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Title
Inherited Pain
Authors
Keywords
-
Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 289, Issue 4, Pages 1971-1980
Publisher
American Society for Biochemistry & Molecular Biology (ASBMB)
Online
2013-12-06
DOI
10.1074/jbc.m113.502211
References
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Related references
Note: Only part of the references are listed.- Two Alternative Conformations of a Voltage-Gated Sodium Channel
- (2013) Ching-Ju Tsai et al. JOURNAL OF MOLECULAR BIOLOGY
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- (2013) Min-Tzu Wu et al. PLoS One
- Small nerve fibres, small hands and small feet: a new syndrome of pain, dysautonomia and acromesomelia in a kindred with a novel NaV1.7 mutation
- (2012) Janneke G. J. Hoeijmakers et al. BRAIN
- Deletion mutation of sodium channel NaV1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability
- (2011) X. Cheng et al. BRAIN
- Inhibition of Nav 4 Peptide-Mediated Resurgent Sodium Currents in Nav1.7 Channels by Carbamazepine, Riluzole, and Anandamide
- (2011) J. W. Theile et al. MOLECULAR PHARMACOLOGY
- The crystal structure of a voltage-gated sodium channel
- (2011) Jian Payandeh et al. NATURE
- Alternative splicing may contribute to time-dependent manifestation of inherited erythromelalgia
- (2010) Jin-Sung Choi et al. BRAIN
- A new Nav1.7 sodium channel mutation I234T in a child with severe pain
- (2010) Hye-Sook Ahn et al. EUROPEAN JOURNAL OF PAIN
- 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
- Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navβ4 peptide-mediated resurgent sodium currents
- (2010) Jonathan W. Theile et al. JOURNAL OF PHYSIOLOGY-LONDON
- Sodium channelopathies and pain
- (2010) Angelika Lampert et al. PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
- Voltage-clamp and current-clamp recordings from mammalian DRG neurons
- (2009) Theodore R Cummins et al. Nature Protocols
- 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
- (2008) M. Estacion 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
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