Published in J Biol Chem on October 24, 2002
Receptor specificity of the fibroblast growth factor family. The complete mammalian FGF family. J Biol Chem (2006) 5.78
Fibroblast growth factor 14 is an intracellular modulator of voltage-gated sodium channels. J Physiol (2005) 2.05
Fibroblast growth factor homologous factors control neuronal excitability through modulation of voltage-gated sodium channels. Neuron (2007) 1.84
The Fibroblast Growth Factor signaling pathway. Wiley Interdiscip Rev Dev Biol (2015) 1.82
Fibroblast growth factor homologous factors: evolution, structure, and function. Cytokine Growth Factor Rev (2005) 1.61
Crystal structure of a fibroblast growth factor homologous factor (FHF) defines a conserved surface on FHFs for binding and modulation of voltage-gated sodium channels. J Biol Chem (2009) 1.56
Crystal structure of the ternary complex of a NaV C-terminal domain, a fibroblast growth factor homologous factor, and calmodulin. Structure (2012) 1.56
FGF14 N-terminal splice variants differentially modulate Nav1.2 and Nav1.6-encoded sodium channels. Mol Cell Neurosci (2009) 1.51
Nav channel mechanosensitivity: activation and inactivation accelerate reversibly with stretch. Biophys J (2007) 1.44
FGF14 regulates the intrinsic excitability of cerebellar Purkinje neurons. Neurobiol Dis (2008) 1.43
Fibroblast growth factor homologous factor 13 regulates Na+ channels and conduction velocity in murine hearts. Circ Res (2011) 1.37
Identification of novel interaction sites that determine specificity between fibroblast growth factor homologous factors and voltage-gated sodium channels. J Biol Chem (2011) 1.27
Long-term inactivation particle for voltage-gated sodium channels. J Physiol (2010) 1.17
Recurrent and Non-Recurrent Mutations of SCN8A in Epileptic Encephalopathy. Front Neurol (2015) 1.17
The fibroblast growth factor 14·voltage-gated sodium channel complex is a new target of glycogen synthase kinase 3 (GSK3). J Biol Chem (2013) 1.14
FGF14 regulates presynaptic Ca2+ channels and synaptic transmission. Cell Rep (2013) 1.12
Voltage-gated sodium channel-associated proteins and alternative mechanisms of inactivation and block. Cell Mol Life Sci (2011) 1.11
Voltage-gated Na+ channels: multiplicity of expression, plasticity, functional implications and pathophysiological aspects. Eur Biophys J (2004) 1.09
Characterization of bipolar disorder patient-specific induced pluripotent stem cells from a family reveals neurodevelopmental and mRNA expression abnormalities. Mol Psychiatry (2015) 1.01
Excitability constraints on voltage-gated sodium channels. PLoS Comput Biol (2007) 1.00
Intracellular FGF14 (iFGF14) Is Required for Spontaneous and Evoked Firing in Cerebellar Purkinje Neurons and for Motor Coordination and Balance. J Neurosci (2015) 0.95
Voltage-gated sodium channels: biophysics, pharmacology, and related channelopathies. Front Pharmacol (2012) 0.94
Bioluminescence methodology for the detection of protein-protein interactions within the voltage-gated sodium channel macromolecular complex. Assay Drug Dev Technol (2012) 0.92
Fibroblast Growth Factor Homologous Factors: New Roles in Neuronal Health and Disease. Neuroscientist (2014) 0.90
Protein assemblies of sodium and inward rectifier potassium channels control cardiac excitability and arrhythmogenesis. Am J Physiol Heart Circ Physiol (2015) 0.89
Regulation of the NaV1.5 cytoplasmic domain by calmodulin. Nat Commun (2014) 0.89
Fibroblast growth factor signaling in the developing neuroendocrine hypothalamus. Front Neuroendocrinol (2010) 0.87
Altered sodium channel-protein associations in critical illness myopathy. Skelet Muscle (2012) 0.85
QTLs of factors of the metabolic syndrome and echocardiographic phenotypes: the hypertension genetic epidemiology network study. BMC Med Genet (2008) 0.85
Interaction between cartilage oligomeric matrix protein and extracellular matrix protein 1 mediates endochondral bone growth. Matrix Biol (2010) 0.84
Proteomic analysis of native cerebellar iFGF14 complexes. Channels (Austin) (2016) 0.82
Trastuzumab alters the expression of genes essential for cardiac function and induces ultrastructural changes of cardiomyocytes in mice. PLoS One (2013) 0.82
Fibroblast growth factor homologous factors in the heart: a potential locus for cardiac arrhythmias. Trends Cardiovasc Med (2011) 0.79
Quantitative proteomics reveals protein-protein interactions with fibroblast growth factor 12 as a component of the voltage-gated sodium channel 1.2 (nav1.2) macromolecular complex in Mammalian brain. Mol Cell Proteomics (2015) 0.79
Deletion of FoxO1 leads to shortening of QRS by increasing Na(+) channel activity through enhanced expression of both cardiac NaV1.5 and β3 subunit. J Mol Cell Cardiol (2014) 0.79
Fibroblast growth factor-12 (FGF12) translocation into intestinal epithelial cells is dependent on a novel cell-penetrating peptide domain: involvement of internalization in the in vivo role of exogenous FGF12. J Biol Chem (2011) 0.78
Physiological and Pathophysiological Insights of Nav1.4 and Nav1.5 Comparison. Front Pharmacol (2016) 0.76
Identification of Amino Acid Residues in Fibroblast Growth Factor 14 (FGF14) Required for Structure-Function Interactions with Voltage-gated Sodium Channel Nav1.6. J Biol Chem (2016) 0.76
Current view on regulation of voltage-gated sodium channels by calcium and auxiliary proteins. Protein Sci (2016) 0.76
Another piece to the intracellular FGF/Na+ channel puzzle. Proc Natl Acad Sci U S A (2016) 0.76
Cardiac Na Channels: Structure to Function. Curr Top Membr (2016) 0.75
Hypoxia-Induced Fibroblast Growth Factor 11 Stimulates Osteoclast-Mediated Resorption of Bone. Calcif Tissue Int (2017) 0.75
Intracellular Fibroblast Growth Factor 14: Emerging Risk Factor for Brain Disorders. Front Cell Neurosci (2017) 0.75
FGF13 modulates the gating properties of the cardiac sodium channel Nav1.5 in an isoform-specific manner. Channels (Austin) (2016) 0.75
High-throughput electrophysiological assays for voltage gated ion channels using SyncroPatch 768PE. PLoS One (2017) 0.75
International Union of Pharmacology. XLVII. Nomenclature and structure-function relationships of voltage-gated sodium channels. Pharmacol Rev (2005) 5.40
De novo pathogenic SCN8A mutation identified by whole-genome sequencing of a family quartet affected by infantile epileptic encephalopathy and SUDEP. Am J Hum Genet (2012) 3.58
Gain of function Naν1.7 mutations in idiopathic small fiber neuropathy. Ann Neurol (2011) 3.53
Sodium channels in normal and pathological pain. Annu Rev Neurosci (2010) 3.47
The Na(V)1.7 sodium channel: from molecule to man. Nat Rev Neurosci (2012) 2.71
Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons. J Physiol (2006) 2.62
A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons. Proc Natl Acad Sci U S A (2006) 2.61
Activated microglia contribute to the maintenance of chronic pain after spinal cord injury. J Neurosci (2006) 2.60
Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders. J Clin Invest (2007) 2.58
Nav1.8 expression is not restricted to nociceptors in mouse peripheral nervous system. Pain (2012) 2.34
From genes to pain: Na v 1.7 and human pain disorders. Trends Neurosci (2007) 2.29
Distinct repriming and closed-state inactivation kinetics of Nav1.6 and Nav1.7 sodium channels in mouse spinal sensory neurons. J Physiol (2003) 2.21
Changes in the expression of tetrodotoxin-sensitive sodium channels within dorsal root ganglia neurons in inflammatory pain. Pain (2004) 2.10
The roles of sodium channels in nociception: Implications for mechanisms of pain. Pain (2007) 2.06
Intense isolectin-B4 binding in rat dorsal root ganglion neurons distinguishes C-fiber nociceptors with broad action potentials and high Nav1.9 expression. J Neurosci (2006) 2.05
Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger. Proc Natl Acad Sci U S A (2004) 1.99
Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones. J Physiol (2005) 1.95
Inherited erythermalgia: limb pain from an S4 charge-neutral Na channelopathy. Neurology (2006) 1.95
Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy. J Neurosci (2004) 1.93
NaN/Nav1.9: a sodium channel with unique properties. Trends Neurosci (2002) 1.93
Fibroblast growth factor homologous factor 2B: association with Nav1.6 and selective colocalization at nodes of Ranvier of dorsal root axons. J Neurosci (2004) 1.91
Nav1.6 channels generate resurgent sodium currents in spinal sensory neurons. FEBS Lett (2005) 1.85
The presence and role of the tetrodotoxin-resistant sodium channel Na(v)1.9 (NaN) in nociceptive primary afferent neurons. J Neurosci (2002) 1.85
Early- and late-onset inherited erythromelalgia: genotype-phenotype correlation. Brain (2009) 1.82
A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons. Exp Neurol (2010) 1.78
Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injury. J Neurosci (2003) 1.76
Intravenous administration of auto serum-expanded autologous mesenchymal stem cells in stroke. Brain (2011) 1.73
GTP-induced tetrodotoxin-resistant Na+ current regulates excitability in mouse and rat small diameter sensory neurones. J Physiol (2003) 1.62
A case of inherited erythromelalgia. Nat Clin Pract Neurol (2007) 1.60
The role of sodium channels in chronic inflammatory and neuropathic pain. J Pain (2006) 1.59
A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis. Ann Neurol (2012) 1.59
Exacerbation of experimental autoimmune encephalomyelitis after withdrawal of phenytoin and carbamazepine. Ann Neurol (2007) 1.56
Early treatment suppresses the development of spike-wave epilepsy in a rat model. Epilepsia (2007) 1.53
An atypical role for collapsin response mediator protein 2 (CRMP-2) in neurotransmitter release via interaction with presynaptic voltage-gated calcium channels. J Biol Chem (2009) 1.51
FGF14 N-terminal splice variants differentially modulate Nav1.2 and Nav1.6-encoded sodium channels. Mol Cell Neurosci (2009) 1.51
Gain-of-function Nav1.8 mutations in painful neuropathy. Proc Natl Acad Sci U S A (2012) 1.50
Extracellular signal-regulated kinase-regulated microglia-neuron signaling by prostaglandin E2 contributes to pain after spinal cord injury. J Neurosci (2007) 1.49
Sporadic onset of erythermalgia: a gain-of-function mutation in Nav1.7. Ann Neurol (2006) 1.48
Human voltage-gated sodium channel mutations that cause inherited neuronal and muscle channelopathies increase resurgent sodium currents. J Clin Invest (2009) 1.46
Nav1.5 sodium channels in macrophages in multiple sclerosis lesions. Mult Scler (2012) 1.45
Primary cortical motor neurons undergo apoptosis after axotomizing spinal cord injury. J Comp Neurol (2003) 1.43
Co-localization of sodium channel Nav1.6 and the sodium-calcium exchanger at sites of axonal injury in the spinal cord in EAE. Brain (2003) 1.42
Differential block of sensory neuronal voltage-gated sodium channels by lacosamide [(2R)-2-(acetylamino)-N-benzyl-3-methoxypropanamide], lidocaine, and carbamazepine. J Pharmacol Exp Ther (2008) 1.42
Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons. J Neurosci (2006) 1.42
Sodium channel Na(v)1.6 is expressed along nonmyelinated axons and it contributes to conduction. Brain Res Mol Brain Res (2002) 1.40
Familial pain syndromes from mutations of the NaV1.7 sodium channel. Ann N Y Acad Sci (2010) 1.40
International Union of Pharmacology. XXXIX. Compendium of voltage-gated ion channels: sodium channels. Pharmacol Rev (2003) 1.40
Differential modulation of sodium channel Na(v)1.6 by two members of the fibroblast growth factor homologous factor 2 subfamily. Eur J Neurosci (2006) 1.39
PGE2 increases the tetrodotoxin-resistant Nav1.9 sodium current in mouse DRG neurons via G-proteins. Brain Res (2004) 1.39
ERK1/2 mitogen-activated protein kinase phosphorylates sodium channel Na(v)1.7 and alters its gating properties. J Neurosci (2010) 1.38
Calmodulin binds to the C terminus of sodium channels Nav1.4 and Nav1.6 and differentially modulates their functional properties. J Neurosci (2003) 1.38
Nav1.7 mutations associated with paroxysmal extreme pain disorder, but not erythromelalgia, enhance Navbeta4 peptide-mediated resurgent sodium currents. J Physiol (2010) 1.38
Multiple sodium channel isoforms and mitogen-activated protein kinases are present in painful human neuromas. Ann Neurol (2008) 1.37
Modulation of thalamic nociceptive processing after spinal cord injury through remote activation of thalamic microglia by cysteine cysteine chemokine ligand 21. J Neurosci (2007) 1.36
Role of hippocampal sodium channel Nav1.6 in kindling epileptogenesis. Epilepsia (2008) 1.36
Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neurons. J Neurosci (2008) 1.35
A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivity. J Physiol (2007) 1.35
Sodium-calcium exchanger and multiple sodium channel isoforms in intra-epidermal nerve terminals. Mol Pain (2010) 1.33
Selective expression of a persistent tetrodotoxin-resistant Na+ current and NaV1.9 subunit in myenteric sensory neurons. J Neurosci (2003) 1.33
Voltage-gated sodium channels: therapeutic targets for pain. Pain Med (2009) 1.33
Transfection of rat or mouse neurons by biolistics or electroporation. Nat Protoc (2009) 1.32
Deletion mutation of sodium channel Na(V)1.7 in inherited erythromelalgia: enhanced slow inactivation modulates dorsal root ganglion neuron hyperexcitability. Brain (2011) 1.32
Voltage-gated sodium channel expression in rat and human epidermal keratinocytes: evidence for a role in pain. Pain (2008) 1.32
Molecular interactions of the gating modifier toxin ProTx-II with NaV 1.5: implied existence of a novel toxin binding site coupled to activation. J Biol Chem (2007) 1.30
Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable. Mol Pain (2008) 1.26