ライフサイエンスコーパス: Na

1 Na humate did not interact with the surfaces of acid-was

2 Na humate was expected to form a coating over favorable

3 Na(+) and K(+) exhibit a significant preference for the

4 Na(+) levels were not increased, and expression levels o

5 Na(+),K(+)-ATPase and H(+),K(+)-ATPase are electrogenic

6 Na(+)-coupled hCNT1 and hCNT2 transport pyrimidine and p

7 Na(+)-influx inhibitors did not improve relaxation or pr

8 Na(+)-NQR uses the energy released by electron transfer

9 Na(+)/Ca(2+) exchanger (NCX) proteins operate through th

10 of a low sodium diet (LSD) containing 0.01% Na(+) , a normal sodium diet (NSD) containing 0.18% Na(+

11 a normal sodium diet (NSD) containing 0.18% Na(+) and a moderately high sodium diet (HSD) containing

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

13 (23)Na MAS NMR spectra of sodium-oxygen (Na-O2) cathodes rev

14 (23)Na NMR experiments show that Na(+) ions are present near

15 present in a measurable quantity in the (23)Na NMR spectra of the cycled electrodes.

16 Average values of the (23)Na quantifications in four healthy volunteer brains were

17 t 7 T, which allows to differentiate the (23)Na signals emanating from three compartments in human br

18 tely high sodium diet (HSD) containing 1.25% Na(+) .

19 A Na(+)/K(+)-ATPase inhibitor (ouabain) potentiated EA-ind

20 A Na-ion solid-state electrolyte, Na3 P0.62 As0.38 S4 , is

21 NCLX is a Na(+)/Ca(2+) exchanger that uses energy stored in the tr

22 Remarkably, the addition of monensin, a Na(+)/H(+) exchanger, completely halts the infection.

23 n our assays, raising the possibility that a Na(+) gradient provides the energy source for Patched1 c

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

25 alter channel selectivity to allow abnormal Na+ conductance, resulting in membrane depolarization, c

26 ABSTRACT: Na(+) excretion by the kidney varies according to dietar

27 , the structure of the first light-activated Na(+) pump, Krokinobacter eikastus rhodopsin 2 (KR2), wa

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

29 optimizing and controlling oxygen activity, Na layered oxide materials with higher capacities can be

30 l epithelial cells express the high affinity Na(+)-coupled glucose carrier SGLT1.

31 Finally, retinoschisin treatment altered Na/K-ATPase localization in photoreceptors of Rs1h(-/Y)

32 y involve, for example, astrocyte Ca(2+) and Na(+) signalling, K(+) buffering, gap junction coupling

33 Intracellular Ca(2+) and Na(+) were simultaneously assessed using Fura-2 and Asan

34 ed for ionophore-based Mg(2+)-, Ca(2+)-, and Na(+)-selective electrodes.

35 e intermediate conformations E2.Pi.2K(+) and Na(+)-bound E1 approximately P.ADP suggest that the dime

36 ting in decreased concentrations of K(+) and Na(+) , as compared to wild-type Z. xanthoxylum grown un

37 ignificant decline in net uptake of K(+) and Na(+) , resulting in decreased concentrations of K(+) an

38 selective electrodes (ISEs) (H(+), K(+), and Na(+)) have outstanding performance characteristics (the

39 llel and antiparallel G-quadruplex in K+ and Na+, respectively).

40 For Li(+) and Na(+), the stabilization is such that hydrogenated dimer

41 Selective Li- and Na-based SEI membranes are produced using Li- or Na-base

42 onized elements (EIEs), i.e., Ca, K, Mg, and Na, as well as the foreign ions (Al, Cu, Fe, Mn, Zn) to

43 g 100 nm particles containing C, Cd, Mn, and Na, respectively.

44 els alone or in combination with NO, PGs and Na(+) /K(+) -ATPase significantly reduced the vasodilata

45 erformance to other PCB-based pH sensors and Na(+) and K(+) PCB-based sensors with comparable perform

46 on of KIR channels, NO and PG synthesis, and Na(+) /K(+) -ATPase would not alter the ability of ATP t

47 l sodium-dependent bile acid transporter and Na(+) -taurocholate cotransporting polypeptide, within t

48 The abundance of apical transporters and Na(+) delivery are the main determinants of Na(+) reabso

49 ese rotations reduce the bond tension around Na and effectively soften the short Na-O bond along the

50 oupling stoichiometry of VcINDY, a bacterial Na(+)-coupled succinate transporter, and further validat

51 landscape of thermodynamic coupling between Na(+) release and inward-opening, and identifies diverse

52 NHE3 directly binds Na(+)/H(+) exchanger regulatory factor (NHERF) family sc

53 KEY POINTS: Body Na(+) content is tightly controlled by regulated urinary

54 Both Na(+) and K(+) conductances suppress low-frequency synap

55 l wires of (Cd2Se3)n(2n-) charge balanced by Na(+) and stabilized by coordinating solvent molecules.

56 onomeric anthocyanin, fructose, glucose, Ca, Na values were higher in the ripe stage.

57 re found to be significantly enriched in Ca, Na, and Se relative to desert soils.

58 The quantification of elements (Mg, Ca, Na and K) through LIBS was done using calibration curve

59 asure total myocardial concentrations of Ca, Na, and other elements.

60 ne, conducts the inward depolarizing cardiac Na(+) current (INa) and is vital for normal cardiac elec

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

62 Interaction with the Lewis acid cation (Na(+) or K(+)) significantly stabilizes the dihydride co

63 anning fluorometry were used to characterize Na(+) and H(+) transport, charge translocation, and ther

64 Chicken Na(+)/H(+) exchanger type I (chNHE1), a multispan transm

65 les containing chloride (mole fraction of Cl/Na >/= 0.1, 90% chloride depletion).

66 vated intracellular Na(+), which compromised Na(+)-dependent nutrient transport, were documented.

67 gle strands in buffered solutions containing Na(+) cations (TEL21/Na(+)).

68 known NCLX-mediated pathway that coordinates Na(+) and Ca(2+) signals to effect mitochondrial redox c

69 with substitution of different counterions (Na:AOT, K:AOT, and Mg:AOT) that consequently also result

70 t SOCE is accompanied by a rise in cytosolic Na(+) that is critical in activating the mitochondrial N

71 High dietary Na(+) intake decreased Na(+) reabsorption in the proximal tubule and increased

72 The sodium-dependent NADH dehydrogenase (Na(+)-NQR) is a key component of the respiratory chain o

73 High dietary Na(+) intake decreased Na(+) reabsorption in the proxima

74 ediating adaptation to variations in dietary Na(+) intake are incompletely characterized.

75 ervations in mice that variations in dietary Na(+) intake do not alter the glomerular filtration rate

76 on by the kidney varies according to dietary Na(+) intake.

77 iverse, yet well-defined roles for different Na(+)-coordinating residues.

78 in the distal nephron because of diminished Na(+) delivery.

79 tentiated EA-induced cytotoxicity and direct Na(+) loading by gramicidin-A caused Pico145-resistant c

80 yophyllales suggested at least two distinct [Na]shoot phenotypes within this order.

81 lex [{U(Tren(TIPS) )}(mu-P){U(Tren(DMBS) )}][Na(12C4)2 ] [7, Tren(DMBS) =N(CH2 CH2 NSiMe2 Bu(t) )3 ].

82 charge compensation at the metal site during Na-ion deintercalation is achieved via the oxidation of

83 d that NhaA could still perform electrogenic Na(+)/H(+) exchange even in the absence of a protonatabl

84 Blocking electroneutral Na(+) movement is predicted to be useful in the treatmen

85 a warming-induced increase in electroneutral Na(+) entry.

86 de and amiloride (blockers of electroneutral Na(+) movement), the action potential amplitude consiste

87 SLC4A7 encodes the electroneutral Na+/HCO3- co-transporter NBCn1 which regulates intracell

88 La and 17 other elements (Na, K, V, Ni, Co, Cu, Zn, Ga, As, Se, Mo, Cd, Sn, Sb, Ba

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

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

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

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

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

94 Structural models indicated that external Na(+) binding opened a large aqueous vestibule (600 A(3)

95 Patched1 specifically requires extracellular Na(+) to regulate Smoothened in our assays, raising the

96 identify that the slow component of the fast Na(+) current is a key determining factor for the onset

97 P test meals containing 5 mg Fe as (57)FeFum+Na(58)FeEDTA or ferrous sulfate ((54)FeSO4).

98 here ENaCs couple the absorption of filtered Na(+) to K(+) secretion, these channels are found in oth

99 tamate- and glycine-gated channels that flux Na(+) and Ca(2+) into postsynaptic neurons during synapt

100 For Na(+) a steadily increasing fraction is observed, which

101 For Na,K-ATPase, bilayer properties can modulate pump activi

102 1 mutant elucidates the structural basis for Na(+) selectivity in mammalian TPCs.

103 Mutations in the genes coding for Na(+),K(+)-ATPase alpha-subunit isoforms lead to severe

104 annel (ENaC) is the limiting entry point for Na(+) reabsorption in the distal kidney nephron and is r

105 precipitate to the calcite surface and form Na acetate.

106 a(2+)-containing solution to a divalent-free Na(+) one, and fast Ca(2+)-dependent inactivation.

107 e biosensor had negligible interference from Na(+),K(+),NH(+4) and Ca(2+) but Mg(2+),Cu(2+) and ascor

108 Li(+) deviates substantially from Na(+) and K(+).

109 Voltage-gated Na(+) (NaV) channels are key regulators of myocardial ex

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

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

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

113 n the gating rates of the fast voltage-gated Na(+) current.

114 ensemble of closed conformations in a highly Na(+)-dependent manner, without evidence of Na(+)-depend

115 pen state that allows permeation of hydrated Na(+), and these results also support a hydrophobic gati

116 in HFpEF are neither a result of an impaired Na(+) gradient nor expression changes in key ion transpo

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

118 esponse was also significantly attenuated in Na(+) free solution.

119 did not prevent the FSS-induced increase in Na(+)/K(+)-ATPase levels.

120 a/K-ATPase complex with proteins involved in Na/K-ATPase signaling, such as caveolin, phospholipase C

121 ation) and superior Na transport kinetics in Na intercalation/extraction processes, as demonstrated b

122 imensions of the respective binding sites in Na,K-ATPase are crucial in determining its selectivity.

123 e is essential for electrogenic transport in Na(+)/H(+) antiporters.

124 as well as acutely stimulated and inhibited Na(+)/H(+) exchange activity.

125 ne depolarization and elevated intracellular Na(+), which compromised Na(+)-dependent nutrient transp

126 KEY POINTS: Intracellular Na(+) -activated Slo2 potassium channels are in a closed

127 In this novel mechanism, slow intracellular Na(+) dynamics endow AOB mitral cells with a weak tenden

128 to a substantial reduction of intracellular [Na(+) ].

129 veral transporters/channels related to K(+) /Na(+) homeostasis, including ZxSKOR, ZxNHX, ZxSOS1 and Z

130 e phases were allowed to separate and Ca, K, Na, and Mg were determined in aqueous phase by means of

131 ernal immune activation, do not display KCC2/Na(+)-K(+)-2Cl(-) cotransporter 1 imbalance when implant

132 onstrated that a low concentration (10 mg/L) Na humate solution in synthetic water significantly impr

133 ites by monitoring diffusion of eGFP-labeled Na(+),K(+)-ATPase constructs in the plasma membrane of H

134 Late Na(+) current inhibition during long-duration VF reduces

135 rose as a result of augmentation of the late Na(+) current.

136 ransgenics accumulated more Cd(2+), but less Na(+) than their wild type counterparts.

137 of record amounts of charge-balancing Li(+), Na(+), and Mg(2+) ions for MOFs.

138 onselective among monovalent cations (Li(+), Na(+), and K(+)).

139 The respective Li(+)-, Na(+)-, and Mg(2+)-loaded materials exhibit high ionic c

140 ploited for the first time to follow a Li(+)/Na(+) ion exchange reaction using in situ powder neutron

141 A set of AAuH2 compounds, A = Li, Na, K, Rb, and Cs, is examined; of these, certain K, Rb,

142 es or the [Co(II)2(bis-salophen)M2] (M = Li, Na) dimers that are present in solution in equilibrium w

143 at had significant longer-lasting localized [Na(+)]i increases mediated through NMDA receptors.SIGNIF

144 SISA14-1 (G03) accumulated low Na and Cl under salinity.

145 10 gene is required to maintain a proper low Na(+)/Ca(2+) ratio in growing tissues allowing tomato gr

146 Our data indicate that low [Na(+)] is required to allow large agonist-induced struct

147 hannels have been shown to be endo/lysosomal Na(+)-selective or Ca(2+)-release channels.

148 3.0 to 0.6 mm upon titration from 0 to 0.3 m Na(+) In the presence of 5 mm Ca(2+), Km was further red

149 ubstantial increase in the abundance of [M + Na](+) adducts was observed in samples from spinal cord

150 The [M + Na](+)/[M + K](+) adducts ratio remained approximately c

151 tion in tissue homeostasis and that the [M + Na](+)/[M + K](+) ratio may be used to detect alteration

152 and phosphorus (P) per unit leaf area (Ma , Na and Pa , respectively), and chlorophyll from 210 spec

153 e total and cell-surface expression of major Na(+) transporters all along the kidney tubule.

154 a new class of promising cathode materials, Na(Li1/3 M2/3 )O2 (M: transition metals featuring stabil

155 itor of palmitoylation reduced ENaC-mediated Na(+) currents within minutes.

156 y while depleting AnkG reduced ENaC-mediated Na(+) transport.

157 ltivariate Cox regression: MELD-sodium (MELD-Na), tumour burden score (TBS), alpha-fetoprotein (AFP),

158 ant APOL1s localized on the plasma membrane, Na(+) and K(+) gradients were maintained, and cells rema

159 floral (Ca, Cr, Mo, Se), common heather (Mg, Na), bearberry (Ba, Fe, Pb) and sage (Ag) honeys.

160 The levels of the minerals: Ca, K, Mg, Na, P, and the trace elements: Cd, Cu, Fe, Mn, Ni, Pb, S

161 i, Se, Th and U), common heather (Co, K, Mg, Na, V), sage (Ag, Cd, Cu), and bearberry (Ba, Fe, Pb, Sb

162 hanger (NCLX) causing enhanced mitochondrial Na(+) uptake and Ca(2+) efflux.

163 is critical in activating the mitochondrial Na(+)/Ca(2+) exchanger (NCLX) causing enhanced mitochond

164 monly used nonvolatile buffers and >/=150 mm Na(+) with conventionally sized nanoelectrospray emitter

165 in the combined RS groups and 108+/-61 mmol Na(+) per day in the LS groups (P<0.001).

166 lected by urinary excretion of 174+/-64 mmol Na(+) per day in the combined RS groups and 108+/-61 mmo

167 f the redox reaction mechanism in Li2 MnO3 , Na(Li1/3 Mn2/3 )O2 is designed as an example of a new cl

168 ns of Ag, As, Ba, Cu, Co, Fe, K, Mg, Mn, Mo, Na, Ni, Se, Sb, U and Th (p<0.05, all) among honeys.

169 ing elevated persistent INa and reverse mode Na/Ca exchange in the mechanism of hyperexcitability.

170 We also monitored Na(+) and Cl(-) ion concentrations and the temporal dyna

171 olation of [Co(I)2(bis-(OMe)salophen)Na2Py4][Na(cryptand)]2, 8.

172 The bimodal distribution of the log-normal [Na]shoot of species within the Caryophyllales suggested

173 SERT-expressing membranes: in the absence of Na(+), the N terminus was rapidly digested.

174 sclosed a marked decrease in the affinity of Na(+) to bind the channel when the conformational equili

175 are readily cationized by the attachment of Na(+) during electrospray ionization operated in the pos

176 NaC, we demonstrate that the augmentation of Na(+) transport is caused predominantly by increasing th

177 lter in which to test competitive binding of Na(+) These experiments disclosed a marked decrease in t

178 s background, we speculated that blockade of Na/K-ATPase-induced ROS amplification with a specific pe

179 of Na(+) At physiological concentrations of Na(+) and Ca(2+), the three HABP2 variants, and particul

180 Saturating concentrations of Na(+) or Ca(2+) specifically modify HDX patterns, reveal

181 e possibilities to study the consequences of Na(+),K(+)-ATPase mutations and provide information abou

182 , but without an appreciable contribution of Na(+) At physiological concentrations of Na(+) and Ca(2+

183 The decay of Na(+) /Ca(2+) exchanger current that followed a stimulat

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

185 Na(+) delivery are the main determinants of Na(+) reabsorption along the kidney tubule.

186 ant factors influencing the effectiveness of Na humate application in improving PAA-nano-ZVI mobility

187 are consistent with electroneutral entry of Na(+) occurring in axons and contributing to setting the

188 Na(+)-dependent manner, without evidence of Na(+)-dependent intermediates.

189 microvilli, and less abundant expression of Na(+)/Pi cotransporter 2, claudin-2, and aquaporin 1.

190 ar Ca(2+) concentration, producing a flux of Na(+) and/or K(+) ions that depolarizes the cell, thus m

191 hose relative occupancies are independent of Na(+) concentration.

192 ke proteins in male organisms, inductions of Na(+)K(+)/ATPases, and strong inhibitions of molt-relate

193 provide information about the interaction of Na(+),K(+)-ATPase alpha-isoforms with cellular matrix pr

194 y constant level despite increased levels of Na(+) under salinity and drought conditions.

195 electron transfer pathways and mechanism of Na(+)-NQR catalysis.

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

197 in mice caused only subtle perturbations of Na(+) homeostasis and provide evidence that the Na(+)/Cl

198 le of females had greater phosphorylation of Na(+)/H(+) exchanger isoform 3 (NHE3), distribution of N

199 s under acidic conditions in the presence of Na(+) that consist of both antiparallel G4s and i-motifs

200 However, in the presence of Na+/H+ exchange activity, the SLC4A7 genotypic effect on

201 Recording of Na currents revealed proexcitatory increases in persiste

202 nt for the role of AnkG in the regulation of Na(+) transport in the distal kidney nephron.

203 and their effects on the reproducibility of Na quantification were explored.

204 impaired Ca(2+) transients, upregulation of Na(+)/Ca(2+) exchanger function, reduction of Ca(2+) upt

205 of Li ions, while the Li-based SEI shuts off Na-ion transport.

206 tissue consumed could be predicted based on Na, N or net primary productivity.

207 gest a regulatory effect of retinoschisin on Na/K-ATPase signaling and localization, whereas Na/K-ATP

208 tions revealed no effect of retinoschisin on Na/K-ATPase-mediated ATP hydrolysis and ion transport.

209 he two H(+) ions that NhaA exchanges for one Na(+) ion during one transport cycle.

210 X-ray absorption spectra of Tl adsorbed onto Na-exchanged IdP indicated a shift from adsorption of (d

211 e driven from the inward to the outward open Na(+)-bound conformation.

212 creased, and expression levels of Ca(2+)- or Na(+)-handling proteins were not altered.

213 from high tissue concentrations of Cl(-) or Na(+) but were due to changes in the pHapo Most of these

214 precycling an electrode in a desired Li- or Na-based electrolyte, and that ionic transport can be ki

215 ased SEI membranes are produced using Li- or Na-based electrolytes, respectively.

216 ate that AtTPC1 is selective for Ca(2+) over Na(+), but nonselective among monovalent cations (Li(+),

217 as TJs dominated by cldn16 favor Mg(2+) over Na(+); (iii) cldn10b does not interact with other TAL cl

218 ding of K(+) and other permeant species over Na(+), there is a selective exclusion of nonpermeant spe

219 (23)Na MAS NMR spectra of sodium-oxygen (Na-O2) cathodes reveals a combination of degradation spe

220 , K and B group) and mineral contents (N, P, Na, K, Ca, Mg and Fe) were stimulated by the irradiation

221 Peak [Na(+)]i changes during single EPSPs are approximately 5

222 olac) inhibition alone, or combined NO, PGs, Na(+) /K(+) -ATPase (ouabain) and KIR channel inhibition

223 ernatively, reaction of [U(Tren(TIPS) )(PH)][Na(12C4)2 ] (5, 12C4=12-crown-4 ether) with [U{N(CH2 CH2

224 higher abundance of total and phosphorylated Na(+)/Cl(-) cotransporter (NCC), claudin-7, and cleaved

225 omplex; (ii) TJs dominated by cldn10b prefer Na(+) over Mg(2+), whereas TJs dominated by cldn16 favor

226 eutral NaCl reabsorption, therefore reducing Na(+)/K(+) exchange.

227 port that AnkG expression directly regulates Na(+) transport by altering ENaC activity in the apical

228 lCBL10 mediates salt tolerance by regulating Na(+) and Ca(2+) fluxes in the vacuole, cooperating with

229 er family and a model system for all related Na(+)/H(+) exchangers, including eukaryotic representati

230 tent, lower water loss rates, lower relative Na(+) content, and higher chlorophyll content and prolin

231 ch then phosphorylate and activate the renal Na-Cl cotransporter (NCC).

232 ophyte algae and marine angiosperms requires Na(+) influx, suggesting that Na(+) /Pi symporters also

233 nae revealed an overlap of the retinoschisin-Na/K-ATPase complex with proteins involved in Na/K-ATPas

234 From the blood samples, Na, P, S, Cl, K, Ca, Fe, Cu, Zn, and Br elemental concen

235 The thiazide-sensitive Na(+)/Cl(-) cotransporter (NCC) is activated by low pota

236 Shoot Na concentrations were determined in 334 angiosperm spec

237 n around Na and effectively soften the short Na-O bond along the polar axis - an effect that is propo

238 Within the A-sites, Na cations are found to be strongly off-centered along t

239 A simple sodium (Na) treatment method was used to modify the morphology a

240 AN pacemaker activity in the atrial-specific Na(+) /Ca(2+) exchange (NCX) knockout (KO) mouse, a mode

241 e transporter, in which multiple spontaneous Na(+) release events were observed.

242 translocation of substrate and co-substrate Na(+) across the lipid bilayer and the transport cycle,

243 ely 2.56% volumetric variation) and superior Na transport kinetics in Na intercalation/extraction pro

244 s provided key insight into how synchronised Na/Fe cooperation operates in these transformations.

245 absorption of UV radiation directly by TEL21/Na(+).

246 ed solutions containing Na(+) cations (TEL21/Na(+)).

247 at NMDG(+) "percolates" 10 times slower than Na(+) in the open state, likely due to a conformational

248 We demonstrated earlier that Na(+)/Ca(2+) exchanger 1 (NCX1), a major calcium exporte

249 We find that Na(+) ions precipitate to the calcite surface and form N

250 (23)Na NMR experiments show that Na(+) ions are present near the gold surface, indicating

251 perms requires Na(+) influx, suggesting that Na(+) /Pi symporters also function in some streptophytes

252 The Na(+) -taurocholate cotransporting polypeptide (NTCP/SLC

253 The Na-based SEI allows easy transport of Li ions, while the

254 B (PTB) proteins are hypothesized to be the Na(+) /Pi symporters catalysing Pi uptake in chlorophyte

255 se media appear to have been screened by the Na humate.

256 on of the baseline membrane potential by the Na(+)/K(+) pump, balanced by an h-current, both of which

257 mobility include the solution chemistry, the Na humate concentration, and the collector properties.

258 5i in binding and unbinding of Na2, i.e. the Na(+) bound in the Na2 site, by carrying out comparative

259 ntegrated ISTDs, both Cs and Li improved the Na peak area reproducibility approximately 2-fold, to fi

260 In human melanoma, the Na(+)/H(+) exchanger NHE1 is an important modifier of th

261 ts, it can be seen that the functions of the Na treatment in our non-vacuum deposited CIGS are mainly

262 rent, both of which affect the gating of the Na(+) current.

263 e transport-associated inward release of the Na(+) ion from the Na2 site to intracellular gating, we

264 The electroneutral C932R mutant of the Na(+),K(+)-ATPase retained a wild-type-like enzyme turno

265 acid causes an imbalanced expression of the Na(+)-K(+)-2Cl(-) cotransporter 1 and the K(+)-Cl(-) cot

266 ng enzyme 2, and increased expression of the Na(+)-K(+)-2Cl(-) cotransporter.

267 Furthermore, the structure of the Na(+)-selective AtTPC1 mutant elucidates the structural

268 ichia coli is the best studied member of the Na(+)/H(+) exchanger family and a model system for all r

269 cterized by compensatory upregulation of the Na(+)/HCO3(-) cotransporter NBCn1.

270 ts of strophanthin induced inhibition of the Na-/K-ATPase in liver cells using a magnetic resonance (

271 The time course of the Na-/K-ATPase inhibition in the cell culture was demonstr

272 of retinoschisin on the functionality of the Na/K-ATPase, its interaction partner at retinal plasma m

273 in binding requires the beta2-subunit of the Na/K-ATPase, whereas the alpha-subunit is exchangeable.

274 These structures portray the Na(+)-bound VcINDY in complexes with succinate and citra

275 +) homeostasis and provide evidence that the Na(+)/Cl(-) cotransporter (NCC) compensated for the inac

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

277 These Na displacements promote off-centering of the neighborin

278 nvertebrate neurons rapidly suppresses these Na(+)-activated K(+) currents and that this effect is me

279 aphy of omnivory driven in part by access to Na.

280 Li apparent selectivity of 47.8 compared to Na ions and 212 compared to K ions, respectively in the

281 This pore-domain chimera is permeable to Na(+), K(+), and Ca(2+) ions, and remarkably, is also ro

282 ylphenyl)imidazol-2-ylidene (IPr)), towards [Na(dioxane)x ][PnCO] (Pn=P, As) is described.

283 rom L2/3 neurons revealed that the transient Na(+) current was significantly larger in fmr1(-/y) neur

284 tion of the co-expressed water-translocating Na(+) /K(+) /2Cl(-) cotransporter promoted TRPV4 activat

285 ithelial cells is dependent on transmembrane Na(+) and/or K(+) flux and the activation of heat shock

286 chemiosmotically driven by the transmembrane Na(+) gradient common to metazoans, regulates Smoothened

287 es the same sites to alternatively transport Na(+) and K(+) This ping-pong mechanism is supported by

288 ATP-hydrolysing sodium/potassium transporter Na(+)/K(+)-ATPase (NKA) into a monoolein-derived LCP.

289 athematical modelling predicted that tubular Na(+) reabsorption decreased in the proximal tubule but

290 athematical modelling predicted that tubular Na(+) reabsorption increased in the proximal tubule but

291 ting the binding sites for substrate and two Na(+) ions.

292 actions that concomitantly increase urinary Na+ excretion and lead to increased urine volume.

293 t is tightly controlled by regulated urinary Na(+) excretion.

294 owing to the lower melting point of the used Na salts compared to the reaction temperature.

295 pyrimidine and purine nucleosides utilizing Na(+) and/or H(+) electrochemical gradients.

296 gh redox potentials ( approximately 4.2 V vs Na/Na(+) ) with high charge capacity (190 mAh g(-1) ).

297 (2+), S-2288 cleavage by wild-type HABP2 was Na(+)-dependent, with Km decreasing from 3.0 to 0.6 mm u

298 d that Rb(+) deocclusion is accelerated when Na(+) binds to an allosteric, nonspecific site, leading

299 K-ATPase signaling and localization, whereas Na/K-ATPase-dysregulation caused by retinoschisin defici

300 The procedure enabled us to evaluate whether Na(+)/K(+)-ATPase uses the same sites to alternatively t