Related references
Note: Only part of the references are listed.Sodium Channels in Human Pain Disorders: Genetics and Pharmacogenomics
Sulayman D. Dib-Hajj et al.
ANNUAL REVIEW OF NEUROSCIENCE, VOL 42 (2019)
The MAP1B Binding Domain of Nav1.6 Is Required for Stable Expression at the Axon Initial Segment
Laura Sole et al.
JOURNAL OF NEUROSCIENCE (2019)
Structures of human Nav1.7 channel in complex with auxiliary subunits and animal toxins
Huaizong Shen et al.
SCIENCE (2019)
THE ROLE OF VOLTAGE-GATED SODIUM CHANNELS IN PAIN SIGNALING
David L. Bennett et al.
PHYSIOLOGICAL REVIEWS (2019)
Building sensory axons: Delivery and distribution of Nav1.7 channels and effects of inflammatory mediators
Elizabeth J. Akin et al.
SCIENCE ADVANCES (2019)
Nonmuscle myosin II isoforms interact with sodium channel alpha subunits
Bhagirathi Dash et al.
MOLECULAR PAIN (2018)
Multiple myosin motors interact with sodium/potassium-ATPase alpha 1 subunits
Bhagirathi Dash et al.
MOLECULAR BRAIN (2018)
Familial gain-of-function Nav1.9 mutation in a painful channelopathy
Chongyang Han et al.
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY (2017)
Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability
Jianying Huang et al.
JOURNAL OF CLINICAL INVESTIGATION (2017)
Single-Molecule Imaging of Nav1.6 on the Surface of Hippocampal Neurons Reveals Somatic Nanoclusters
Elizabeth J. Akin et al.
BIOPHYSICAL JOURNAL (2016)
Nav1.7-A1632G Mutation from a Family with Inherited Erythromelalgia: Enhanced Firing of Dorsal Root Ganglia Neurons Evoked by Thermal Stimuli
Yang Yang et al.
JOURNAL OF NEUROSCIENCE (2016)
Decreased Nav1.9 channel expression in Hirschsprung's disease
Anne-Marie O'Donnell et al.
JOURNAL OF PEDIATRIC SURGERY (2016)
Biophysical and Pharmacological Characterization of Nav1.9 Voltage Dependent Sodium Channels Stably Expressed in HEK-293 Cells
Zhixin Lin et al.
PLOS ONE (2016)
NaV 1.9: a sodium channel linked to human pain
Sulayman D. Dib-Hajj et al.
NATURE REVIEWS NEUROSCIENCE (2015)
The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy
Chongyang Han et al.
NEUROMOLECULAR MEDICINE (2015)
Heterologous expression of NaV1.9 chimeras in various cell systems
R. Oliver Goral et al.
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY (2015)
Cold-aggravated pain in humans caused by a hyperactive NaV1.9 channel mutant
Enrico Leipold et al.
NATURE COMMUNICATIONS (2015)
The phenotype of congenital insensitivity to pain due to the NaV1.9 variant p.L811P
Christopher Geoffrey Woods et al.
EUROPEAN JOURNAL OF HUMAN GENETICS (2015)
Preferential Targeting of Nav1.6 Voltage-Gated Na+ Channels to the Axon Initial Segment during Development
Elizabeth J. Akin et al.
PLOS ONE (2015)
Gain-of-function mutations in sodium channel NaV1.9 in painful neuropathy
Jianying Huang et al.
BRAIN (2014)
Multiple roles for NaV1.9 in the activation of visceral afferents by noxious inflammatory, mechanical, and human disease-derived stimuli
James R. F. Hockley et al.
PAIN (2014)
Mechanism of sodium channel NaV1.9 potentiation by G-protein signaling
Carlos G. Vanoye et al.
JOURNAL OF GENERAL PHYSIOLOGY (2013)
A de novo gain-of-function mutation in SCN11A causes loss of pain perception
Enrico Leipold et al.
NATURE GENETICS (2013)
Mechanisms of polarized membrane trafficking in neurons - Focusing in on endosomes
Zofia M. Lasiecka et al.
MOLECULAR AND CELLULAR NEUROSCIENCE (2011)
Human embryonic kidney (HEK293) cells express endogenous voltage-gated sodium currents and Nav1.7 sodium channels
Bingjun He et al.
NEUROSCIENCE LETTERS (2010)
Multiplexed transposon-mediated stable gene transfer in human cells
Kristopher M. Kahlig et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2010)
Voltage-clamp and current-clamp recordings from mammalian DRG neurons
Theodore R. Cummins et al.
NATURE PROTOCOLS (2009)
Transfection of rat or mouse neurons by biolistics or electroporation
Sulayman D. Dib-Hajj et al.
NATURE PROTOCOLS (2009)
Occurrence, function and evolutionary origins of '2A-like' sequences in virus genomes
Garry A. Luke et al.
JOURNAL OF GENERAL VIROLOGY (2008)
A case for StopGo'': Reprogramming translation to augment codon meaning of GGN by promoting unconventional termination (Stop) after addition of glycine and then allowing continued translation (Go)
John F. Atkins et al.
RNA (2007)
Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons
Anthony M. Rush et al.
JOURNAL OF PHYSIOLOGY-LONDON (2007)
PiggyBac transposon-mediated gene transfer in human cells
Matthew H. Wilson et al.
MOLECULAR THERAPY (2007)
A single sodium channel mutation produces hyperor hypoexcitability in different types of neurons
Anthony M. Rush et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2006)
Site-specific labeling of cell surface proteins with biophysical probes using biotin ligase
I Chen et al.
NATURE METHODS (2005)
The C-terminal region as a modulator of rNav1.7 and rNav1.8 expression levels
K Vijayaragavan et al.
FEBS LETTERS (2004)
Functional role of the C-terminus of voltage-gated sodium channel Nav1.8
JS Choi et al.
FEBS LETTERS (2004)
Identification of an axonal determinant in the C-terminus of the sodium channel Nav1.2
JJ Garrido et al.
EMBO JOURNAL (2001)
Integration of PCR fragments at any specific site within cloning vectors without the use of restriction enzymes and DNA ligase
M Geiser et al.
BIOTECHNIQUES (2001)
Share Paper
