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

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

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

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

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

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

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

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

12 keletal scaffolds (CSs) that stabilize nodal Na(+) channels.

13 ivation phase of mammalian voltage-activated Na(+) channels.

14 l activity but not on tetrodotoxin-sensitive Na(+) channels.

15 ility, and the localization of voltage-gated Na(+) channels.

16 mutations of either voltage-gated Ca(2+) or Na(+) channels.

17 (V)1.x CTs, and the consequent regulation of Na(+) channels.

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

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

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

21 s of the ions appear to be weakly coupled in Na(+)-channels.

22 is essential for the biological function of Na(+)-channels.

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

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

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

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

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

28 es unexpectedly identified the voltage-gated Na(+) channel accessory subunit Navbeta1.

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

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

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

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 Na(V)1.5 is a cardiac voltage-gated Na(+) channel alphasubunit and is encoded by the SCN5a g

38 of the first high-resolution structure of a Na(+)-channel, an anionic coordination site was proposed

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

40 t demonstrates that a specific voltage-gated Na(+) channel and its associated impairment of SCN inter

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

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

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

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

45 corpions toxins bind to the resting state of Na(+) channels and inhibit fast inactivation by interact

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

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

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

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

50 of the resting state of a voltage sensor of Na(+) channels and reveals its mode of interaction with

51 VSD's is remarkably conserved among K(+) and Na(+) channels and that pathways for gating-pore current

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 4; K(+) channel antagonist) and lamotrigine (Na(+) channel antagonist) were found to significantly in

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 In vivo, these Na(+) channels are formed as complexes of pore-forming a

60 Voltage-gated Na(+)-channels are transmembrane proteins that are respo

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

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

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

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

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

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

69 tivity of the drug is caused by reduction of Na(+) channel availability and by an increase in the thr

70 1.5-reduced Na(+) current density, decreased Na(+) channel availability, and slowed Na(V)1.5-reduced

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

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

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

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

75 The final step in Na(+) channel biosynthesis in central neurons is concomi

76 d atrial-selectivity, AF-selectivity (atrial Na(+)-channel block at AF rates versus ventricular block

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 racellular antiarrhythmic effect mediated by Na(+) channel blockade.

80 State-dependent Na(+)-channel blockade potentially allows for the develo

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

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

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

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

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

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

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

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

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

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

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

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

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

94 cap-ET elicited entry of permanently charged Na(+) channel blockers to effectively suppress Na(+) cur

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

96 lied a mathematical model of state-dependent Na(+)-channel blocking (class I antiarrhythmic drug) act

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

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

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

100 cn2b (encoding beta2) null mice have reduced Na(+) channel cell surface expression in neurons, and ac

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

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

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

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

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

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

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

108 The spatial pattern of Na(+) channel clustering in the axon initial segment (AI

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

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

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

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

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

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

115 ity and stationary site size were similar at Na(+) channel clusters and other axonal regions.

116 n-deficient rat, which contain voltage-gated Na(+) channel clusters but lack paranodal specialization

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

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

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

120 ssibility that beta subunit availability and Na(+) channel composition and functional regulation may

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

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

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

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

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

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

127 We found that functional Na(+) channel density is approximately four times lower

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

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

130 e their use as an accurate model for cardiac Na(+) channel disease.

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

132 tuning neuronal computations, and changes in Na(+) channel distribution have been shown to mediate no

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

134 The dynamics of Na(+) channels during repetitive spiking were indirectly

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

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

137 Epithelial Na(+) channel (ENaC) activity is regulated, in part, by

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

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

140 xtracellular Zn(2+) activates the epithelial Na(+) channel (ENaC) by relieving Na(+) self-inhibition.

141 lications of loss of function for epithelial Na(+) channel (ENaC) containing a pseudohypoaldosteronis

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

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

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

145 t the extracellular domain of the epithelial Na(+) channel (ENaC) functions as a sensor that fine tun

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

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

148 The epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal

149 The epithelial Na(+) channel (ENaC) in the aldosterone-sensitive distal

150 The epithelial Na(+) channel (ENaC) is critical for Na(+) homeostasis a

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

152 The epithelial Na(+) channel (ENaC) is regulated by a variety of extern

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

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

155 1 (SPLUNC1) effectively inhibits epithelial Na(+) channel (ENaC)-dependent Na(+) absorption and pres

156 Regulation of epithelial Na(+) channel (ENaC)-mediated transport in the distal ne

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

158 ain K(+) channels (TREK1) and the epithelial Na(+) channel (ENaC).

159 CFTR) and the amiloride-sensitive epithelial Na(+) channel (ENaC).

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

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

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

163 The epithelial Na(+) channel, ENaC, and the Cl(-)/HCO(3)(-) exchanger,

164 Epithelial Na(+) channels (ENaCs) are expressed in the most distal

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

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

167 Epithelial Na(+) channels (ENaCs) play an essential role in the reg

168 learance because of inhibition of epithelial Na(+) channels (ENaCs) promotes cardiogenic lung edema.

169 the maturation and activation of epithelial Na(+) channels (ENaCs).

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 ort the crystal structure of a voltage-gated Na(+) channel from Arcobacter butzleri (NavAb) captured

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

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

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

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

183 1.1) and loss of modulation of the resultant Na(+) channel function.

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

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

186 have revealed that animal-type voltage-gated Na(+) channels had evolved in choanoflagellates, one of

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

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

189 NaC (degenerin and epithelial Na(+) channel) Na(+) channels have been implicated in touch sensation.

190 and coexpressed PDGFRalpha and voltage-gated Na(+) channels (I(Na)).

191 Na(V)1.1 is the primary voltage-gated Na(+) channel in several classes of GABAergic interneuro

192 ectly to, and colocalizes with, the Na(V)1.5 Na(+) channel in the sarcolemma of adult mouse ventricul

193 ings show that FHFs are potent regulators of Na(+) channels in adult ventricular myocytes and suggest

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

195 as a multifunctional regulatory platform for Na(+) channels in mice.

196 We tested whether FHFs regulate Na(+) channels in murine heart.

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

198 Voltage-gated Na(+) channels in the brain are composed of a single por

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

200 ation during attacks, which in turn leads to Na(+) channel inactivation and inexcitability of muscles

201 While it is commonly assumed that Na(+) channel inactivation is the primary mechanism of t

202 action potentials by increasing the rate of Na(+) channel inactivation, resulting in a marked reduct

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

204 moves a small degree of the resting level of Na(+) channel inactivation.

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

206 In CF and non-CF epithelia, the Na(+) channel inhibitor amiloride produced similar reduc

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

208 io response patterns, but treatment with the Na(+)-channel inhibitor riluzole reverses corticosteroid

209 Voltage-gated Na(+) channels initiate action potentials during electri

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

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

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

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

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

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

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

217 veal that TRP family and amiloride-sensitive Na(+) channels mediate touch-evoked currents in differen

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 ics of a combined gain- and loss-of-function Na(+) channel mutation and that the electrophysiological

221 we generated multiple PSC lines containing a Na(+) channel mutation causing a cardiac Na(+) channel o

222 The cardiac Na(+) channel Na(V)1.5 current (I(Na)) is critical to ca

223 ulation of the primary cardiac voltage-gated Na(+) channel (Na(v)1.5) by Ca(2+)/calmodulin-dependent

224 Neuronal DEG/ENaC (degenerin and epithelial Na(+) channel) Na(+) channels have been implicated in to

225 n myocytes and caused S-nitrosylation of the Na(+) channel, Na(v)1.5.

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

227 lular end of the S1 segment of the bacterial Na(+) channel NaChBac detects molecular interactions tha

228 ltage-Sensor Domain (VSD) of the prokaryotic Na(+) channel NaChBac in a lipid bilayer.

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

239 a1 subunit of Na/K-ATPase (alpha1-NaKA), the Na(+) channel NaV1.6, and the AIS anchoring protein anky

240 ats, humans) by activating the voltage-gated Na(+) channel Nav1.7, but has no effect on Nav1.8.

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

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

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

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

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

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

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

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

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

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

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

252 ot been shown to regulate endogenous cardiac Na(+) channels or to participate in cardiac pathophysiol

253 or potential (Trp) channels, but not sodium (Na(+)) channels or ligand-gated channels.

254 g a Na(+) channel mutation causing a cardiac Na(+) channel overlap syndrome.

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

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

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

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

259 e in part to activation of expression of the Na(+) channel protein Nav1.5.

260 sidues for the binding of beta-toxins to its Na(+) channel receptor site.

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

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

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

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

265 t adenoviral delivery of the skeletal muscle Na(+) channel (SkM1) to epicardial border zones normaliz

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

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

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

269 mall peptide fragment of the auxiliary beta4 Na(+) channel subunit into immature calyces (postnatal d

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

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

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

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

274 10 seconds was relatively rapid in wild-type Na(+) channels (tau; 639 +/- 90 milliseconds, n = 8).

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

276 dendrite has a higher density of functional Na(+) channels than more distal regions, suggesting that

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

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

279 dotoxin sensitive and tetrodotoxin-resistant Na(+) channels that underlie the unique electrical prope

280 acetycholine and tetrodotoxin, a blocker of Na(+) channels, that lowered the acetylcholine concentra

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

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

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

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

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

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

287 Here we identified a voltage-gated Na(+) channel (VGSC) that was essential for positive sel

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

289 +) current (I(Na)) mediated by voltage-gated Na(+) channels (VGSCs).

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 tween the Sig1R and the Nav1.5 voltage-gated Na(+) channel, which has also been implicated in promoti

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

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

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

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

297 bunit with that of Na(v)1.7, a TTX-sensitive Na(+) channel widely expressed in both small and large D

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

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

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