Sodium channel slow inactivation interferes with open channel block
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/srep25974.pdf
Reference44 articles.
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2. Eberhardt, M. et al. Inherited pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation. J Biol Chem 289, 1971–1980 (2014).
3. Emery, E. C. et al. Novel SCN9A mutations underlying extreme pain phenotypes: unexpected electrophysiological and clinical phenotype correlations. J Neurosci 35, 7674–7681 (2015).
4. Lampert, A., O’Reilly, A. O., Reeh, P. & Leffler, A. Sodium channelopathies and pain. Pflugers Arch 460, 249–263 (2010).
5. Estacion, M. et al. NaV1.7 gain-of-function mutations as a continuum: A1632E displays physiological changes associated with erythromelalgia and paroxysmal extreme pain disorder mutations and produces symptoms of both disorders. J Neurosci 28, 11079–11088 (2008).
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