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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Na channels also bind exogenous compounds, such as lidoc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 inates SAF more effectively than traditional Na+-channel blockade by flecainide.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 ssion of mRNA encoding several voltage-gated Na+ channels by the E11.5 gut was detected using RT-PCR.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 Dietary salt intake controls epithelial Na+ channel (ENaC)-mediated Na+ reabsorption in the dist

163 regulates the amiloride-sensitive epithelial Na+ channel (ENaC/SCNN1) to mediate Na+ homeostasis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 larization refractoriness and more effective Na-channel inhibition.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 Activity of voltage-gated Na channels (Na(v)) is modified by alternative splicing.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

270 10 seconds was relatively rapid in wild-type Na(+) channels (tau; 639 +/- 90 milliseconds, n = 8).

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

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

273 Na channels that generate resurgent current express an i

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

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

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

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

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

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

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

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

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

288 hine, the steady-state voltage dependence of Na channels was shifted to the left with almost 50% of c

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 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 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 ugh I(NaP) is sufficient for activation of K(Na) channels, without substantial contribution from the

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