ライフサイエンスコーパス: sodium channel

1 the deactivated voltage sensor of bacterial sodium channel.

2 -gated sodium channel, the principle cardiac sodium channel.

3 p.E1483K) in SCN8A, encoding a voltage-gated sodium channel.

4 f sodium ions in the selectivity filter of a sodium channel.

5 c3818C > T; pAla1273Val) in the NaV1.1 brain sodium channel.

6 borated a revised PyR1 model of the mosquito sodium channel.

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

8 separation as a compliment or alternative to sodium channels.

9 contribution to plasma membrane delivery of sodium channels.

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

11 and 500-fold selectivity against off-target sodium channels.

12 of the effects of this compound on isolated sodium channels.

13 and epilepsy-associated mutant voltage-gated sodium channels.

14 ays inactivation of vertebrate voltage-gated sodium channels.

15 otoxin resistance through point mutations in sodium channels.

16 y inhibited a number of mammalian and insect sodium channels.

17 channels, resulting in prolonged opening of sodium channels.

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

19 nservation of this mechanism among mammalian sodium channels.

20 seizure agent that targets voltage-dependent sodium channels.

21 CaMKII as a plausible modulator of neuronal sodium channels.

22 enom able to inhibit the human voltage-gated sodium channel 1.7 (hNaV1.7), a channel reported to be i

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

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

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

26 ins are well known blockers of voltage-gated sodium channels, a property that is of broad interest in

27 esent a structural and functional study of a sodium channel activation inhibitor from crab spider ven

28 ess was associated with enhanced endothelial sodium channel activation, attenuated endothelial nitric

29 n conjunction with reductions in endothelial sodium channel activation, oxidative stress and macropha

30 tion of a WD plays a key role in endothelial sodium channel activation, reduced nitric oxide producti

31 prevent WD-induced increases in endothelial sodium channel activation, reductions in bioavailable ni

32 can increase cardiac contractility, but most sodium channel activators have proarrhythmic effects tha

33 her discovered that SMA MNs exhibit enhanced sodium channel activities with increased current amplitu

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

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

36 insecticide, and pyrethroid insecticides are sodium channel agonists.

37 slices, we find that dendritic voltage-gated sodium channels allow somatic action potentials to activ

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

39 ations in the coding region of voltage-gated sodium channel alpha 1 subunit gene, SCN1A, were identif

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

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

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

43 the ventricle is to chaperone voltage-gated sodium channel alpha-subunits to the plasma membrane.

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

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

46 ules via activation of the apical epithelial sodium channel and the basolateral Na(+)/K(+)ATPase pump

47 posium, with a focus on the role of aberrant sodium channels and abnormal sodium homeostasis in cardi

48 and ranolazine enhance slow inactivation of sodium channels and are approved by the US Food and Drug

49 oids have been shown to target voltage-gated sodium channels and cannabidiol has recently received at

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

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

52 the interaction of FGF14 with voltage-gated sodium channels and neuronal excitability.

53 in diabetic animals by targeting epithelial sodium channels and stimulating keratinocyte proliferati

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

55 e nephron cannot be compensated for by other sodium channels and/or transporters, only by a high-sodi

56 e's putative molecular target (voltage-gated sodium channels) and mechanism of action (inhibition of

57 ward currents (primarily through calcium and sodium channels) and outward currents (primarily through

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

59 n part, through its actions on voltage-gated sodium channels, and resurgent current may be a promisin

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

61 l characterization of the western honeybee's sodium channel (Apis Mellifera NaV1).

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

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

64 Activation and inactivation of voltage-gated sodium channels are critical for proper electrical signa

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

66 Voltage-gated sodium channels are crucial determinants of neuronal exc

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

68 Voltage-gated sodium channels are essential for electrical signalling

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

70 However, when voltage-gated sodium channels are temporarily blocked, cell volume and

71 Voltage-gated sodium channels are the primary target of pyrethroid ins

72 Drugs that block sodium channels are used in local anesthesia and the tre

73 on potentials suggested slow inactivation of sodium channels as an important contributor to warmup.

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

75 ves requires the clustering of voltage-gated sodium channels at nodes of Ranvier.

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

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

78 Thus, low somatic sodium channel availability appears to enhance fidelity

79 However, it was not clear how low sodium channel availability in the soma influenced the t

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

81 ere we describe the use of small prokaryotic sodium channels (BacNav) to create de novo excitable hum

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

83 We report that sodium channel beta1 subunit proteins encoded by this mu

84 Mutations in SCN2B, encoding voltage-gated sodium channel beta2-subunits, are associated with human

85 hat Ae1a potently inhibits the voltage-gated sodium channel BgNaV1 from the German cockroach Blattell

86 the efficacy of both drugs to mexiletine, a sodium channel blocker currently used to treat myotonia.

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

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

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

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

91 The clinical suspicion and use of a sodium-channel blocker to unmask BrS has allowed earlier

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

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

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

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

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

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

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

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

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

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

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

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

104 hey preferably bind to the open state of the sodium channel by interacting with two distinct receptor

105 iracid (50 nM) inhibited the activity of the sodium channel by over 50%.

106 g mechanisms of resistance and modulation of sodium channels by structurally different ligands.

107 well known that specific mutations in insect sodium channels confer knockdown resistance (kdr) to pyr

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

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

110 ntains the pore-forming degenerin/epithelial sodium channel (DEG/ENaC) proteins MEC-4 and MEC-10.

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

112 The activity of background potassium and sodium channels determines neuronal excitability, but ph

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

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

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

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

117 Conversely, epithelial sodium channel (ENaC) activity was largely preserved, su

118 icoid receptors (MRs) to increase epithelial sodium channel (ENaC) activity.

119 ations of the amiloride-sensitive epithelial sodium channel (ENaC) and characterized by neonatal life

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

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

122 thality associated with increased epithelial sodium channel (ENaC) expression in lung and kidney.

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

124 Inhibitors of the epithelial sodium channel (ENaC) have therapeutic potential in CF a

125 The epithelial sodium channel (ENaC) is a member of the ENaC/degenerin

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

127 The epithelial sodium channel (ENaC) of the kidney is necessary for ext

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

129 porter (NCC) and alpha- and gamma-epithelial sodium channel (ENaC) subunits from the discovery set we

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

131 mice, whereas upregulation of the epithelial sodium channel (ENaC) sufficient to increase the electro

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

133 2, which negatively regulates the epithelial sodium channel (ENaC), Na(+)/Cl(-) cotransporter (NCC),

134 +):Cl(-) cotransporter (NCC), the epithelial sodium channel (ENaC), the renal outer medullary potassi

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

136 Regulation of the epithelial sodium channel (ENaC), which regulates fluid homeostasis

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

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

139 how formaldehyde regulates human epithelial sodium channels (ENaC) in H441 and expressed in Xenopus

140 electrochemical gradient through epithelial sodium channels (ENaC).

141 fluid absorption, mainly via the epithelial sodium channel, ENaC.

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

143 x in keratinocytes is mediated by epithelial sodium channels (ENaCs) and causes increased secretion o

144 g to a receptive class-related difference of sodium channel equipment.

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

146 ch of the four S6 segments of the eukaryotic sodium channel form an occlusion for ions in the closed

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

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

149 ); however, the mechanisms that link loss of sodium channel function to arrhythmic instability remain

150 wet/dry weight ratios, increased epithelial sodium channel gamma expression, and more lymphatic vess

151 tions associated with LQT3 promote a mode of sodium channel gating in which some channels fail to ina

152 s therefore concluded to represent the first sodium channel gating modifier from an araneomorph spide

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

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

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

156 nderstand the mechanism of a mutation in the sodium channel gene SCN1B linked to genetic epilepsy wit

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

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

159 De novo mutations of the sodium channel gene SCN8A, encoding the sodium channel N

160 intron 16 of SCN5A, a voltage-gated cardiac sodium channel gene.

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

162 gate residue in the eukaryotic voltage-gated sodium channel has been identified, the minimal molecula

163 Slow inactivation of voltage-gated sodium channels has been discussed to be the underlying

164 Mutations in brain isoforms of voltage-gated sodium channels have been identified in patients with di

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

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

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

168 rvations showing an upregulation of neuronal sodium channels in the brain during epilepsy, we tested

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

170 We studied this using dynamic clamp to mimic sodium channels in the soma, which yielded normal, overs

171 ng nonovershooting action potentials and few sodium channels in the soma.

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

173 ation (PAD) normally mediates inhibition via sodium channel inactivation and shunting but can evoke s

174 ight into a rare form of CMS precipitated by sodium channel inactivation defects.

175 ates the rate of closed-state and open-state sodium channel inactivation, which synergizes with tempe

176 Knocking out TTXr sodium channels influences use-dependent changes of cond

177 In this study we aimed to establish whether sodium-channel inhibition with phenytoin is neuroprotect

178 dine (GS967) is a recently described, novel, sodium channel inhibitor exhibiting potent antiarrhythmi

179 ons or silencing them with QX-314, a charged sodium channel inhibitor that enters via large-pore ion

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

181 Voltage-gated sodium channels initiate action potentials in nerve, mus

182 vides crucial information for development of sodium channel insecticides that target key insect pests

183 throids, the atomic mechanisms of pyrethroid-sodium channel interactions are not clearly understood.

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

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

186 50 on skeletal (Nav1.4) and cardiac (Nav1.5) sodium channels is above 3000 nm The lead molecules have

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

188 in SCN10A, encoding the voltage-gated Nav1.8 sodium channel, is associated with PR-interval prolongat

189 human pain syndrome linked to voltage-gated sodium channels, is widely regarded as a genetic model o

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

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

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

193 v.1.7, the main pain signaling voltage-gated sodium channel, lead to its truncations and, consequentl

194 Axonal organelles and sodium channel localization are sensitive to local block

195 ation of splicing of mammalian voltage-gated sodium channels may be exploitable to provide effective

196 endent mechanism required the Degenerin/ENaC sodium channel MEC-4, the L-type voltage-gated calcium c

197 docking of DDT into the Kv1.2-based mosquito sodium channel model, we predict that two DDT molecules

198 Axonal voltage-gated sodium channel mRNA and local trafficking were examined

199 incomplete inactivation of the major cardiac sodium channel Na(V)1.5 is correlated with an increased

200 codes the alpha subunit of the major cardiac sodium channel Na(V)1.5, are associated with multiple ca

201 codes the alpha subunit of the major cardiac sodium channel Na(V)1.5.

202 ia was linked to gain-of-function changes of sodium channel Na(v)1.7 only a decade ago, the literatur

203 showed decreased mRNA production, whereas a sodium channel (Na(V)beta4) associated with burst firing

204 ndous therapeutic potential of voltage-gated sodium channels (Na(v)s) has been the subject of many st

205 Voltage-gated sodium channels (Na(V)s) provide the initial electrical

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

207 SCN4A, the gene encoding the skeletal muscle sodium channel Nav 1.4, revealed a homozygous mutation p

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

209 ibution of the tetrodotoxin-resistant (TTXr) sodium channels Nav 1.8 and Nav 1.9 to these changes.

210 dependence in tetrodotoxin-resistant (TTXr) sodium channel (Nav 1.8, Nav 1.9) knockout and wildtype

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

212 iation at the axon initial segment relies on sodium channel (Nav)-associated fibroblast growth factor

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

214 glutamate receptor-1 (mGluR1), voltage-gated sodium channels (Nav ) and glutamate transporters.

215 he domain IV voltage sensor of voltage-gated sodium channels (Nav ) and slows down their fast inactiv

216 which select for TTX-resistant voltage-gated sodium channels (Nav) [12-16].

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

218 40, like Nfasc186, can cluster voltage-gated sodium channels (Nav) at the developing node of Ranvier

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

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

221 Voltage-gated sodium channels (NaV) play an important role in general

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

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

224 tations in SCN1A, the gene encoding neuronal sodium channel Nav1.1.

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

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

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

228 blished that MOG1 interacts with the cardiac sodium channel Nav1.5 and regulates cell surface traffic

229 genome sequencing suggested a variant in the sodium channel NaV1.5 encoded by SCN5A, NM_000335:c.5284

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

231 5A gene, coding for the alpha-subunit of the sodium channel NaV1.5.

232 the sodium channel gene SCN8A, encoding the sodium channel Nav1.6, result in EIEE13 (OMIM 614558), w

233 This is due to the voltage-gated sodium channel Nav1.7 (Scn9a), previously associated wit

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

235 Mutations in the voltage-gated sodium channel Nav1.7 are linked to inherited pain syndr

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

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

238 Voltage-gated sodium channel Nav1.7 is a central player in human pain.

239 Trafficking of the voltage-gated sodium channel NaV1.7 is dysregulated in neuropathic pai

240 (IEM) in which gain-of-function mutations of sodium channel NaV1.7 make dorsal root ganglion (DRG) ne

241 The human voltage-gated sodium channel Nav1.7 plays a crucial role in transmissi

242 cond intracellular loop of the voltage-gated sodium channel NaV1.7, encoded by the SCN9A gene, was id

243 iggered by warmth, is caused by mutations in sodium channel Nav1.7, which are preferentially expresse

244 physiological conditions, the voltage-gated sodium channel Nav1.8 is expressed almost exclusively in

245 , MrVIB, and MfVIA inhibit the voltage-gated sodium channel NaV1.8, a well described target for the t

246 .5, but selectively activated the brain-type sodium channels Nav1.6 or Nav1.3 in cellular electrophys

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

248 subunit of the skeletal muscle voltage-gated sodium channel (Nav1.4).

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

250 Cardiac voltage-gated sodium channels (Nav1.5) play an essential role in regul

251 m channel (SCN5A gene encoding voltage-gated sodium channel [NaV1.5]) cause congenital long-QT syndro

252 The main cardiac sodium channel, NaV1.5, carries the sodium current (INa)

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

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

257 Improper function of voltage-gated sodium channels (NaVs), obligatory membrane proteins for

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

259 substantial level of sequence homology among sodium channels, our data also implicate MMP proteolysis

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

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

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

263 omote activation and inhibit inactivation of sodium channels, resulting in prolonged opening of sodiu

264 Mutations of the cardiac voltage-gated sodium channel (SCN5A gene encoding voltage-gated sodium

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

266 exon 6B towards fetal exon 6A in the cardiac sodium channel, SCN5A.

267 centrations at which it blocks voltage-gated sodium channels selectively.

268 s and the crystal structure of a prokaryotic sodium channel, showing for the first time the detailed

269 Splicing of the Drosophila sodium channel shows many similarities to its mammalian

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

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

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

273 ut (CKO) mice, in which Myd88 was deleted in sodium channel subunit Nav1.8-expressing primary sensory

274 human-specific isoform of the voltage-gated sodium channel subunit SCN4B was significantly correlate

275 no acid substitutions in the skeletal muscle sodium channel that reduce TTX binding, suggesting that

276 to have evolved from ancestral voltage-gated sodium channels that are widely expressed in prokaryotes

277 gously expressed human cardiac voltage-gated sodium channel, the principle cardiac sodium channel.

278 ter splicing of the Drosophila voltage-gated sodium channel to favour inclusion of exon K, rather tha

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

280 cretory organelles are capable of delivering sodium channels to the plasma membrane in isolated axons

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

282 Voltage-gated sodium channel (VGSC) beta subunits signal through multi

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

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

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

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

287 ly overexpress large mammalian voltage-gated sodium channels (VGSC).

288 nd functional relationships of voltage-gated sodium channels (VGSC).

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

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

291 Voltage-gated sodium channels (VGSCs) are responsible for the initiati

292 ave recently demonstrated that voltage-gated sodium channels (VGSCs) in dorsal root ganglion (DRG) ne

293 Voltage-gated sodium channels (VGSCs) regulate invasion and metastasis

294 Clustering of voltage-gated sodium channels (VGSCs) within the neuronal axon initial

295 The pioneering model of the housefly sodium channel visualized the first receptor for pyrethr

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

297 dins220 association with brain voltage-gated sodium channels was shown by co-immunoprecipitation expe

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

299 correlating increased expression of neuronal sodium channels within the heart to epilepsy-related car

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