| Q24679655 | A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity |
| Q37232148 | A SCN10A SNP biases human pain sensitivity |
| Q34616126 | A case of inherited erythromelalgia |
| Q43773926 | A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis. |
| Q86045082 | A new Nav1.7 mutation in an erythromelalgia patient |
| Q39287807 | A new Nav1.7 sodium channel mutation I234T in a child with severe pain |
| Q33918510 | A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia |
| Q37403813 | A painful neuropathy-associated Nav1.7 mutant leads to time-dependent degeneration of small-diameter axons associated with intracellular Ca2+ dysregulation and decrease in ATP levels. |
| Q39972794 | A pore-blocking hydrophobic motif at the cytoplasmic aperture of the closed-state Nav1.7 channel is disrupted by the erythromelalgia-associated F1449V mutation. |
| Q24546007 | A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons |
| Q39759228 | A sodium channel gene SCN9A polymorphism that increases nociceptor excitability |
| Q43061175 | Alternative splicing may contribute to time-dependent manifestation of inherited erythromelalgia |
| Q28186422 | Annexin II/p11 is up-regulated in Purkinje cells in EAE and MS |
| Q91085254 | Building sensory axons: Delivery and distribution of NaV1.7 channels and effects of inflammatory mediators |
| Q28577237 | CAP-1A is a novel linker that binds clathrin and the voltage-gated sodium channel Na(v)1.8 |
| Q39161394 | COL6A5 variants in familial neuropathic chronic itch. |
| Q34511133 | Calmodulin regulates current density and frequency-dependent inhibition of sodium channel Nav1.8 in DRG neurons |
| Q24304239 | Characterization of a de novo SCN8A mutation in a patient with epileptic encephalopathy |
| Q28277714 | Contactin associates with sodium channel Nav1.3 in native tissues and increases channel density at the cell surface |
| Q28586003 | Contactin regulates the current density and axonal expression of tetrodotoxin-resistant but not tetrodotoxin-sensitive sodium channels in DRG neurons |
| Q35719847 | Contactin-1 and Neurofascin-155/-186 Are Not Targets of Auto-Antibodies in Multifocal Motor Neuropathy |
| Q33591220 | Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas |
| Q28118989 | De novo gain-of-function and loss-of-function mutations of SCN8A in patients with intellectual disabilities and epilepsy |
| Q28111582 | De novo pathogenic SCN8A mutation identified by whole-genome sequencing of a family quartet affected by infantile epileptic encephalopathy and SUDEP |
| Q49125035 | Deletion mutation of sodium channel Na(V)1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability. |
| Q94552696 | Dendritic Spine Dynamics after Peripheral Nerve Injury: An Intravital Structural Study |
| Q28250012 | Differential modulation of sodium channel Na(v)1.6 by two members of the fibroblast growth factor homologous factor 2 subfamily |
| Q34481049 | Diverse functions and dynamic expression of neuronal sodium channels |
| Q47927525 | Dynamic-clamp analysis of wild-type human Nav1.7 and erythromelalgia mutant channel L858H. |
| Q34156496 | Dynamics of sodium channel Nav1.5 expression in astrocytes in mouse models of multiple sclerosis |
| Q39744096 | ERK1/2 mitogen-activated protein kinase phosphorylates sodium channel Na(v)1.7 and alters its gating properties |
| Q48001757 | Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation |
| Q34350866 | Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. |
| Q39792047 | Erythromelalgia mutation L823R shifts activation and inactivation of threshold sodium channel Nav1.7 to hyperpolarized potentials. |
| Q34422995 | Erythromelalgia: a hereditary pain syndrome enters the molecular era. |
| Q33705386 | FGF14 N-terminal splice variants differentially modulate Nav1.2 and Nav1.6-encoded sodium channels |
| Q48045901 | Familial gain-of-function Nav1.9 mutation in a painful channelopathy. |
| Q24300238 | Fibroblast growth factor homologous factor 2B: association with Nav1.6 and selective colocalization at nodes of Ranvier of dorsal root axons |
| Q28254063 | From genes to pain: Na v 1.7 and human pain disorders |
| Q48430447 | Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy. |
| Q40526727 | Functional role of the C-terminus of voltage-gated sodium channel Na(v)1.8. |
| Q30048469 | Gain of function NaV1.7 mutations in idiopathic small fiber neuropathy |
| Q34309236 | Gain-of-function Nav1.8 mutations in painful neuropathy. |
| Q45771999 | Gain-of-function mutations in sodium channel Na(v)1.9 in painful neuropathy |
| Q112080560 | Hominini-specific regulation of CBLN2 increases prefrontal spinogenesis |
| Q35609134 | Human Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons |
| Q34567504 | Inherited erythermalgia: limb pain from an S4 charge-neutral Na channelopathy |
| Q28587249 | Interaction of voltage-gated sodium channel Nav1.6 (SCN8A) with microtubule-associated protein Map1b |
| Q28289125 | International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels |
| Q35642815 | Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7. |
| Q39308636 | Mexiletine-responsive erythromelalgia due to a new Na(v)1.7 mutation showing use-dependent current fall-off. |
| Q28240813 | Modulation of thalamic nociceptive processing after spinal cord injury through remote activation of thalamic microglia by cysteine cysteine chemokine ligand 21 |
| Q24313401 | Modulation of the cardiac sodium channel Nav1.5 by fibroblast growth factor homologous factor 1B |
| Q34321453 | Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger |
| Q36678533 | Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons |
| Q36487377 | Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decade |
| Q33875626 | Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders |
| Q34585853 | Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons. |
| Q28215683 | NaN/Nav1.9: a sodium channel with unique properties |
| Q35003780 | Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons |
| Q84389261 | Nav1.8 expression is not restricted to nociceptors in mouse peripheral nervous system |
| Q36290427 | Network topology of NaV1.7 mutations in sodium channel-related painful disorders. |
| Q28278802 | Neurobiology: a channel sets the gain on pain |
| Q89340974 | Nonmuscle myosin II isoforms interact with sodium channel alpha subunits |
| Q34971951 | Novel SCN1A mutation in a proband with malignant migrating partial seizures of infancy |
| Q35572913 | Oral administration of PF-01247324, a subtype-selective Nav1.8 blocker, reverses cerebellar deficits in a mouse model of multiple sclerosis |
| Q34262020 | PKCε phosphorylation of the sodium channel NaV1.8 increases channel function and produces mechanical hyperalgesia in mice. |
| Q38253772 | Painful neuropathies: the emerging role of sodium channelopathies |
| Q38306520 | Painful peripheral neuropathy and sodium channel mutations |
| Q36916035 | Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable |
| Q30835612 | Pharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a |
| Q46691815 | Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neurons |
| Q35432154 | Preferential targeting of Nav1.6 voltage-gated Na+ Channels to the axon initial segment during development |
| Q33187322 | Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury |
| Q33739335 | Reduced thermal sensitivity and Nav1.8 and TRPV1 channel expression in sensory neurons of aged mice |
| Q93249605 | Resilience to Pain: A Peripheral Component Identified Using Induced Pluripotent Stem Cells and Dynamic Clamp |
| Q47977892 | Reverse pharmacogenomics: carbamazepine normalizes activation and attenuates thermal hyperexcitability of sensory neurons due to Nav 1.7 mutation I234T. |
| Q27334074 | Screening fluorescent voltage indicators with spontaneously spiking HEK cells |
| Q34569783 | Size matters: Erythromelalgia mutation S241T in Nav1.7 alters channel gating |
| Q48686306 | 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. |
| Q46987387 | Small-fiber neuropathy Nav1.8 mutation shifts activation to hyperpolarized potentials and increases excitability of dorsal root ganglion neurons. |
| Q34277762 | Small-fibre neuropathies--advances in diagnosis, pathophysiology and management |
| Q35659204 | Sodium channel Nav1.7 in vascular myocytes, endothelium, and innervating axons in human skin |
| Q38691016 | Sodium channel Nav1.8: Emerging links to human disease |
| Q38260278 | Sodium channel genes in pain-related disorders: phenotype-genotype associations and recommendations for clinical use. |
| Q37724336 | Sodium channels in normal and pathological pain |
| Q34481638 | Sporadic onset of erythermalgia: a gain-of-function mutation in Nav1.7. |
| Q101038915 | Status of peripheral sodium channel blockers for non-addictive pain treatment |
| Q42211742 | Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(V)1.7 mutant channel. |
| Q28214636 | Structure of the sodium channel gene SCN11A: evidence for intron-to-exon conversion model and implications for gene evolution |
| Q28601095 | Subtype-Selective Small Molecule Inhibitors Reveal a Fundamental Role for Nav1.7 in Nociceptor Electrogenesis, Axonal Conduction and Presynaptic Release |
| Q21203947 | Temperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7 |
| Q36258703 | The AMPK Activator A769662 Blocks Voltage-Gated Sodium Channels: Discovery of a Novel Pharmacophore with Potential Utility for Analgesic Development |
| Q41190621 | The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy. |
| Q85637494 | The G1662S NaV1.8 mutation in small fibre neuropathy: impaired inactivation underlying DRG neuron hyperexcitability |
| Q30487520 | The ataxia3 mutation in the N-terminal cytoplasmic domain of sodium channel Na(v)1.6 disrupts intracellular trafficking |
| Q38241746 | The role of sodium channels in painful diabetic and idiopathic neuropathy. |
| Q34674268 | The roles of sodium channels in nociception: Implications for mechanisms of pain |
| Q84255216 | Transfection of rat or mouse neurons by biolistics or electroporation |
| Q34074334 | Two Nedd4-binding motifs underlie modulation of sodium channel Nav1.6 by p38 MAPK. |
| Q28574005 | Upregulation of Sodium Channel Nav1.3 and Functional Involvement in Neuronal Hyperexcitability Associated with Central Neuropathic Pain after Spinal Cord Injury |
| Q30580969 | Voltage-gated sodium channel Nav 1.5 contributes to astrogliosis in an in vitro model of glial injury via reverse Na+ /Ca2+ exchange |
| Q34433609 | Voltage-gated sodium channel Nav1.6 is modulated by p38 mitogen-activated protein kinase. |