NaV1.4 DI-S4 periodic paralysis mutation R222W enhances inactivation and promotes leak current to attenuate action potentials and depolarize muscle fibers

Author:

Bayless-Edwards Landon,Winston Vern,Lehmann-Horn Frank,Arinze Paula,Groome James R.,Jurkat-Rott Karin

Funder

U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke

U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences

German DGM Disease Society Taro Pharmaceuticals German BMBF Ministry for the IonNeurOnet project

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

Reference43 articles.

1. Jurkat-Rott, K., Groome, J. R. & Lehmann-Horn, F. Pathophysiological role of omega pore current in channelopathies. Front. Neuropharmacol. 3, 1–15 (2012).

2. Cannon, S. C. Channelopathies of skeletal muscle excitability. Compr. Physiol. 5, 761–90 (2015).

3. Cheng, C.-J., Kuo, E. & Huang, C.-L. Extracellular potassium homeostasis: insights from hypokalemic periodic paralysis. Semin. Nephrol. 33, 237–247 (2013).

4. Groome, J. R., Moreau, A. & Delemotte, L. Gating pore currents in sodium channels. In: Handbook of Experimental Pharmacology: Sodium channels and related disorders (ed. Chahine, M.) (Springer, Berlin, Heidelberg) (2017).

5. Rudel, R., Lehmann-Horn, F., Ricker, K. & Kuther, G. Hypokalemic periodic paralysis: in vitro investigation of muscle fiber membrane parameters. Muscle Nerve 7, 110–120 (1984).

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