Gotowa bibliografia na temat „Kv7.2/3”
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Artykuły w czasopismach na temat "Kv7.2/3"
Hernandez, Ciria C., Björn Falkenburger i Mark S. Shapiro. "Affinity for phosphatidylinositol 4,5-bisphosphate determines muscarinic agonist sensitivity of Kv7 K+ channels". Journal of General Physiology 134, nr 5 (26.10.2009): 437–48. http://dx.doi.org/10.1085/jgp.200910313.
Pełny tekst źródłaMiceli, Francesco, Maria V. Soldovieri, Paolo Ambrosino, Laura Manocchio, Ilaria Mosca i Maurizio Taglialatela. "Pharmacological Targeting of Neuronal Kv7.2/3 Channels: A Focus on Chemotypes and Receptor Sites". Current Medicinal Chemistry 25, nr 23 (4.07.2018): 2637–60. http://dx.doi.org/10.2174/0929867324666171012122852.
Pełny tekst źródłaPeretz, Asher, Anton Sheinin, Cuiyong Yue, Nurit Degani-Katzav, Gilad Gibor, Rachel Nachman, Anna Gopin i in. "Pre- and Postsynaptic Activation of M-Channels By a Novel Opener Dampens Neuronal Firing and Transmitter Release". Journal of Neurophysiology 97, nr 1 (styczeń 2007): 283–95. http://dx.doi.org/10.1152/jn.00634.2006.
Pełny tekst źródłaWright, Andrew B., Khrystyna Yu Sukhanova i Keith S. Elmslie. "KV7 channels are potential regulators of the exercise pressor reflex". Journal of Neurophysiology 126, nr 1 (1.07.2021): 1–10. http://dx.doi.org/10.1152/jn.00700.2020.
Pełny tekst źródłaBarro-Soria, Rene. "Effects of small molecules on neurodevelopmental disorder-associated Kv7.2/3 mutations". Biophysical Journal 123, nr 3 (luty 2024): 528a. http://dx.doi.org/10.1016/j.bpj.2023.11.3192.
Pełny tekst źródłaPeretz, Asher S., Eti Patrich, Polina Kornilov, Nataly Menaker i Bernard Attali. "A Novel Compound Targeting Kv7.2/3 Channels Relieves Inflammatory and Neuropathic Pain". Biophysical Journal 106, nr 2 (styczeń 2014): 141a. http://dx.doi.org/10.1016/j.bpj.2013.11.820.
Pełny tekst źródłaLiu, Wenjing, i 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 (styczeń 2014): 40–52. http://dx.doi.org/10.1016/j.mcn.2013.12.005.
Pełny tekst źródłaSurur, Abdrrahman S., Christian Bock, Kristin Beirow, Konrad Wurm, Lukas Schulig, Markus K. Kindermann, Werner Siegmund, Patrick J. Bednarski i Andreas Link. "Flupirtine and retigabine as templates for ligand-based drug design of KV7.2/3 activators". Organic & Biomolecular Chemistry 17, nr 18 (2019): 4512–22. http://dx.doi.org/10.1039/c9ob00511k.
Pełny tekst źródłaLi, S., V. Choi i 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, nr 24 (28.05.2013): 9980–85. http://dx.doi.org/10.1073/pnas.1302770110.
Pełny tekst źródłaMiranda, Pablo, Alba Cadaveira-Mosquera, Rafaela Gonzalez-Montelongo, Alvaro Villarroel, Jose Antonio Lamas, Diego Alvarez de la Rosa i Teresa Giraldez. "Regulation of the Kv7.2/3 Channels by the Neuronal Serum-and Gluococorticoids-Regulated Kinase 1.1". Biophysical Journal 104, nr 2 (styczeń 2013): 268a. http://dx.doi.org/10.1016/j.bpj.2012.11.1505.
Pełny tekst źródłaRozprawy doktorskie na temat "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.
Pełny tekst źródłaWhile 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