Nav1.7 is the Predominant Sodium Channel in Rodent Olfactory Sensory Neurons
Published 2011 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Nav1.7 is the Predominant Sodium Channel in Rodent Olfactory Sensory Neurons
Authors
Keywords
-
Journal
Molecular Pain
Volume 7, Issue -, Pages 1744-8069-7-32
Publisher
SAGE Publications
Online
2011-05-12
DOI
10.1186/1744-8069-7-32
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Loss-of-function mutations in sodium channel Nav1.7 cause anosmia
- (2011) Jan Weiss et al. NATURE
- Sodium Channels in Normal and Pathological Pain
- (2010) Sulayman D. Dib-Hajj et al. Annual Review of Neuroscience
- 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
- Two novel mutations of SCN9A (Nav1.7) are associated with partial congenital insensitivity to pain
- (2010) Roland Staudl 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
- ERK1/2 Mitogen-Activated Protein Kinase Phosphorylates Sodium Channel Nav1.7 and Alters Its Gating Properties
- (2010) S. Stamboulian et al. JOURNAL OF NEUROSCIENCE
- Signaling by olfactory receptor neurons near threshold
- (2010) V. Bhandawat et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Early- and late-onset inherited erythromelalgia: genotype–phenotype correlation
- (2009) Chongyang Han et al. BRAIN
- Mexiletine-responsive erythromelalgia due to a new Nav1.7 mutation showing use-dependent current fall-off
- (2009) Jin-Sung Choi et al. EXPERIMENTAL NEUROLOGY
- The ataxia3 Mutation in the N-Terminal Cytoplasmic Domain of Sodium Channel Nav1.6 Disrupts Intracellular Trafficking
- (2009) L. M. Sharkey et al. JOURNAL OF NEUROSCIENCE
- Two novel SCN9A mutations causing insensitivity to pain
- (2009) K. B. Nilsen et al. PAIN
- Adult neurogenesis and the olfactory system
- (2009) Mary C. Whitman et al. PROGRESS IN NEUROBIOLOGY
- Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas
- (2008) Joel A. Black et al. ANNALS OF NEUROLOGY
- 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
- Voltage-gated sodium channel expression in rat and human epidermal keratinocytes: Evidence for a role in pain
- (2008) Peng Zhao et al. PAIN
Discover Peeref hubs
Discuss science. Find collaborators. Network.
Join a conversationPublish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn More