. http://dx.doi.org/10.1016/j.bpj.2012.11.1505.
Texto completo da fonteTeses / dissertações sobre o assunto "Kv7.2/3"
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.
Texto completo da fonteWhile 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