ライフサイエンスコーパス: Na channel

1 ssing of the gamma isoform of the epithelial Na(+) channel.

2 non-identical voltage-sensing domains of the Na(+) channel.

3 ioned in the detection of low salt and was a Na(+) channel.

4 ema may be reversed by temporary blockade of Na(+) channels.

5 pon simultaneous activation of both LCCs and Na(+) channels.

6 recovery from inactivation) of voltage-gated Na(+) channels.

7 Nav1.5 and Nav1.5-CW inactivation-deficient Na(+) channels.

8 tween bacterial and eukaryotic voltage-gated Na(+) channels.

9 h lidocaine remains specific for inactivated Na(+) channels.

10 encode prematurely truncated, nonfunctional Na(+) channels.

11 ermediate preopen and open states of hNav1.5 Na(+) channels.

12 the NMDA receptor (NMDAR) and voltage-gated Na(+) channels.

13 raded potential models lacking voltage-gated Na(+) channels.

14 distinct effects on inactivation of cardiac Na(+) channels.

15 lux of sodium (Na(+)) ions via voltage-gated Na(+) channels.

16 ischarge associated with a deficit in Nav1.6 Na(+) channels.

17 rminals with undefined molecular partners of Na(+) channels.

18 nels (LCCs), ryanodine receptors and sodium (Na(+)) channels.

19 y, inhibition of amiloride-sensitive sodium (Na(+)) channels.

20 nce, characteristic of mammalian Ca(2+), not Na(+), channels.

21 ns, light-mediated REST inhibition increased Na(+)-channel 1.2 and brain-derived neurotrophic factor

22 C-to-DAC transmission requires voltage-gated Na(+) channels; (2) this transmission is partly dependen

23 cleotide phosphate, as also as intracellular Na(+) channels able to control endolysosomal fusion, a k

24 JI Epistasis assays show that voltage-gated Na(+) channels act downstream of H2O2 to modulate regene

25 y carbamazepine and additional commonly used Na(+) channel-acting anticonvulsants, both in control an

26 In this work, we tested whether truncated Na+ channels activate the unfolded protein response (UPR

27 transmitter release; decreases threshold for Na(+) channel activation; and slows Na(+) channel inacti

28 e model exhibit proexcitatory alterations in Na channel activity, some of which were not seen in hipp

29 Together these channel proteins promote K(Na) channel activity and dampen neuronal excitability.

30 r study thus reveals that TMEM16C enhances K(Na) channel activity in DRG neurons and regulates the pr

31 More broadly, voltage-gated Na channels adopt this same modulatory principle.

32 ions in the mRNA level of Scn5a (the cardiac Na(+) channel alpha subunit gene), as well as a 56% redu

33 Thus, Nav1.3 is the functionally important Na(+) channel alpha subunit in both alpha- and beta-cell

34 gene classically defined as ancillary to the Na(+) channel alpha subunit, can be partly consequent to

35 gene classically defined as ancillary to the Na(+) channel alpha subunit, can be partly consequent to

36 beta4 depends on its direct interaction with Na(+) channel alpha subunits through an extracellular di

37 gene classically defined as ancillary to the Na+ channel alpha subunit, can be partly consequent to d

38 plicing of the type V, voltage-gated cardiac Na+ channel alpha-subunit (SCN5A), generating variants e

39 Na channels also bind exogenous compounds, such as lidoc

40 feature is curiously absent for the related Na channels, also potently regulated by calmodulin.

41 mbryonic kidney (HEK) cells expressing human Na channels and by modeling human action potentials.

42 iated with mutation in the gene encoding the Na(+) channel and acquired conditions associated with he

43 lazine and predicted the combined effects of Na(+) channel and IKr blockade by both the parent compou

44 tation-contraction coupling and arrhythmias: Na(+) channel and Na(+) transport.

45 tation-contraction coupling and arrhythmias: Na(+) channel and Na(+) transport.

46 of neurofascin 186, followed by the loss of Na(+) channels and ankyrin G, and then betaIV spectrin,

47 BTX targets voltage-gated Na(+) channels and enables them to open persistently.

48 nsporters to study the communication between Na(+) channels and mitochondria.

49 Mechanistically, 4 inhibited voltage-gated Na(+) channels and N-type Ca(2+) channels and was effect

50 The ubiquity of disruption of Na(+) channels and Na(+) homeostasis in cardiac disorder

51 tering signal) resulted in a gradual loss of Na(+) channels and other axonal components from the node

52 gate the relationship between the density of Na(+) channels and the spatiotemporal pattern of AP init

53 to derive from primary interactions with the Na(+) channel, and benefit may be gained from an alterna

54 th tetrodotoxin (TTX)-dependent block of the Na(+) channel, and molecular manipulation of mitochondri

55 inhibition of hERG K(+) channels and hNaV1.5 Na(+) channels, and no effects were observed on cardiova

56 hannel clustering, progressive loss of nodal Na(+) channels, and seizures.

57 Although voltage-dependent Na(+) channels are abundantly expressed in beta cells an

58 Voltage-dependent Na(+) channels are crucial for electrical signalling in

59 Recent studies have shown that Na(+) channels are highly clustered at the myocyte inter

60 f a covalent tether of peptide to its target Na channels at a distinct ligand-binding site.

61 ion is crucial for the initial clustering of Na(+) channels at heminodes.

62 A high density of Na(+) channels at nodes of Ranvier is necessary for rapi

63 t neural conduction requires accumulation of Na(+) channels at nodes of Ranvier.

64 contributes to the long-term maintenance of Na(+) channels at nodes of Ranvier.

65 mplexes exist in myelinated axons to cluster Na(+) channels at nodes of Ranvier.

66 n depends on the myelin sheath and clustered Na(+) channels at nodes of Ranvier.

67 dal junction-dependent mechanism can cluster Na(+) channels at nodes.

68 such as NaVbeta4 (Scn4b), which blocks open Na(+) channels at positive voltages, competing with the

69 secreted gliomedin induces the clustering of Na(+) channels at the edges of each myelin segment to fo

70 Clustering of Na(+) channels at the nodes of Ranvier is coordinated by

71 sting membrane potential, thereby increasing Na(+) channel availability for action potential propagat

72 ling prokaryote single-domain, voltage-gated Na(+) channels (BacNa(v)s) [4].

73 K mutant and batrachotoxin-activated hNav1.5 Na(+) channels became completely lacosamide resistant, i

74 pulses from -90 to -50 mV; however, hNav1.5 Na(+) channels became sensitive to lacosamide with IC50

75 d membrane voltage, we demonstrate here that Na(+) channel beta2 subunits (Navbeta2s) are required to

76 AP waveforms independent of morphology, (2) Na(+) channel beta2 subunits modulate AP-evoked Ca(2+)-i

77 cardiomyocyte-, tissue-, and state-dependent Na(+)-channel block mathematical models, optical mapping

78 Combining optimized Na(+)-channel block with blockade of atrial K(+) current

79 ling reproduced an enhanced effectiveness of Na-channel block when resting membrane potential was sli

80 ve anti-AF effects obtainable with optimized Na(+)-channel blockade.

81 e S-enantiomer of propafenone, an equipotent Na channel blocker but much weaker RyR2 inhibitor, did n

82 We show that phenytoin, a Na channel blocker used clinically for treatment of epil

83 Treatment with the epithelial Na(+) channel blocker amiloride, improving airway surfac

84 n a use-dependent manner by the prototypical Na(+) channel blocker carbamazepine.

85 reducing axonal electrical activity with the Na(+) channel blocker flecainide.

86 The pure Na(+) channel blocker lidocaine and the antianginal rano

87 mate receptors after 48 h silencing with the Na(+) channel blocker tetrodotoxin.

88 strains co-expressing Hybrid toxin and AaIT (Na(+) channel blocker) produced synergistic effects, req

89 The effects of flecainide, a sodium (Na(+))-channel blocker, and d,l-sotalol, a potassium cha

90 tively terminated AF compared with optimized Na(+)-channel blocker alone.

91 Combining optimized Na(+)-channel blocker with IKr block increased rate-depe

92 Combining optimized Na(+)-channel blocker with IKur block had similar effect

93 ivity was obtained with an inactivated-state Na(+)-channel blocker.

94 ydroartemisinin (DHA) and various Ca(2+) and Na(+) channel blockers and showed positively correlated

95 cal profile and anti-AF effects of optimized Na(+)-channel blockers.

96 tial and thereby alters the effectiveness of Na-channel blockers.

97 letine, which is structurally related to the Na(+) channel-blocking anesthetic lidocaine, is used to

98 e by introducing them into rat Nav1.4 muscle Na(+) channel, both individually and in combination.

99 In addition to blocking Na(+) channels, bupivacaine affects the activity of many

100 only are potent modulators of voltage-gated Na+ channels but also affect Ca2+ channels and their fun

101 re intracellular modulators of voltage-gated Na+ channels, but their cellular distribution in cardiom

102 gs indicate that gain-of-function in Slack K(Na) channels causes hyperexcitability in both isolated n

103 may be attributable to modulation of cardiac Na(+) channels, causing an increase in the late current

104 because of a larger contribution of neuronal Na channels characterized by their high sensitivity to t

105 Here we show that while Na(+) channels cluster at nodes in the absence of NF186,

106 caffolding protein ankyrin-G is required for Na(+) channel clustering at axon initial segments.

107 It is also considered essential for Na(+) channel clustering at nodes of Ranvier to facilita

108 ial propagation in myelinated axons requires Na(+) channel clustering at nodes of Ranvier.

109 ins and dystroglycan complexes contribute to Na(+) channel clustering at peripheral nodes by unknown

110 n, NrCAM, and NF186 not only plays a role in Na(+) channel clustering during development, but also co

111 cking nodal beta spectrins have normal nodal Na(+) channel clustering during development, but progres

112 etal scaffolds traditionally associated with Na(+) channel clustering in neurons and are important fo

113 here that ankyrin-G is dispensable for nodal Na(+) channel clustering in vivo.

114 tein complexes function as secondary reserve Na(+) channel clustering machinery, and two independent

115 BMP1)/Tolloid (TLD)-like proteinases confine Na(+) channel clustering to these sites by negatively re

116 alone, including profound disruption of AIS Na(+) channel clustering, progressive loss of nodal Na(+

117 taI spectrin substitute for and rescue nodal Na(+) channel clustering.

118 oskeletal mechanisms ensure robust CNS nodal Na(+) channel clustering.

119 motor dysfunction, and significantly reduced Na(+) channel clustering.

120 he paranodal junction-dependent mechanism of Na(+)channel clustering is mediated by the spectrin-base

121 Na+ channel clustering is thought to depend on two axona

122 results in the formation of numerous ectopic Na(+) channel clusters along axons that are devoid of my

123 dal spectrins are required to maintain nodal Na(+) channel clusters and the structural integrity of a

124 of a molecular aggregate (the voltage-gated Na(+) channel complex) that includes the beta subunit fa

125 resurgent current depends on a factor in the Na(+) channel complex, probably a subunit such as NaVbet

126 fferences in the specific composition of the Na(+) channel complexes enriched at the AIS and nodes co

127 ntally important question: just what makes a Na(+) channel conduct Na(+) ions?

128 Pancreatic beta-cell Na(+) channels control global Ca(2+) signaling and oxida

129 autoresistance found in P. terribilis muscle Na(+) channels could emerge primarily from a single AA s

130 plicated in the regulation of the epithelial Na(+) channel critical for proper airway surface hydrati

131 Moreover, they presented Nav1.6 Na(+) channel deficiency, which contributed to arrhythmi

132 SIC) is a member of the degenerin/epithelial Na(+) channel (Deg/ENaC) family of ion channels.

133 nnels, allowing full axon repolarization and Na(+) channel deinactivation.

134 that small plastic changes in the local AIS Na(+) channel density could have a large influence on ne

135 initial segment (AIS) because that is where Na(+) channel density is highest.

136 oxical mismatch between the AP threshold and Na(+) channel density, which could be explained by the l

137 backpropagation and excitability, based on a Na(+) channel-dependent broadening of backpropagating ac

138 Cardiac Na(+) channels display less and incomplete slow inactiva

139 es distance-dependent inactivation of axonal Na(+) channels due to somatic depolarization propagating

140 ctrin cytoskeletal proteins to cluster nodal Na(+) channels during development.

141 cyte alterations, connexin dysregulation and Na(+)-channel dysfunction), electrical refractoriness, a

142 fect may form the basis for Ca(2+)-dependent Na(+) channel dysregulation in SCN4A channelopathies ass

143 Our simulations revealed that Na(+) channel effects are insufficient to explain flecai

144 Model predictions suggest that Na(+) channel effects are insufficient to explain flecai

145 Furthermore, our study suggests that Na+ channel effects alone are insufficient to explain th

146 verse ion channels to include the epithelial Na(+) channel ENaC.

147 igh-salt (HS)-induced increase in epithelial Na(+) channel (ENaC) activity in the cortical collecting

148 , claudin-7, and cleaved forms of epithelial Na(+) channel (ENaC) alpha and gamma subunits, which ass

149 odium via the amiloride-sensitive epithelial Na(+) channel (ENaC) and nonselective cyclic-nucleotide-

150 The renal epithelial Na(+) channel (ENaC) expression and function were measur

151 Canonical vertebrate epithelial Na(+) channel (ENaC) formed by alpha-, beta-, and gamma-

152 Epithelial Na(+) channel (ENaC) function is regulated by the intrac

153 The epithelial Na(+) channel (ENaC) functions as a pathway for Na(+) ab

154 The epithelial Na(+) channel (ENaC) has a key role in the regulation of

155 to and regulates stability of the epithelial Na(+) channel (ENaC) in salt-absorbing epithelia in the

156 Scnn1b-Tg mice overexpress the epithelial Na(+) channel (ENaC) in their lungs, driving increased s

157 ensitive distal nephron where the epithelial Na(+) channel (ENaC) is expressed, we hypothesized that

158 ABSTRACT: All three epithelial Na(+) channel (ENaC) subunits (alpha, beta and gamma) ar

159 Na(+) hyperabsorption through the epithelial Na(+) channel (ENaC), which contribute to reduced airway

160 1 (SPLUNC1) effectively inhibits epithelial Na(+) channel (ENaC)-dependent Na(+) absorption and pres

161 a key role in trafficking of the epithelial Na(+) channel (ENaC).

162 ) crosses the apical membrane via epithelial Na(+) channels (ENaC) and is extruded into the interstit

163 +) absorption is mediated by both epithelial Na(+) channels (ENaC) and Na-H exchangers (NHE), inhibit

164 epithelia absorb Na+ through the epithelial Na+ channel (ENaC) and secrete Cl- through the cystic fi

165 The epithelial Na+ channel (ENaC) is essential for Na+ homeostasis, and

166 ension caused by mutations in the epithelial Na+ channel (ENaC) that interfere with its ubiquitylatio

167 se to amiloride (a blocker of the epithelial Na(+) channel, ENaC).

168 Epithelial Na(+) channels (ENaCs) are members of the ENaC/degenerin

169 ng body of evidence suggests that epithelial Na(+) channels (ENaCs) in the brain play a significant r

170 ng ion channels (ASICs) are proton-activated Na(+) channels expressed in the nervous system, where th

171 The normal segregation of Na(+) channel expression and dynamics at the heminode an

172 The subcellular segregation of Na(+) channel expression and intracellular Na(+) dynamic

173 n mice lacking both ankyrin-G and ankyrin-R, Na(+) channels fail to cluster at nodes.

174 ncodes an auxiliary protein of voltage-gated Na(+) channels, fibroblast growth factor 13 (Fgf13).

175 Within the P. terribilis muscle Na(+) channel, five amino acid (AA) substitutions have b

176 zed to enhance slow inactivation of neuronal Na(+) channels for its therapeutic action.

177 , as expected for the paracellular water and Na(+) channel formed by claudin-2.

178 ized during the ISIs, preventing recovery of Na(+) channels from inactivation.

179 The present review focuses on Na(+) channel function and regulation, Na(+) channel str

180 gamma trimer dramatically reduces epithelial Na(+) channel function and surface expression, and impai

181 CRT improves DHF-induced alterations of Na(+) channel function, especially suppression of INa-L,

182 Na(+) channel gain of function (GOF), arising in both in

183 failure (DHF); however, the role of altered Na(+) channel gating in CRT remains unexplored.

184 ) current results from a distinctive form of Na(+) channel gating, originally identified in cerebella

185 consequences of four mutations in the human Na+ channel gene SCN8A causing either mild (E1483K) or s

186 in a drug-induced (sea anemone toxin, ATXII) Na(+) channel GOF isolated heart model and modulate extr

187 tes cardiac repolarization in the setting of Na(+) channel GOF.

188 ons required the activation of voltage-gated Na(+) channels, had the same frequency as the field pote

189 ntroduce roNaV2, an engineered voltage-gated Na(+) channel harboring a selenocysteine in its inactiva

190 However, Na channels have only shown subtler Ca2+ modulation that

191 Voltage-gated Na(+) channel ( I(Na)) function is critical for normal c

192 Interestingly, somatic Na(+) channels in interneurons and persistent Na(+) curr

193 tability, but physiological roles for "leak" Na(+) channels in specific mammalian neurons have not be

194 d the interaction of ranolazine with cardiac Na(+) channels in the setting of normal physiology, long

195 als depends on the presence of voltage-gated Na(+) channels in the spine head, while NMDARs are not e

196 Magi-1 scaffolds Na(V)1.8 and Slack K(Na) channels in dorsal root ganglion neurons regulating

197 me 2) or with sea anemone toxin II to impair Na(+) channel inactivation (mimicking long QT syndrome 3

198 petitive firing rates, possibly by relieving Na(+) channel inactivation, and thus contribute to maint

199 hold for Na(+) channel activation; and slows Na(+) channel inactivation.

200 A-Na(V)1.5) and demonstrated that incomplete Na+ channel inactivation is sufficient to drive structur

201 el of GS-458967 interaction with the cardiac Na+ channel, informed by experimental data recorded from

202 t blockade of ryanodine receptors (RyR2) and Na(+) channel inhibition.

203 larization refractoriness and more effective Na-channel inhibition.

204 The dual RyR2 and Na channel inhibitor R-propafenone (3 mumol/L) significa

205 (-/-) mice with ranolazine, a broadly acting Na(+) channel inhibitor that should increase NCX1 forwar

206 erefore be less susceptible to use-dependent Na channel inhibitors used as local anesthetic, antiarrh

207 e BTX receptor has been delineated along the Na(+) channel inner cavity, which is formed jointly by f

208 s, malathion) or a different mode of action (Na(+)channel-interfering insecticides; permethrin, cyper

209 als by voltage-dependent inactivation of the Na(+) channels involved in action potential generation.

210 Na(+) channels, the structure of eukaryotic Na(+) channels is still undefined.

211 A distinctive feature of prokaryotic Na(+)-channels is the presence of four glutamate residue

212 The contributions of different Na(+) channel isoforms, apart from the cardiac isoform,

213 genetic knockout (KO) mouse strain lacking K(Na) channels (KCNT1 and KCNT2) shows only a modest hyper

214 However, the Na(+) channel late component ( I(Na,L)) is directly asso

215 ectrin cytoskeletal proteins maintains nodal Na(+) channels (Liu et al., 2020).

216 lexes located beneath the myelin sheath from Na(+) channels located at nodes of Ranvier.

217 , we identify an endolysosomal ATP-sensitive Na(+) channel (lysoNa(ATP)).

218 in amplifies mGluR5 signaling independent of Na(+) channel modification.

219 ine the association of SCN5A cardiac sodium (Na(+)) channel mRNA splice variants in white blood cells

220 UPR can be initiated by Na+ channel mRNA splice variants and is involved in the

221 Kv4.3 mRNA levels resulting from expressing Na+ channel mRNA splice variants.

222 APD prolongation and EADs in the presence of Na(+) channel mutations because of increased intercellul

223 also studied mice haplo-insufficient for the Na(+) channel Na(v)1.5 (Na(v)1.5(+/)) and mice in which

224 Modification of voltage-gated Na(+) channel (Na(V) ) function by intracellular Ca(2+)

225 Skeletal muscle voltage-gated Na(+) channel (Na(V)1.4) activity is subject to calmodul

226 such inactivation is observed in the cardiac Na(+) channel (Na(V)1.5).

227 stsynaptic local activation of voltage-gated Na(+)-channels (Na(v)s), that is a spine spike.

228 derlying Na(+) sensing involves the atypical Na(+) channel, Na(X).

229 Pancreatic alpha-cells express voltage-gated Na(+) channels (NaChs), which support the generation of

230 Here, we show that a leak Na(+) channel, Nalcn, is expressed in the CO2/H(+)-sensi

231 We tested if Na(+) channel (Nav) neuronal isoforms contribute to INaL

232 annel protein family, as a new voltage-gated Na(+) channel (NaV) that generates ulAPs, and that estab

233 Thus, influx of Na(+) via voltage-gated Na(+) channels (NaV ) has emerged as an important regula

234 Voltage-gated Na(+) channels (Nav ) modulate neuronal excitability, bu

235 roles of oligodendroglial voltage-activated Na(+) channels (Nav) and electrical excitability in rela

236 zation leads to the opening of voltage-gated Na(+) channels (Nav) and subsequently voltage-dependent

237 Voltage-gated Na(+) channels (Nav) are essential for myocyte membrane

238 We tested if Na+ channel (Nav) neuronal isoforms contribute to INaL a

239 r that results from de novo mutations in the Na channel Nav1.6.

240 n-of-function mutations in the voltage-gated Na channel Nav1.6.

241 n the SCN5A gene, encoding the voltage-gated Na(+) channel NaV1.5.

242 ns in the human SCN11A-encoded voltage-gated Na(+) channel NaV1.9 cause severe pain disorders ranging

243 The voltage-gated cardiac Na(+) channel (Nav1.5), encoded by the SCN5A gene, condu

244 he absence of CNO, as well as an increase in Na(+) channel (NaV1.7) expression.

245 Dysregulation of voltage-gated cardiac Na(+) channels (NaV1.5) by inherited mutations, disease-

246 f protein, but not mRNA, for a voltage-gated Na(+) channel, Nav1.8, that is expressed almost exclusiv

247 transmitter release depends on voltage-gated Na(+) channels (Navs) to propagate an action potential (

248 potential generation: (1) the voltage-gated Na(+) channels necessary for action potential generation

249 e axon initial segment compared with somatic Na(+) channels of pyramidal neurons, suggesting converge

250 ing via use-dependent block of voltage-gated Na(+) channels on GABAergic inhibitory micronetworks in

251 brane was 10 mV hyperpolarized compared with Na(+) channels on the anterior membrane, with no differe

252 embrane revealed that activation voltage for Na(+) channels on the posterior membrane was 10 mV hyper

253 ificantly increased CaMKII-dependent cardiac Na channel phosphorylation (Na(V)1.5, at serine 571, Wes

254 undly inactivating somatic and proximal axon Na(+) channels, plateaus evoked action potentials that r

255 Voltage-gated Na(+) channels play an essential role in electrical sign

256 ls (ASICs) are widely expressed proton-gated Na(+) channels playing a role in tissue acidosis and pai

257 rystal structures of bacterial voltage-gated Na(+) channels predict that the side chain of rNaV1.4 Tr

258 ease onto Na channels, we reset this view of Na channel regulation.

259 that paranode-dependent clustering of nodal Na(+) channels requires axonal betaII spectrin which is

260 ns, the tetrodotoxin-sensitive voltage-gated Na(+) channels responsible for action potential firing h

261 way inflammation in juvenile beta-epithelial Na(+) channel (Scnn1b)-transgenic (Tg) mice.

262 The blocking of cardiac Na(+) channels should be taken into consideration when p

263 so express the sodium-activated potassium (K(Na)) channel Slack.

264 lar, aprotic R-substituent potently promoted Na+ channel slow inactivation and displayed frequency (u

265 es on Na(+) channel function and regulation, Na(+) channel structure and function, and Na(+) channel

266 Two following papers focus on Na(+) channel structure, function and regulation, and Na

267 lar localization of Navbeta4, the modulatory Na(+) channel subunit thought to underlie resurgent Na(+

268 CN1A which encodes the voltage gated sodium (Na(+)) channel subunit Nav1.1.

269 The extracellular regions of epithelial Na(+) channel subunits are highly ordered structures com

270 sayed, inhibitory synchrony was dependent on Na(+) channels, suggesting that action potentials in gra

271 tein and the alpha-subunit of the epithelial Na(+) channel, supporting impaired MR signaling.

272 ts K(ATP) channel trafficking also regulates Na(+) channel surface expression.

273 10 seconds was relatively rapid in wild-type Na(+) channels (tau; 639 +/- 90 milliseconds, n = 8).

274 samide block at -70 mV was slow in wild-type Na(+) channels (tau; 8.04 +/- 0.39 seconds, n = 8).

275 ensing ion channels (ASICs) are proton-gated Na(+) channels that are expressed throughout the nervous

276 ls (ASICs) are neuronal, voltage-independent Na(+) channels that are transiently activated by extrace

277 rystal structures of bacterial voltage-gated Na(+) channels, the structure of eukaryotic Na(+) channe

278 m, which causes a block of voltage-dependent Na+ channels throughout the myocardial wall and interrup

279 amily M member 4 (TRPM4), and perhaps TRPM5, Na(+) channels to control Ca(2+)-mediated secretion of b

280 o eliminate any contribution of plasmalemmal Na(+) channels to the observed actions of the drug at th

281 tamate receptor antagonists, a voltage-gated Na(+) channel toxin, extracellular Ca(2+) ion exclusion,

282 n, Na(+) channel structure and function, and Na(+) channel trafficking, sequestration and complexing.

283 properties of the pore-forming voltage-gated Na(+) channel (VGSC) alpha subunit, but also by the inte

284 Voltage-gated Na(+) channel (VGSC) beta1 subunits, encoded by SCN1B, a

285 properties of the pore-forming voltage-gated Na+ channel (VGSC) alpha subunit, but also by the integr

286 Functional expression of voltage-gated Na(+) channels (VGSCs) has been demonstrated in multiple

287 d the onset response by moving voltage-gated Na+ channels (VGSCs) to closed-state inactivation (CSI)

288 We monitored the cardiac Na(+) channel voltage-sensing domain (VSD) conformationa

289 Here, by rapid Ca2+ photorelease onto Na channels, we reset this view of Na channel regulation

290 rmeate the selectivity filter of prokaryotic Na(+)-channels when one or more Glu177 residues are prot

291 vating an exogenously expressed ligand-gated Na(+) channel, which depolarizes horizontal cells, cause

292 ified in SCN1A, the gene encoding the Nav1.1 Na(+) channel, which is also a major target of epileptog

293 ithin the nodal gap at the location of nodal Na(+) channels, which are known to be critical for propa

294 -dependent blocking effects on voltage-gated Na(+) channels, which are thought to underlie the inhibi

295 vity of four-domain voltage-gated Ca(2+) and Na(+) channels, which is controlled by the selectivity f

296 g during development, but progressively lose Na(+) channels with increasing age.

297 Our results show that communication of the Na(+) channels with mitochondria shape both global Ca(2+

298 rebrocortical nerve terminals after blocking Na(+) channels with tetrodotoxin.

299 ause of synaptic activation of voltage-gated Na(+) channels within the spine.

300 Depolarization and the number of inactivated Na(+) channels would build with successive spikes, resul