Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navβ4 peptide-mediated resurgent sodium currents

Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents

(2010) Brian W. Jarecki et al.   JOURNAL OF CLINICAL INVESTIGATION

Control of transient, resurgent, and persistent current by open-channel block by Na channel  4 in cultured cerebellar granule neurons

(2010) J. S. Bant et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Subtype-selective targeting of voltage-gated sodium channels

(2009) Steve England et al.   BRITISH JOURNAL OF PHARMACOLOGY

Regulation of Persistent Na Current by Interactions between   Subunits of Voltage-Gated Na Channels

(2009) T. K. Aman et al.   JOURNAL OF NEUROSCIENCE

Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation

(2008) Brian W. Jarecki et al.   JOURNAL OF PHYSIOLOGY-LONDON

Functional properties and differential neuromodulation of Nav1.6 channels

(2008) Yuan Chen et al.   MOLECULAR AND CELLULAR NEUROSCIENCE

Paroxysmal Extreme Pain Disorder M1627K Mutation in Human Nav1.7 Renders DRG Neurons Hyperexcitable

(2008) Sulayman D Dib-Hajj et al.   Molecular Pain