ライフサイエンスコーパス: Na

1 Na(+) /H(+) exchanger NHE3 of human or primates differs

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

3 Na(+) current-driven early afterdepolarizations in untub

4 Na(+)-depleted mice showed robust preferences to "light

5 Na(+)-K(+) pump current, I(p), was measured in voltage-c

6 Na(v) 1.8-Cre-tdTomato mice label 80% of nodose and dors

7 Na(V)1.7(-/-) showed substantial scratch reduction mainl

8 Na(V)1.8(-/-) impaired histamine and 5-HT-induced scratc

9 rylacetophenone with sodium sulfinate (RSO(2)Na), and (iii) the CuBr(2)-mediated intramolecular Fried

10 , namely [(C(2) B(9) H(11) )(2) Ln(THF)(2) ][Na(THF)(5) ] (Ln=Dy, 1Dy) and [(THF)(3) (mu-H)(3) Li](2)

11 ough the separation of K(+), Ba(2+), Mg(2+), Na(+), Li(+), and Tris(+) in approximately 30 s, with ef

12 (204)Tl, 277 us for (137)Cs, 258 us for (22)Na).

13 for (204)Tl, 26 us for (137)Cs, 9 us for (22)Na).

14 (23) Na T(2) -contrast MRI of metallic sodium offers a clear,

15 rff-perfused mouse hearts are studied by (23)Na, (31)P, (13)C NMR followed by (1)H-NMR metabolomic pr

16 interstitial sodium stores determined by (23)Na-magnetic resonance imaging.

17 ecursor [Mn(II)(ptac)(3)-Na-Fe(III)(acac)(3)-Na-Mn(II)(ptac)(3)] (3) with an appropriate metal ratio

18 heterotrimetallic precursor [Mn(II)(ptac)(3)-Na-Fe(III)(acac)(3)-Na-Mn(II)(ptac)(3)] (3) with an appr

19 ctive four-domain voltage-gated channels (4D-Na(v)s) in animals allowed rapid Na(+)-dependent electri

20 stricted to animals or to the presence of 4D-Na(v)s.

21 pically exhibit much slower kinetics than 4D-Na(v)s, and are not thought to have crossed the prokaryo

22 insufficient for the Na(+) channel Na(v)1.5 (Na(v)1.5(+/)) and mice in which the cAMP-dependent regul

23 excitability and three subtypes - Na(V)1.7, Na(V)1.8 and Na(V)1.9 - are preferentially expressed in

24 A Na(V)Sp1-specific S4-S5(L) peptide, containing the resid

25 discovery and characterization of ST-2262, a Na(V)1.7 inhibitor that blocks the extracellular vestibu

26 we identified, in adult cardiac myocytes, a Na(V)1.5 subpopulation in close proximity to subjacent s

27 We have recently found that a Na(+)/H(+) exchanger expressed on synaptic vesicles prom

28 Additionally, [Na(+)](o) modulates cardiomyocyte contractility via a so

29 While the mechanisms of AIS Na(+) and K(+) channel clustering are understood, the mo

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

31 table, in particular metals such as Ca, Al, Na, Zn, and Fe and halogens like Cl and F, occurring in

32 lic mechanism regulated by astrocytic alpha2-Na/K ATPase that triggers episodic motor paralysis in mi

33 neuroimaging reveals that conditional alpha2-Na/K ATPase knockout triggers spontaneous cortical sprea

34 Mutations of the ion pump alpha2-Na/K ATPase cause familial hemiplegic migraine, but the

35 ic and metabolomic analyses show that alpha2-Na/K ATPase loss alters metabolic gene expression with c

36 Here, we show that mice in which alpha2-Na/K ATPase is conditionally deleted in astrocytes displ

37 migraine, but the mechanisms by which alpha2-Na/K ATPase mutations lead to the migraine phenotype rem

38 for their contribution to itch by analysing Na(V)-specific knockout mice.

39 and energy efficiency in aprotic Li-O(2) and Na-O(2) batteries.

40 etails of the competition between Mg(2+) and Na(+) cations for specific sites, 3) estimates of bindin

41 odel demonstrated that changes in Ca(2+) and Na(+) homeostasis are responsible for the surprisingly m

42 llowed changes in cardiac myocyte Ca(2+) and Na(+) regulation from the formation of compensated hyper

43 et sodium channel isoforms, Na(V)1.1-1.6 and Na(V)1.8.

44 int mutants and tested them for Na(v)1.7 and Na(v)1.2 activity.

45 and three subtypes - Na(V)1.7, Na(V)1.8 and Na(V)1.9 - are preferentially expressed in the periphera

46 system L amino acid transporter activity and Na(+) K(+) -ATPase activity using sarcolemmal membranes

47 perature water, 90 degrees C-water, CDTA and Na(2)CO(3).

48 n a state that is permeable to both K(+) and Na(+), which is reminiscent of the SF in the nonselectiv

49 oxide in the presence of Li ions (Li(+)) and Na ions (Na(+)) is the fundamental root cause for the po

50 Spectral lines of C, Ca, Fe, Mg, N and Na were selected as input variables for prediction model

51 ) affected the corresponding minerals, P and Na content.

52 Consequently, multiple Na(V)1.7-specific and Na(V)1.8-specific blockers have undergone clinical trial

53 50) ~ +75 mV), in contrast to other TPCs and Na(V) channels that activate between -20 and 0 mV.

54 he levels of intracellular Ca(2+) uptake and Na, K-ATPase mRNA were determined in the cultured epithe

55 The cv HI10 papillae were shown to act as Na(+) sinks when plants were grown under saline conditio

56 pported for small precharged species such as Na(+).

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

58 d to their mammalian counterparts, bacterial Na(V) channels possess a simpler, fourfold symmetric str

59 The modulation was eliminated by blocking Na(V) channels (tetrodotoxin, 1 mum), persistent Na(+) c

60 nesthetics ambroxol and lidocaine block both Na(V)1.7 and NaChBac but affect activation and inactivat

61 binding sites dysregulate targeting of both Na(+) and K(ATP) channels to the ICD, but not to lateral

62 resence of saturating concentrations of both Na(+) and succinate.

63 ) exchange across the ER membrane induced by Na(+) influx via the light-sensitive channels.

64 te that rapid store depletion is mediated by Na(+)/Ca(2+) exchange across the ER membrane induced by

65 oncentrations of macroelements (C, N, P, Ca, Na, K, Mg) and micronutrients (Fe, Zn, Co, Mn, I) were s

66 tent (0.85) and plateau-free P2-type cathode-Na(0.85) Li(0.12) Ni(0.22) Mn(0.66) O(2) (P2-NLNMO) was

67 ice haplo-insufficient for the Na(+) channel Na(v)1.5 (Na(v)1.5(+/)) and mice in which the cAMP-depen

68 Ca(2+) affects CDI, we recorded one-channel Na(+) currents to quantify the receptor gating mechanism

69 gain-of-function mutations of sodium channel Na(v) 1.6 that result in neuronal hyperactivity.

70 Voltage-gated sodium channel Na(v)1.5 generates cardiac action potentials and initiat

71 that binds to voltage-gated sodium channels (Na(v) proteins), arresting electrical activity in nerves

72 ith high pH (>7.5) and high sodium/chloride (Na/Cl) ratios resulting from cation exchange.

73 ons because of increased intercellular cleft Na(+) ion depletion.

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

75 The nodes of Ranvier have clustered Na(+) and K(+) channels necessary for rapid and efficien

76 ysis of the bis(azide)cobaltate(II) complex [Na(THF)(x)][((ket)guan)Co(N(3))(2)] ((ket)guan = [(tBu(2

77 imals, sodium is essential to running costly Na-K ATPases.

78 The zeolite X product, Pb,Br,H,Cs,Na-X, shows superior stability toward moisture, maintain

79 n primarily hindered by dendritic and "dead" Na formation that leads to low Coulombic efficiency, sho

80 The family of K(+)-dependent Na(+)/Ca(2+)-exchangers, NCKX, are important mediators o

81 ful impairment of this interaction disrupted Na(V) 1.5's ability to recover from inactivation.

82 While bacteria encode single-domain Na(+)-selective voltage-gated channels (BacNa(v)), they

83 tates and limited reversible capacity during Na(+) de/insertion.

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

85 The electrogenic Na(+)/H(+) antiporter was active in asymmetric liposomes

86 bonic anhydrases (CAs) with the electrogenic Na/HCO(3) cotransporter NBCe1-A speeds transport by rege

87 sodium niobate contains only three elements (Na, Nb, and O).

88 , ischemia, and atrial fibrillation, enhance Na(+) influx, generating a late Na(+) current that prolo

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

90 h sodium 1,4-bis-2-ethylhexylsulfosuccinate (Na-AOT).

91 These results suggest that, in eukaryotic Na(V) channels, the S4-S5(L) of DI, DII and DIII domains

92 except Na), while addition of Si reversed Buta-induced alterati

93 n toxic newts and found that newts expressed Na(v) channels with modified TTX binding sites, conferri

94 ardiac ion channels from all three families (Na(V), Ca(V), and K(V)).

95 getics and a 2nd 2-component ion circuit for Na(+) bioenergetics in a strictly anaerobic rumen bacter

96 Free energy profiles for Na(+) and for Cl(-) ions within the open state pore reve

97 he most improved potency and selectivity for Na(V)1.7, examined alongside off-target Na(V)s, compared

98 prove gHwTx-IV's potency and selectivity for Na(V)1.7.

99 illae function as specialized structures for Na(+) sequestration in P. vaginatum, illustrating a poss

100 ary of 373 point mutants and tested them for Na(v)1.7 and Na(v)1.2 activity.

101 nfirm that energy differences resulting from Na(+) or K(+) co-occlusion promote the formation of 6-MR

102 enetic gain-of-function and loss-of-function Na(V)1.7 mutations have been identified in select indivi

103 ould stimulate non- HCO3- transporters (e.g. Na-H exchangers) by accelerating CO(2) / HCO3- -mediated

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

105 proteins that function as coupled glutamate/Na(+)/H(+)/K(+) transporters and as anion-selective chan

106 allosteric modulator of many class A GPCRs, Na(+), synergistically regulated pH sensing by maintaini

107 In 2015, use of MELD-GRAIL-Na as compared with MELD-Na resulted in reclassification

108 ir [M + 2H](2+), [M + 2Na](2+), and [M + H + Na](2+) ions acquired by positive-ion electrospray ioniz

109 Here, Na(V)1.7, 1.8 and 1.9 were compared for their contributi

110 The hexanuclear [Na(12)Fe(6)(tris-cyclo-salophen)(2)(THF)(14)], 1-THF, an

111 How Na(V) -CaM, CaMKII and FGF/fibroblast growth factor homo

112 ose of the monovalent peptides for the human Na(V)1.4 channel.

113 .5-generated voltage-gated sodium current I (Na) and Nav1.5 surface protein levels in rabbit cardiomy

114 blunted the negative effect of NEDD4-2 on I (Na) We conclude that LITAF controls cardiac excitability

115 Cardiac sodium channel expression, I(Na) and atrial action potential duration were reduced an

116 ogical techniques, we found an increase in I(Na,late) from -0.34 to -0.59 A F(-1) and a decrease in N

117 gative shifts in the voltage dependence of I(Na) inactivation (within 10 min) and subsequent superimp

118 was the result of actions of amiodarone on I(Na), I(Kur), I(CaL), I(CaT), I(f) and beta-adrenergic re

119 ects of even resting cytosolic [Ca(2+)] on I(Na).

120 al antioxidant reduced AF burden, restored I(Na), I(Ca,L), I(Kur), action potential duration, and rev

121 These findings implicate Na(V)1.7 as a key pharmacotherapeutic target for the tre

122 rom -0.34 to -0.59 A F(-1) and a decrease in Na(+) ,K(+) -ATPase current from 1.09 A F(-1) to 0.54 A

123 n unexpected stimulus-dependent diversity in Na(V) channel-mediated itch signalling.

124 (V)Ms structure, induced both an increase in Na(V)Sp1 current density and a negative shift in the act

125 ting the synthesis-property relationships in Na(3)PS(4).

126 rsisting for >10 min and rapid increases in [Na(+) ](i) .

127 matic compartment included fast-inactivating Na(+) and delayed-rectifier K(+) conductances, while an

128 everal voltage-gated ion channels, including Na(V), Ca(V), and K(V) channels.

129 nsing domain targeting toxin BDS-I increases Na(V)1.7 but decreases NaChBac peak currents.

130 ced salinity uptake and dilution of internal Na(+) and Cl(-) as well as other ions.

131 Our results provide detailed insights into Na(v)1.5 structure, pharmacology, activation, inactivati

132 ncy of action potentials and convert it into Na(+) current availability.

133 Intracellular Na elevation in the heart is a hallmark of pathologies w

134 plateau phase, (2) increasing intracellular Na(+) (Na(i)) that decreases the depolarizing I(NCX) the

135 rated against 13 other competing metal ions (Na(+), K(+), Mg(2+), Ca(2+), Mn(2+), Fe(2+), Al(3+), Ni(

136 the presence of Li ions (Li(+)) and Na ions (Na(+)) is the fundamental root cause for the poor stabil

137 The voltage-gated sodium channel isoform Na(V)1.7 is highly expressed in dorsal root ganglion neu

138 ity over off-target sodium channel isoforms, Na(V)1.1-1.6 and Na(V)1.8.

139 tations in KCNT1, the gene encoding Slack (K(Na)1.1) channels, result in epilepsy of infancy with mig

140 e average migration times and %RSD for K(+), Na(+), and Li(+) were measured to be 22.04 s (1.59%), 26

141 useful for the realization of ISEs for K(+), Na(+), Ca(2+), and NO(3)(-).

142 under purely monovalent salt conditions (K+, Na+), TALEs bind to specific and non-specific DNA with n

143 Concentrations of 16 elements (K, Na, Mg, Ca, Fe, Zn, Hg, Se, As, Cu, Cd, Mn, Ni, Cr, Pb a

144 drites, and highlighting the deep-eutectic K-Na alloying approaches for room temperature liquid anode

145 hypoglycaemic conditions and generate large Na(+) - and Ca(2+) -dependent action potentials.

146 ion, enhance Na(+) influx, generating a late Na(+) current that prolongs action potential duration (A

147 otic agents individually do not enhance late Na(+) current.

148 Understanding cation (H(+) , Li(+) , Na(+) , Al(3+) , etc.) intercalation/de-intercalation ch

149 rcalation/de-intercalation (including Li(+), Na(+), and K(+)) at low redox potentials, carbon materia

150 In nine structures, A(+) (A=Li, Na, K, Rb and Cs), AE(2+) (AE=Ca, Sr, Ba) and Mn(2+) dem

151 e obstacles for practical applications of Li/Na-CO(2) batteries.

152 abolism in the kidney after 2 weeks of a low Na(+) diet.

153 oxygen metabolism following 2 weeks of a low Na(+) diet.

154 t upon oxygen delivery during normal and low Na(+) conditions, while aldosterone receptors mainly aff

155 in both groups after candesartan in the low Na(+) group.

156 mains, HCNL1 evolutionarily adapted to a low-Na(+) freshwater environment to conserve sperm's ability

157 of the membrane Na(+)-K(+) pump should lower Na(+) concentrations, and the beta3 adrenoceptor (beta3

158 Our data suggest that lower Na(+) K(+) -ATPase activity, which reduces the driving f

159 eatment of [MoCl(4)(THF)(2)] with MOtBu (M = Na, Li) does not result in simple metathetic ligand exch

160 MA(2) RuX(6) (X=Cl or Br), MA(2) MRuX(6) (M=Na, K or Ag; X=Cl or Br) and MA(3) Ru(2) X(9) (X=Br) bas

161 Ca(2+) transporters, including the mammalian Na(+)/Ca(2+) exchanger (NCX), our study provides a regul

162 onfidence interval [CI], 3.160, 36.084; MELD-Na, OR = 7.594, 95% CI, 2.578, 22.372; P < 0.001, respec

163 an the previously published cutoff at a MELD-Na of 20 points (vWF-Ag, OR = 10.873, 95% confidence int

164 have consistently higher creatinine and MELD-Na values.

165 lysis, CysC >= 1.5 mg/L, sarcopenia and MELD-Na were independent predictors of ACLF in the WL, while

166 Clinical characteristics, MELD-Na, and mortality on the waiting list were recorded.

167 However, MELD-Na may underestimate complications arising from portal h

168 Despite persistently low MELD-Na scores, patients with cirrhosis still experience high

169 The mean MELD-Na score per sample ranged from 14 to 38.

170 Combining vWF-Ag levels with MELD-Na improves risk stratification and may help to prioriti

171 , use of MELD-GRAIL-Na as compared with MELD-Na resulted in reclassification of 16.7% (n = 672) of pa

172 ched1 uses the energy of the plasma membrane Na(+) gradient, thus functioning as an SHH/Na(+) antipor

173 Stimulation of the membrane Na(+)-K(+) pump should lower Na(+) concentrations, and t

174 and isovitexin) and minerals (K, P, Ca, Mg, Na and Fe) were predominant in WJP.

175 drial Ca(2+) extrusion via the mitochondrial Na(+)/Ca(2+) exchanger, NCLX.

176 use of Normal Saline, which contains 155 mM [Na(+)](o), with cardiac ischemia may require further inv

177 The content of minerals (Ca, Fe, K, Mg, Mn, Na and Zn), dietary fiber (total, soluble and insoluble)

178 functional minerals (Ca, Cu, Fe, K, Mg, Mn, Na, P, Se and Zn) and trace metals (As, Cd, Pb, U and V)

179 (As, Ba, Be, Bi, Cd, Co, Cr, Cu, K, Mn, Mo, Na, Ni, P, Pb, Th, Tl, Sb, U, V, Y and Zn) in 73 commerc

180 Consequently, multiple Na(V)1.7-specific and Na(V)1.8-specific blockers have un

181 olution containing 10 mM NaClO(4) and 10 muM Na(2)C(2)O(4).

182 has long been recognized that smooth muscle Na/K ATPase modulates vascular tone and blood pressure (

183 u phase, (2) increasing intracellular Na(+) (Na(i)) that decreases the depolarizing I(NCX) thereby su

184 preferentially host the mitochondrial NCLX (Na(+)/Ca(2+) exchanger).

185 X (tetrodotoxin) exposure, mitochondria near Na(V)1.5 channels accumulated more Ca(2+) and showed inc

186 F cleanly forms the binuclear cobalt nitride Na(THF)(4){[((ket)guan)Co(N(3))](2)(mu-N)} (1).

187 ve been advanced to clinical development, no Na(V)1.7-selective compound has shown convincing efficac

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

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

190 her linked to reactivation of nonequilibrium Na(+) current, as they were rapidly blocked by tetrodoto

191 duced repolarization reserve and normalizing Na(i).

192 Mitochondrial Ca(2+) channels, and not Na(+) -dependent transport, regulate CRAC channels under

193 on intracellular Ca(2+), and the activity of Na(+)/Ca(2+) exchanger (NCX) may be altered when the Na(

194 a: see text], but it can also be composed of Na(+) Here, we show that the strictly anaerobic rumen ba

195 tiapin-Q also improved cardiac conduction of Na(v)1.5(+/-) mice by 24%.

196 1.7 and indicated an overall contribution of Na(V)1.9.

197 etention is based on an efficient control of Na(+) -permeable slow- and fast-vacuolar channels that m

198 f the high natural abundance and low cost of Na resources, as well as electrochemical similarities wi

199 itine and veratridine block peak currents of Na(V)1.7 and shift activation (aconitine) and inactivati

200 We also observe separable effects of Na(+) and succinate binding at several positions suggest

201 The evolution of Na(+)-selective four-domain voltage-gated channels (4D-N

202 a homologue of the eukaryotic SLC6 family of Na(+) -dependent symporters for amino acids, neurotransm

203 Identification of Na(V)1.7 inhibitors with all of the desired properties t

204 revention of Na(i) overload or inhibition of Na/Ca(mito) may be a new approach to ameliorate metaboli

205 otency, selectivity, and binding kinetics of Na(V) channel ligands.

206 uolar channels that mediate the back-leak of Na(+) into cytosol and, if not regulated tightly, could

207 d the kinetic transitions of the movement of Na(+) and K(+) ions through the Na(+)/K(+)-ATPase and pr

208 Recently CaM was found to engage part of Na(V) 1.5 that is required for channel inactivation with

209 f lithium and the low discharge potential of Na-CO(2) batteries create obstacles for practical applic

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

211 P for Al(3+) was also proved in presence of Na(2)EDTA by both UV-Vis and fluorometric titration.

212 Prevention of Na(i) overload or inhibition of Na/Ca(mito) may be a new

213 )(3)] (3) with an appropriate metal ratio of Na:Mn:Fe = 2:2:1.

214 y 100% without compromising the rejection of Na(2)SO(4).

215 rized together with the potential release of Na(+) and Ca(2+) cations, revealing suitable for RT albu

216 ve image analysis revealed reorganization of Na(V)1.5 away from dense clusters localized near GJs and

217 rallel beta3 AR agonists-induced reversal of Na(+)-K(+) pump inhibition and indices of congestion sug

218 all pruritogens confirmed a leading role of Na(V)1.7 and indicated an overall contribution of Na(V)1

219 The honeycomb superstructure of Na(0.75)[Li(0.25)Mn(0.75)]O(2), present in almost all ox

220 nteractions with both the C-terminal tail of Na(v)1.6 and FGF14.

221 reclinical development, and the targeting of Na(V)1.9, although hampered by technical constraints, mi

222 male Drosophila, para Despite being the only Na(V) channel in the fly, we show that only 23 +/- 1% of

223 [Formula: see text]-dependent and the other Na(+)-dependent, which was validated by biochemical anal

224 In contrast to other Na(V)1.7 inhibitors that preferentially inhibit the inac

225 ck-in site is highly selective for K(+) over Na(+).

226 improvement in solubility, selectivity over Na(V)1.5, and CYP2C9 inhibition.

227 P(Cl) /P(Na) of airway epithelia was unaltered by pH 7.4 vs.

228 2-layered sodium transition metal oxides (P2-Na(x)TmO(2)) often suffer from structural/chemical trans

229 mposition pattern yielding the phase-pure P2-Na(2)Mn(2)FeO(6) quaternary oxide with high uniformity o

230 d the evaluation rules towards air-stable P2-Na(x)TmO(2) have not yet been clearly elucidated.

231 PELD-Na-Cr better ordered the sickest children and should bet

232 As a result, PELD-Na-Cr could increase pediatric transplant rates and redu

233 drites/trunk compartment included persistent Na(+), hyperpolarization-activated cation (I (h) ), slow

234 ) channels (tetrodotoxin, 1 mum), persistent Na(+) current (I (NaP); riluzole, 10 mum), or Ca(V) chan

235 exed, in situ potentiometric analysis of pH, Na(+), and K(+) in sweat.

236 val of either extracellular or intra-pipette Na(+) had no effect on the selectivity, kinetics, amplit

237 The dendrite-free sodium-potassium (Na-K) liquid alloy composed of two alkali metals is one

238 hannels (4D-Na(v)s) in animals allowed rapid Na(+)-dependent electrical excitability, and enabled the

239 ults demonstrate that the capacity for rapid Na(+)-based signaling in eukaryotes is not restricted to

240 As such, the capacity for rapid Na(+)-selective signaling is considered to be confined t

241 underlying ionic mechanisms by which reduced Na(v) availability in Fhf2 knockout (Fhf2(KO)) mice pred

242 ting important roles of I(NaL) in regulating Na(i).

243 ical role of the FHF2A isoform in regulating Na(v) channel function.

244 hen large amounts of glutamate are released, Na(+) accumulated in the terminals, activated vesicular

245 enome-wide association study (GWAS) for root Na(+) /K(+) ratio in a population consisting of 369 toma

246 With the most performing sample (Na/Ca_0.27), a comprehensive study on simultaneous adsor

247 VirChR1 shows that it is a highly selective, Na(+)/K(+)-conducting channel and, in contrast to known

248 e Na(+) gradient, thus functioning as an SHH/Na(+) antiporter.

249 elix dividing two distinct regulatory sites: Na(+) and the inhibitory peptide.

250 and the lack of any observed hypertonic skin Na(+) excess, but the lymphatic drainage was impaired (i

251 solute carrier family 9 member A6 (SLC9A6)/(Na(+),K(+))/H(+) exchanger 6 (NHE6) gene that cause Chri

252 Persistently depolarizing sodium (Na(+)) leak currents enhance electrical excitability(1,2

253 sitive to the specific voltage-gated sodium (Na(V)) channel blocker tetrodotoxin.

254 Voltage-gated sodium (Na(V)) channels are pore-forming transmembrane proteins

255 dotoxin (TTX) to block voltage-gated sodium (Na(v)) channels as a chemical defense against predation.

256 Voltage-gated sodium (Na(V)) channels drive neuronal excitability and three su

257 ntials are initiated by an influx of sodium (Na(+)) ions via voltage-gated Na(+) channels.

258 Rechargeable sodium (Na) based batteries have gained tremendous research inte

259 latively small changes in perfusate sodium ([Na(+)](o)) composition significantly affect cardiac elec

260 ion and subcellular localization of the sole Na(V) channel in both male and female Drosophila, para D

261 crystal structures have revealed a specific Na(+) binding site and molecular dynamics (MD) simulatio

262 Thrombin binds a specific Na(+) ion next to Asp189, which is absent in trypsin.

263 e neuronal excitability and three subtypes - Na(V)1.7, Na(V)1.8 and Na(V)1.9 - are preferentially exp

264 for Na(V)1.7, examined alongside off-target Na(V)s, compared with HwTx-IV and gHwTx-IV.

265 While several small molecules targeting Na(V)1.7 have been advanced to clinical development, no

266 four important "beyond Li-ion" technologies: Na-ion batteries, K-ion batteries, all-solid-state batte

267 Here, we report that Na(+) substantially accumulated in the calyx of Held ter

268 Here we report that Na(+) substantially accumulated in the mouse calyx of He

269 These results reveal that Na(+) controls OXPHOS function and redox signalling thro

270 We show that Na(v)1.5 organizes as distinct clusters in the groove an

271 The Na ion participates in the formation of hybrid passivati

272 The Na(+)/I(-) symporter (NIS), the plasma membrane protein

273 fect clusters preferentially align along the Na/Li ion diffusion channels (a-b planes), which is like

274 These asymmetric proteoliposomes contain the Na(+)/H(+) antiporter NhaA from Salmonella Typhimurium.

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

276 marker in the human SLC4A7 gene encoding the Na/HCO(3) transporter NBCn1 suggest that this pH-regulat

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

278 le energy storage, the implementation of the Na metal anode has been primarily hindered by dendritic

279 the Pd(0)-catalyst, transmetallation of the Na- or K-enolate generated in situ, and subsequent reduc

280 Additionally, we sequenced the Na(v) channel gene family in toxic newts and found that

281 We have previously demonstrated that the Na(+)/H(+) exchanger regulatory factor 1 (NHERF1) promot

282 Replicate (urban) samples indicate that the Na(2)CO(3) solution is significantly less selective for

283 movement of Na(+) and K(+) ions through the Na(+)/K(+)-ATPase and propose the significance that this

284 osed to interact with S6(T) according to the Na(V)Ms structure, induced both an increase in Na(V)Sp1

285 In turn, the Na(+) current can control neuronal firing frequency in a

286 (2+) exchanger (NCX) may be altered when the Na(+) gradient is changed.

287 proposed water-independent nature of tissue Na(+) could induce local pathogenic changes, but lacks f

288 ut also reinforcing the importance of tissue Na(+) excess, are both mechanistic and clinical.

289 substituents (23e) abrogated the binding to Na(v)1.6.

290 own ether derivatives exhibit selectivity to Na(+) and K(+) ions within detection ranges of 0-100 and

291 current knowledge of regulation of tonoplast Na(+) -permeable channels and discusses the energy cost

292 en)(2)(THF)(14)], 1-THF, and the trinuclear [Na(6)Fe(3)(tris-cyclo-salophen)(py)(9)], 1-py, Fe(II) cl

293 In contrast, C-21 did not increase urine Na(+) excretion or renal interstitial cGMP in SHR.

294 ls and discusses the energy cost of vacuolar Na(+) sequestration, under different scenarios.

295 ulated in the terminals, activated vesicular Na(+)/H(+) exchanger, and regulated glutamate loading as

296 2,4,6-Pr(i)(3))(2)-3,5-Pr(i)(2)) with 5% w/w Na/NaCl in hexanes gave a dark red solution from which t

297 histamine and 5-HT-induced scratching while Na(V)1.9 was involved in itch signalling towards 5-HT, C

298 isms, and evolutionary origins of widespread Na(+)-coupled transporters.

299 tions, except for Li(+), which competes with Na(+) for binding, but does not support channel activity

300 Treatment of [Ph(3) EMe][I] with [Na{N(SiMe(3) )(2) }] affords the ylides [Ph(3) E=CH(2) ]