ライフサイエンスコーパス: sodium channel

1 A gene encoding a neuronal voltage-activated sodium channel.

2 the deactivated voltage sensor of bacterial sodium channel.

3 possible mechanism for CBD interactions with sodium channels.

4 resembling the properties of F1.Q54 neuronal sodium channels.

5 separation as a compliment or alternative to sodium channels.

6 ntry through NMDA receptors or voltage-gated sodium channels.

7 otoxin resistance through point mutations in sodium channels.

8 e unbinding rate of these two compounds with sodium channels.

9 nservation of this mechanism among mammalian sodium channels.

10 seizure agent that targets voltage-dependent sodium channels.

11 CaMKII as a plausible modulator of neuronal sodium channels.

12 contribution to plasma membrane delivery of sodium channels.

13 The prominent role of voltage-gated sodium channel 1.7 (Nav1.7) in nociception was revealed

14 The voltage-gated sodium channel 1.7 (Nav1.7) plays an important role in m

15 s effect is mediated solely by voltage-gated sodium channel 1.8 (NaV1.8).

16 We concluded that for prokaryotic sodium channels, a fine balance among filter size, bindi

17 indirectly reduces principal cell epithelial sodium channel abundance and function.

18 The extent to which sodium channel activity after injury contributes to syna

19 even mutations which cause small changes in sodium channel activity can have devastating consequence

20 early infantile epilepsy result in increased sodium channel activity with gain-of-function, character

21 orption, transepithelial voltage, epithelial sodium channel activity, and pendrin abundance and subce

22 e reduced chloride absorption and epithelial sodium channel activity, despite principal cell mineralo

23 ional changes in mitochondria resulting from sodium channel activity.

24 The presence of sodium channels, along with the submembranous location o

25 owever, expression analysis of voltage-gated sodium channel alpha subunits revealed NaV 1.7 mRNA tran

26 IN-cleavable peptide on the human epithelial sodium channel alpha-subunit (ENaC-alpha).

27 bited increased expression of the epithelial sodium channel alpha-subunit, largely abolished basolate

28 Unlike potassium channels, sodium channel alpha-subunits are believed to form funct

29 Here we demonstrate that sodium channel alpha-subunits not only physically intera

30 ological targets include human voltage-gated sodium channels, among other membrane proteins.

31 The link between an axonal sodium channel and ASD, a disorder typically attributed

32 Sodium channel and clathrin linker 1 (SCLT1) mutations w

33 nformational cycle in a single voltage-gated sodium channel and give insight into the structural basi

34 ented protein expression of gamma-epithelial sodium channel and NHE3 (sodium-hydrogen antiporter 3).

35 clude that for a non-uniform distribution of sodium channels and a sufficiently small intercellular d

36 extracellularly can powerfully inhibit both sodium channels and calcium channels, thereby blocking b

37 of the tyrosine phosphatase SHP-1, inhibited sodium channels and caused hyperpolarization through act

38 trodotoxin (TTX)-sensitive and TTX-resistant sodium channels and hyperpolarization-activated cyclic n

39 omponent of tarantula venom, potently blocks sodium channels and is an attractive scaffold for engine

40 y, this chimera, DII S1-S4, forms functional sodium channels and is potently inhibited by the NaV1.7

41 ytes pretreated with tetrodotoxin to inhibit sodium channels and isolate the effect of flecainide on

42 c coupling can influence the dynamics of the sodium channels and potentially provide cell-to-cell cou

43 ough NMDA receptors or through voltage-gated sodium channels and that the spine neck is not a signifi

44 ions between CBD and the NavMs voltage-gated sodium channel, and electrophysiology to show the functi

45 nctional interaction between VCL and cardiac sodium channel, and suggests an important role for respi

46 the axon, alters activation dynamics of the sodium channels, and prevents the traveling of the invad

47 native splicing also changes the activity of sodium channels, and while it is highly conserved, it is

48 arrhythmogenic Ca release even when cardiac sodium channels are blocked.

49 important site on the myelinated axon where sodium channels are clustered and regeneration of action

50 ABSTRACT: Voltage-gated sodium channels are critical for neuronal activity, and

51 Voltage-gated sodium channels are critical for peripheral sensory neur

52 KEY POINTS: Sodium channels are critical for supporting fast action

53 Fast opening and closing of voltage-gated sodium channels are crucial for proper propagation of th

54 e novel evidence that multiple voltage-gated sodium channels are involved in schizophrenia pathogenes

55 study, we investigated whether voltage-gated sodium channels are involved in the development of vincr

56 Voltage gated sodium channels are key players in aberrant pain signali

57 Voltage-gated sodium channels are responsible for action potentials an

58 Voltage-gated sodium channels are subjected to S-palmitoylation and ex

59 Voltage-gated sodium channels are targets for a range of pharmaceutica

60 establish the extracellular vestibule of the sodium channel as a viable receptor site for the design

61 y shifts conventional paradigms in regard to sodium channel assembly, structure, and function but imp

62 Enrichment of sodium channels at nodes of Ranvier, a hallmark of myeli

63 hwann cells, such as clustered voltage-gated sodium channels at the node of Ranvier and Shaker-type p

64 exon 1b, PV interneurons lack voltage-gated sodium channels at their axonal initial segments and hav

65 we addressed how the bacterial voltage-gated sodium channel (BacNa(V)) C-terminal cytoplasmic domain

66 Bacterial voltage-gated sodium channels (BacNavs) serve as models of their verte

67 In DRG neurons, siRNA knockdown of sodium channel beta4 subunits fails to significantly alt

68 In mice with CPVT, sodium channel block alone did not prevent ventricular t

69 of antiarrhythmic action and concluded that sodium channel block alone is responsible for flecainide

70 ect on arrhythmia burden, despite comparable sodium channel block.

71 s demonstrate unexpected efficacy of a novel sodium channel blocker in Dravet syndrome and suggest a

72 lencing motor neurons with the intracellular sodium channel blocker QX-314 also disrupted premotor rh

73 acerbated by GS967, a potent, unconventional sodium channel blocker.

74 nd carvedilol), flecainide, and the neuronal sodium-channel blocker riluzole; a direct antiarrhythmic

75 BIIB074, a Nav1.7-selective, state-dependent sodium-channel blocker, can be administered at therapeut

76 on between age at disease onset, response to sodium channel blockers and the functional properties of

77 r trigeminal neuralgia is treatment with the sodium channel blockers carbamazepine and oxcarbazepine,

78 Further, a good response to sodium channel blockers clinically was found to be assoc

79 The potential role of sodium channel blockers in patients with potassium chann

80 The response to sodium channel blockers indicates a therapeutic overlap

81 ike cationic derivatives of local anesthetic sodium channel blockers like QX-314, this cationic compo

82 Most sodium channel blockers reduce the early (peak) and late

83 Site 1 sodium channel blockers such as tetrodotoxin (TTX) are e

84 We find that the use of sodium channel blockers was often associated with clinic

85 -onset forms and an insufficient response to sodium channel blockers were associated with loss-of-fun

86 In contrast, sodium channel blockers were rarely effective in epileps

87 for most patients, concomitant therapy with sodium channel blockers, like mexiletine, is often utili

88 e treatment of pain using novel and existing sodium channel blockers.

89 ate onset epilepsies and lack of response to sodium channel blockers.

90 e clinical observations suggest conventional sodium channel blocking antiepileptic drugs may worsen t

91 ry from inactivation compared with the other sodium channel blocking drugs we tested.

92 uctural basis for state-dependent binding of sodium channel-blocking drugs.

93 Alternative splicing modifies sodium channels, but the functional relevance and adapti

94 Na(V)1.5 is distinguished from other sodium channels by a unique glycosyl moiety and loss of

95 We show here that sodium channels can implement a molecular leaky integrat

96 Mutations in voltage-dependent sodium channels cause severe autism/intellectual disabil

97 Previous studies have shown that sodium channels cluster together in specific cellular su

98 scribe an anatomic hub (a couplon) formed by sodium channel clusters and subjacent subsarcolemmal mit

99 Voltage-gated sodium channels comprise an ion-selective alpha-subunit

100 acellular potassium diffusion and persistent sodium channel conductance.

101 ytes-lacking intact sarcolemma and devoid of sodium channel contribution-flecainide, but not its anal

102 terations in the properties of voltage-gated sodium channel currents in Jedi-1 null neurons.

103 x through Dmca1D channels, likely to enhance sodium channel de-inactivation via a fast afterhyperpola

104 annels belonging to the degenerin/epithelial sodium channel (DEG/ENaC) family activate in response to

105 TATEMENT Members of the degenerin/epithelial sodium channel (DEG/ENaC) family are broadly expressed i

106 The protein family of degenerin/epithelial sodium channels (DEG/ENaCs) is composed of diverse anima

107 ) are proton-gated members of the epithelial sodium channel/degenerin (ENaC/DEG) superfamily of ion c

108 We conclude that a non-uniform sodium channel distribution increases the conduction vel

109 n in the fraction of available voltage-gated sodium channels due to insufficient recovery from inacti

110 ghly conserved impact on the availability of sodium channels during trains of rapid stimulations, and

111 p with trigeminal neuralgia, suggesting that sodium channels dysfunction may be a key pathophysiologi

112 Through this mechanism, sodium channels effectively measure the frequency of act

113 f the gene encoding the alpha-subunit of the sodium channel ENaC in cell lines and primary epithelial

114 (2020) report that the epithelial sodium channel ENaC, which serves as the salty receptor,

115 lial cells is rate-limited by the epithelial sodium channel (ENaC) activity in lung, kidney, and the

116 of the extracellular loops of the epithelial sodium channel (ENaC) alpha and gamma subunits increases

117 ng tubule mass and attenuation of epithelial sodium channel (ENaC) and ROMK expression and apical loc

118 ice displayed upregulation of the epithelial sodium channel (ENaC) and the Ca(2+)-activated K(+) chan

119 The epithelial sodium channel (ENaC) has an important role in regulatin

120 Overexpression in the epithelial sodium channel (ENaC) in membrane platelets can be relat

121 The epithelial sodium channel (ENaC) is present in the apical membrane

122 The epithelial sodium channel (ENaC) is the limiting entry point for Na

123 The epithelial sodium channel (ENaC) mediates Na(+) transport in severa

124 ow overexpression or silencing of epithelial sodium channel (ENaC) subunits and claudin-8 affect para

125 of loss-of-function mutations in epithelial sodium channel (ENaC) subunits exhibit meibomian gland (

126 a downregulates the expression of epithelial sodium channel (ENaC) subunits in enterocytes (ECs) to m

127 the ability of insulin to augment epithelial sodium channel (ENaC) transport.

128 Co-localization of epithelial sodium channel (ENaC) with the plasma membrane was reduc

129 oride cotransporter (NCC) and the epithelial sodium channel (ENaC), are regulated is paramount.

130 2, which negatively regulates the epithelial sodium channel (ENaC), Na(+)/Cl(-) cotransporter (NCC),

131 ion channel for sodium taste, the epithelial sodium channel (ENaC), throughout development dramatical

132 ductance regulator (CFTR) and the epithelial sodium channel (ENaC).

133 the beta- or gamma-subunit of the epithelial sodium channel (ENaC).

134 bined with hyperactivation of the epithelial sodium channel (ENaC).

135 transport, with dysregulation of epithelial sodium channels (ENaC).

136 ought to increase the activity of epithelial sodium channels (ENaC).

137 s transfected with siRNAs against epithelial sodium channel ENaCalpha or ENaCdelta compared to untran

138 -sensing ion channels (ASICs) and epithelial sodium channel (ENaCs), these channel families display v

139 ition and protease-sensitivity in epithelial sodium channels (ENaCs) are not fully understood.

140 inide's inhibitory activity on human cardiac sodium channels expressed in HEK293T cells.

141 stically reduced the sensitivity of mosquito sodium channels expressed in Xenopus oocytes to both typ

142 Reduced cardiac sodium channel expression is a known causal mechanism in

143 were not associated with changes in relevant sodium channel expression or differences in capacitance

144 Cardiac sodium channel expression, I(Na) and atrial action poten

145 PPK25), a member of the degenerin/epithelial sodium channel family (DEG/ENaC).

146 acillus alcalophilus) and NaChBac (bacterial sodium channel from Bacillus halodurans) (IC50 = 112 nM

147 cted two mutations (V410L and F1534C) in the sodium channel from this resistant strain.

148 efasciatus display CNV for the voltage-gated sodium channel gene (Vgsc), target-site of pyrethroid an

149 Missense variants in the SCN8A voltage-gated sodium channel gene are linked to early-infantile epilep

150 cation and cloning of the full-length of the sodium channel gene in pyrethroid resistant mosquitoes r

151 unction mutations in the brain voltage-gated sodium channel gene SCN1A.

152 iomyocytes bearing nonsense mutations in the sodium channel gene SCN5A, which are associated with con

153 novo missense mutations in the voltage-gated sodium channel gene SCN8A Here, we investigated the neur

154 De novo mutations of the sodium channel gene SCN8A result in an epileptic encepha

155 n associated with mutations in voltage-gated sodium channel genes.

156 These sodium channels have been implicated in painful and pain

157 The human voltage-gated sodium channel, hNa(V)1.5, is responsible for the rapid

158 tions impair the encoded protein Na(V)1.2, a sodium channel important for action potential initiation

159 y whereas Scn2a encodes voltage-gated Nav1.2 sodium channels important for action potential initiatio

160 structure of the complete NavMs prokaryotic sodium channel in a fully open conformation.

161 e VCL-M94I was co-expressed with the cardiac sodium channel in HEK293 cells and also overexpressed in

162 STATEMENT Na(v)1.6 is a major voltage-gated sodium channel in human brain, where it regulates neuron

163 g for the alpha-subunit of the most abundant sodium channel in the heart) and PKP2 (the gene coding f

164 SCN5A, which encodes the major voltage-gated sodium channel in the heart.

165 Na(v)1.6 (SCN8A) is a major voltage-gated sodium channel in the mammalian CNS, and is highly conce

166 e demonstrated that lacosamide, which blocks sodium channels in a use-dependent manner, attenuates pa

167 known requirement for tetrodotoxin-sensitive sodium channels in action potential firing in a discrete

168 lar pharmacology of GS-967 and eleclazine on sodium channels in human induced pluripotent stem cell-d

169 l axons, inhibition of Na(V)1.7 and Na(V)1.8 sodium channels in incoming presynaptic DRG axons is no

170 Na(v)1.7 and other voltage-gated sodium channels in mouse DRG are considered threshold ch

171 isms in human pain and advances in targeting sodium channels in peripheral neurons for the treatment

172 ave demonstrated an essential role of Nav1.7 sodium channels in the sensation of pain, thus making th

173 bunit and the supramolecular organization of sodium channels, in an important model cell system that

174 selectively to the slow-inactivated state of sodium channels, in contrast to drugs like carbamazepine

175 The mechanism of inhibition involved sodium channel inactivation and shunting.

176 ltiple human pain disorders to voltage-gated sodium channels, including disorders characterized by in

177 Sodium channel inhibition by GS-967 and eleclazine has u

178 ation of 30 muM, lacosamide acts as a potent sodium channel inhibitor of Nav1.7 variants carried by r

179 gly, the compound is also a highly effective sodium channel inhibitor when applied extracellularly, p

180 hibitors [ Bicyclic sulfonamide compounds as sodium channel inhibitors and their preparation .

181 GS-967 and eleclazine (GS-6615) are novel sodium channel inhibitors exhibiting antiarrhythmic effe

182 nding site is different from that of classic sodium channel inhibitors like lidocaine, which also bin

183 Voltage-gated sodium channels initiate electrical signals and are freq

184 The Nav1.1 voltage-gated sodium channel is a critical contributor to excitability

185 The voltage-gated sodium channel is critical for cardiomyocyte function an

186 The NaV1.7 voltage-gated sodium channel is implicated in human pain perception by

187 ensitivity to pain (CIP); this voltage-gated sodium channel is therefore a key target for analgesic d

188 Inhibition of voltage-gated sodium channels is neuroprotective in preclinical models

189 Nav1.6 is the primary voltage-gated sodium channel isoform expressed in mature axon initial

190 The voltage-gated sodium channel isoform Na(V)1.7 is highly expressed in d

191 Three pore-forming sodium channel isoforms are primarily expressed in the p

192 E STATEMENT It is unclear whether individual sodium channel isoforms exert differential roles in acti

193 er than 200-fold selectivity over off-target sodium channel isoforms, Na(V)1.1-1.6 and Na(V)1.8.

194 xhibit high levels of selectivity over other sodium channel isoforms.

195 is capable of binding to these voltage-gated sodium channels, it has a very different mode and site o

196 of the soma: the voltage-gated potassium and sodium channels Kv1.4 and Nav1.6 and the glycoprotein CD

197 iological role of MAP1B in the regulation of sodium channel localization and will contribute to futur

198 iletine, is often utilized for patients with sodium channel-mediated type 3 long QT syndrome (LQT3).

199 The sodium channel modulator GS967/Prax330 prolonged surviva

200 The finding of voltage-gated sodium channel mutations in small fibre neuropathy (with

201 ent of two types of epilepsy associated with sodium channel mutations.

202 sed by de novo gain-of-function mutations of sodium channel Na(v) 1.6 that result in neuronal hyperac

203 the SCN1A gene encoding brain voltage-gated sodium channel Na(V)1.1.

204 The sarcolemmal voltage gated sodium channel Na(V)1.4 conducts the key depolarizing cu

205 the gene encoding the cardiac voltage-gated sodium channel Na(v)1.5 cause various cardiac arrhythmia

206 Voltage-gated sodium channel Na(v)1.5 generates cardiac action potenti

207 assium channel K(V)1.3 and the voltage-gated sodium channel Na(V)1.7 as examples of targeting ion cha

208 Voltage-gated sodium channel Na(V)1.7 is a genetically validated targe

209 Sodium channel Na(V)1.7 is a major target in pain resear

210 humans, functional loss of the voltage-gated sodium channel Na(v)1.7 leads to pain insensitivity with

211 or potential channel TRPA1 and voltage-gated sodium channel Na(v)1.7, that accompany algogen insensit

212 SCN9A encodes the voltage-gated sodium channel Na(v)1.7, which is present in DRG nocicep

213 t two disease mutations in the voltage-gated sodium channel Na(v)1.8 that induce nociceptor hyperexci

214 Here, we engineered the model sodium channel Na(V)Ab with voltage-shifting mutations a

215 osslink in the VS of the ancestral bacterial sodium channel Na(V)Ab.

216 neurons via a paracrine mechanism involving sodium channel Na(x) expressed by astrocytes and the epe

217 The sodium channels Na(V)1.8 and Na(V)1.9, as well as the TR

218 biophysical analysis revealed voltage-gated sodium channel (Na(V)) currents in menthol-sensitive Vgl

219 or homologous factors) are key regulators of sodium channel (Na(V)) inactivation.

220 nsory neurons express multiple voltage-gated sodium channels (Na(V) ) critical for the initiation and

221 X), a neurotoxin that binds to voltage-gated sodium channels (Na(v) proteins), arresting electrical a

222 Voltage-gated sodium channels (Na(V)) are indispensable for transforma

223 alated disk (ID) nanodomains rich in cardiac sodium channels (Na(V)1.5) and slowing cardiac conductio

224 Voltage-gated sodium channels (Na(v)s) initiate the action potential w

225 urane binding to the bacterial voltage-gated sodium channel NaChBac.

226 ABSTRACT: Voltage-gated sodium channel NaV 1.7 is required for acute and inflamm

227 Voltage-gated sodium channel (NaV) mutations cause genetic pain disord

228 mmunostaining for tyrosine hydroxylase (TH), sodium channels (Nav ) and ankyrin-G (Ank-G) was used to

229 They are rich in voltage-gated sodium channels (Nav) and thus underpin rapid nerve impu

230 We examined the repertoire of voltage-gated sodium channels (NaV) in fluorescence-sorted mouse EC ce

231 vertebrates, target conserved voltage-gated sodium channels (NaV) of nerve and muscle, causing paral

232 uman SAN excitability requires voltage-gated sodium channels (Nav) remains controversial.

233 e thermal random motion of the voltage-gated sodium channels (Nav), which are bound to ankyrin partic

234 unction mutations in the brain voltage-gated sodium channel NaV1.1.

235 gene (SCN2A) coding for human voltage-gated sodium channel NaV1.2 (P = 9 x 10(-4)).

236 SCN2A gene that disrupt the encoded neuronal sodium channel NaV1.2 are important risk factors for aut

237 in SCN2A, a gene encoding the voltage-gated sodium channel Nav1.2, have been associated with a spect

238 re, EC cells use Scn3a-encoded voltage-gated sodium channel NaV1.3 for electrical excitability and 5-

239 role for the regulation of the voltage-gated sodium channel NaV1.5 in the heart by the serum and gluc

240 mportant functional regulator of the cardiac sodium channel Nav1.5, and some beta3 mutations predispo

241 ted the effect of LITAF on the voltage-gated sodium channel Nav1.5, which is critical for cardiac dep

242 Our data show that TTX-S sodium channel Nav1.6 is involved in the functional chan

243 expression and function of the voltage-gated sodium channel Nav1.7 are increased in a preclinical mod

244 ic studies have implicated the voltage-gated sodium channel NaV1.7 as a therapeutic target for the tr

245 Furthermore, FGF13 interacted with the sodium channel Nav1.7 in a heat-facilitated manner.

246 The sodium channel Nav1.7 is crucial for impulse generation

247 this concept to the analysis of variants in sodium channel NaV1.7 subunit found in patients with chr

248 Gain-of-function mutations of voltage-gated sodium channel Nav1.7 underlie dorsal root ganglion neur

249 rmed an important role for the voltage-gated sodium channel Nav1.9 in human pain disorders.

250 etween the rat skeletal muscle voltage-gated sodium channel (Nav1.4) and fluorescently labeled Nav1.4

251 n-of-function mutations in the voltage-gated sodium channel (Nav1.5) are associated with the long-QT-

252 hysiological regulator of the heart-specific sodium channel, Nav1.5.

253 clearly demonstrated that the voltage-gated sodium channel, Nav1.7, is critical to pain sensation in

254 Voltage-gated sodium channels (NaVs) are activated by transiting the v

255 Mutations in voltage-gated sodium channels (Navs) can cause alterations in pain sen

256 Voltage-gated sodium channels (Navs) play crucial roles in excitable c

257 Voltage-gated sodium channels (Navs) play essential roles in excitable

258 bles spikes to be generated efficiently (few sodium channels needed) and with rapid recovery that enh

259 er 60 mutations of SCN4A encoding the NaV1.4 sodium channel of skeletal muscle have been identified i

260 e drugs is thought to be due to the block of sodium channels on excitatory neurons, primarily Na(V)1.

261 nserved sites were enriched in voltage-gated sodium channels, particularly the alpha subunits (p = 8.

262 Voltage-gated sodium channels play a critical role in cellular excitab

263 KEY POINTS: Voltage-gated sodium channels play a fundamental role in determining n

264 lity, and that the first domain of all three sodium channels plays a role in determining the rate at

265 Calcium (Cav1 and Cav2) and sodium channels possess homologous CaM-binding motifs, k

266 ed that ENaC evolved from a proton-activated sodium channel present in ionocytes of freshwater verteb

267 Importantly, the expression of the sodium channel protein NaV1.5 was altered in AV nodal ce

268 ed on high-resolution structures of a single sodium channel protein.

269 esthetic and antiepileptic drug binding to a sodium channel, revealing sites and pathways that may of

270 pagated by a single isoform of voltage gated sodium channels - SCN5A.

271 tion selectivity of eukaryotic voltage-gated sodium channels showed a sharp size cut-off for ion perm

272 under control of the sensory neuron-specific sodium channel (sns) gene to selectively silence these n

273 y and in vitro activity at the voltage-gated sodium channel subtype 1.7 (Na(V)1.7), a channel targete

274 Specifically, voltage-gated sodium channel subtype NaV 1.7 is required for sensing a

275 d by gain-of-function mutations in Nav1.8, a sodium channel subtype predominantly expressed in periph

276 ral nerve fibers, but clarifying the role of sodium channel subtypes in different axonal segments may

277 ke of the insecticide or when binding at the sodium channel, the presumed destination of the neurotox

278 Yet zebrafish lack epithelial sodium channels, the primary conduit land animals use to

279 te exon encoding part of the first domain of sodium channels to compare how splicing modifies differe

280 be a good exemplar for drug binding to human sodium channels, to examine the structural and functiona

281 - or C- termini of Shaker monomers or within sodium channels two-domain fragments.

282 determined the structure of a voltage-gated sodium channel, two-pore channel 3 (TPC3), which generat

283 late sodium current across a panel of 7 LQT3 sodium channel variants and suppressing arrhythmic activ

284 der long QT syndrome 3 (LQT3) carrying SCN5A sodium channel variants.

285 Voltage-gated sodium channel (VGSC) beta1 subunits are multifunctional

286 notyping and sequencing of the voltage gated sodium channel (VGSC) gene did not detect the common L10

287 Veratridine (VTD) is a voltage-gated sodium channel (VGSC) modifier that is used as an "agoni

288 Voltage-gated sodium channel (VGSC) mutations cause severe epilepsies

289 studies have linked pathogenic voltage-gated sodium channel (VGSC) variants to human pain disorders.

290 Voltage-gated sodium channels (VGSC) are transmembrane proteins that g

291 We hypothesize that the voltage-gated sodium channels (VGSC) on the dorsal root ganglion (DRG)

292 Notably, voltage-gated sodium channels (VGSC) that are crucial for neuronal exc

293 er than the activation time of voltage-gated sodium channels (VGSC) would evoke action potentials (AP

294 ted fibres, however, show that voltage-gated sodium channels (VGSCs) aggregate with cell adhesion mol

295 NQ2/3 (Kv7.2/7.3) channels and voltage-gated sodium channels (VGSCs) are enriched in the axon initial

296 in which the alpha-subunit of the epithelial sodium channel was conditionally deleted in taste buds (

297 Using heterologously expressed human Nav1.7 sodium channels, we examined the state-dependent effects

298 We used the prokaryotic NavMs sodium channel, which has been shown to be a good exempl

299 Dysfunction of Na(V)1.1 sodium channels, which are chiefly expressed in inhibito

300 cold stimuli in Adelta-fibers by activating sodium channels without producing heat or mechanical all