ライフサイエンスコーパス: NHE

1 NHE activities contribute to the control of the cell cyc

2 NHE activity was inhibited significantly (approximately

3 NHE dysfunction has been linked to many diseases, and th

4 NHE inhibition involved a decrease of both NHE2 and NHE3

5 NHE is a non-redundant toxin to haemolysin BL (HBL) desp

6 NHE mediates killing of cells from multiple lineages and

7 NHE-1 activation preceding TRPV1 stimulation suggests th

8 NHE-1 inhibition also reduced plasma levels alanine amin

9 NHE-1 inhibition also resulted in reduced plasma levels

10 NHE-1 inhibition facilitated the hemodynamic response to

11 NHE-1 inhibition may represent a highly potent novel str

12 NHE-1 inhibition, however, replicated previously reporte

13 NHE-1 protein was co-localized with cytoskeletal protein

14 capsazepine, or sodium-hydrogen exchanger 1 (NHE-1) inhibitor dimethyl amiloride were perfused with o

15 The sodium/hydrogen exchanger 1 (NHE-1) is linked to the cytoskeleton by ezrin/radixin/mo

16 roposed that Na(+)/H(+) exchanger isoform 1 (NHE-1) is important in microglial migration.

17 nsitive sodium-hydrogen exchanger isoform 1 (NHE-1), intracellular pH, Bcl-x(L) deamidation, and apop

18 olemmal sodium-hydrogen exchanger isoform-1 (NHE-1) could facilitate return of spontaneous circulatio

19 whether sodium-hydrogen exchanger isoform-1 (NHE-1) inhibition attenuates myocardial injury during re

20 basolateral Na(+)-H(+) exchanger isoform-1 (NHE-1) was investigated in neural adaptation of rat tast

21 othesis that sodium-proton exchanger type 1 (NHE-1) is a regulator of extracellular signal-regulated

22 The sodium/proton exchanger type 1 (NHE-1) plays an important role in the proliferation of v

23 Nuclease hypersensitivity element III(1) (NHE III(1)) of the c-Myc promoter can form transcription

24 he nuclease hypersensitivity element III(1) (NHE III(1)) of the c-MYC promoter strongly controls the

25 pendent Na(+)-HCO(3)(-) cotransporter, and a NHE-like Na(+)/H(+) exchanger.

26 of G-quadruplex structures within the PDGF-A NHE can silence PDGF-A expression.

27 After the desired duration of acidosis, NHE was reactivated (by reintroduction of [Na+]o or remo

28 Hypertonicity rapidly activated NHE-1 in a concentration-dependent manner as assessed by

29 5-HT and Ang II rapidly activated NHE-1 via their G protein-coupled receptors (5-HT(2A) an

30 strong acid, an increase in Ca(2+) activates NHE-1, and increases neural adaptation to all acidic sti

31 In addition, NHE-1 activation resulted in intracellular Na(+) loading

32 In addition, NHE-1 and NCXrev play a concerted role in BK-induced mic

33 Here, we found that all NHE isoforms were expressed in wild-type (WT) mouse coch

34 ected by feed intake (P = 0.003) as were all NHE genes (NHE1, NHE2, and NHE3; P < 0.05).

35 Although NHE inhibitors are known to lower intraocular pressure (

36 with choline and significantly reduced by an NHE inhibitor, cariporide.

37 The fluxes are blocked by an NHE inhibitor, ethylisopropylamiloride, and are absent i

38 SNP and dimethyl amiloride (DMA), an NHE inhibitor, inhibited pH(i) recovery to a similar deg

39 Finally, zoniporide, an NHE inhibitor being explored as a therapeutic agent to t

40 ction complexes that included Jak2, CaM, and NHE-1.

41 favour of the module containing CatSper and NHE and highlight experimentally testable predictions th

42 roduced by a model featuring the CatSper and NHE module but not by those including the pH-independent

43 e treated with 5-HT (.1 micromol/L, 1 h) and NHE activity was measured as ethyl-isopropyl-amiloride (

44 Kinetic flux expressions for the CU, NCE and NHE were developed and individually parameterized based

45 Ang II, suggesting that the EGF receptor and NHE-1 work in parallel to stimulate ERK activity in RASM

46 l restitution, we evaluated whether TFFs and NHE isoforms share a common pathway to promote epithelia

47 ongly reducing hydrated electrons (e(aq)(-); NHE = -2.9 V) that have been shown to effectively degrad

48 Blocking NHE-1 activity not only attenuated loss of dendritic mit

49 Interestingly, blocking NHE-1 activity with its potent inhibitor HOE 642 not onl

50 f heart failure by inhibiting either or both NHE isoforms, and drugs used to treat heart failure may

51 E activity (likely through acid extrusion by NHE isoform 1).

52 H(+) exchanger (NHE) activity is mediated by NHE isoform 1 (NHE1), which is subject to regulation by

53 molecular mechanisms that stimulate cardiac NHE activity in disease may be targeted to attenuate suc

54 ic target for indirectly suppressing cardiac NHE activity warrants further investigation.

55 This suggests that SNP causes NHE inhibition.

56 Depriving NHEs of intracellular protons by buffering HC cytosol wi

57 II (CAII), which is colocalized with either NHE or NBC.

58 V (relative to the normal hydrogen electrode NHE) which supports the feasibility of a low pH iron rel

59 m -0.1 V versus a normal hydrogen electrode (NHE) when a mixture of water and ionic liquid ([H2O] = 1

60 489 mV versus the normal hydrogen electrode (NHE), were used to immobilize and "wire" GcGDH to the sp

61 +0.6 V versus the normal hydrogen electrode (NHE).

62 +/- 0.2 V vs. the normal hydrogen electrode (NHE).

63 .95 and 0.28 V vs normal hydrogen electrode (NHE)], respectively.

64 ch lies the nuclease hypersensitive element (NHE) III(1) region containing the CT-element.

65 The KRAS nuclease-hypersensitive element (NHE) region contains a G-rich element (22RT; 5'-AGGGCGGT

66 ontains one nuclease hypersensitive element (NHE) that is critical for PDGF-A gene transcription.

67 88) and the nuclease-hypersensitive element (NHE; -92 to -48).

68 effects not through NBCe1-A, but endogenous NHEs.

69 newly defined family of eukaryotic endosomal NHE as novel targets for pharmacological inhibition to a

70 human disorders linked to loss of endosomal NHE function.

71 nsport activity of the orthologous endosomal NHE Nhx1 is important for multivesicular body (MVB)-vacu

72 , the molecular basis of how these endosomal NHEs control endocytic trafficking is unclear.

73 Here, we show non-haemolytic enterotoxin (NHE) from the neglected human foodborne pathogen Bacillu

74 rdiac pathology activate RSK, an established NHE kinase, and several selective RSK inhibitors have be

75 ologue of the medically important eukaryotic NHE Na(+)/H(+) exchangers.

76 termine the kinetics of Na(+)/H(+) exchange (NHE) and the activity of the Na(+)/K(+) pump, and ATP le

77 selective inhibitors of Na(+)-H(+) exchange (NHE).

78 he effects of serotonin on Na+ /H+ exchange (NHE) activity in the human intestine have not been inves

79 ulates intracellular pH via Na+/H+ exchange (NHE) antiporters; however, this mechanism has not been d

80 O3- cotransport (NBC) and Na+ / H+ exchange (NHE), expressed in enzymically isolated mammalian ventri

81 The sodium/hydrogen exchange (NHE) gene family plays an integral role in neutral sodiu

82 ly via V-ATPase with sodium-proton exchange (NHE) playing a minor role.

83 y EZA and blocked by EIPA, a Na-H exchanger (NHE) inhibitor.

84 Na-H exchanger (NHE) was examined by immunolocalization.

85 rdial stretch: (i) the Na(+)-H(+) exchanger (NHE) (ii) nitric oxide (NO) and the ryanodine receptor (

86 Here we show that Na(+)/H(+) exchanger (NHE) activity appears to, in part, contribute to this sy

87 Sarcolemmal Na(+)/H(+) exchanger (NHE) activity is mediated by NHE isoform 1 (NHE1), which

88 that inhibition of the Na(+)/H(+) exchanger (NHE) affords significant protection to myocardium subjec

89 ) exchanger (NCE), and Na(+)-H(+) exchanger (NHE) into an existing computational model of mitochondri

90 llular distribution of Na(+)/H(+) exchanger (NHE), which is localized in a punctate distribution in t

91 48), thereby promoting Na(+)-H(+) exchanger (NHE)-3 degradation.

92 cking H(+) efflux by a Na(+)-H(+) exchanger (NHE; Ddnhe1(-)), chemotaxis is impaired and the assembly

93 ndent and sensitive to Na(+)/H(+)-exchanger (NHE) inhibitors.

94 increase cleft acidity via Na+/H+ exchanger (NHE) proton extrusion, which results in inhibition of co

95 porter (MCT), the sodium hydrogen exchanger (NHE), and V-Type ATPase mediate acid extrusion to counte

96 The type 1 sodium-hydrogen exchanger (NHE-1) is a ubiquitous electroneutral membrane transport

97 e-dependent neutral sodium-proton exchanger (NHE).

98 Conversely, Na/H exchangers (NHE) are often implicated in cellular migration but have

99 l Na(+) channels (ENaC) and Na-H exchangers (NHE), inhibition of NHE-mediated Na(+) absorption is the

100 oblasts and organizes Na(+)/H(+) exchangers (NHEs) and the PTH receptor.

101 Na(+) /H(+) exchangers (NHEs) are ancient membrane-bound nanomachines that work

102 Multiple Na(+)/H(+) exchangers (NHEs) are implicated in maintenance of neural pH homeost

103 human endosomal Na(+)(K(+))/H(+) exchangers (NHEs) NHE6 and NHE9 are implicated in neurological disor

104 Mammalian Na(+)/H(+) exchangers (NHEs) regulate numerous physiological processes and are

105 tic vesicles and (3) Na(+) /H(+) exchangers (NHEs).

106 ne encodes a homologue of Na+/H+ exchangers (NHEs) located on the parasite's plasma membrane.

107 Sodium/hydrogen exchangers (NHEs) are ubiquitous ion transporters that serve multipl

108 As an alternative to direct and global NHE inhibition, which may trigger non-cardiac adverse ef

109 of CaM --> association of CaM with NHE-1 --> NHE-1 activation.

110 Hence, NHEs are being targeted for pharmaceutical-based clinica

111 trate substrate-tolerant nano-heteroepitaxy (NHE) of high-quality formamidinium-lead-tri-iodide (FAPb

112 These studies identify NHE as a new regulator of ERK activity in RASM cells.

113 The nuclease hypersensitivity element III1 (NHE III1) upstream of the P1 and P2 promoters of c-MYC c

114 , ethylisopropylamiloride, and are absent in NHE-deficient AP-1 cells.

115 are needed to understand whether changes in NHE activity contribute to the IOP-lowering effect of NO

116 presence of 30 microM cariporide to inhibit NHE, acid extrusion via NBC was also slowed at 27 degree

117 JAK2V617F inhibits NHE-1 upregulation in response to DNA damage and consequ

118 on cytosolic and membrane-bound CA isoforms, NHE-1, and TRPV1.

119 ucture of the G-rich element within the KRAS NHE.

120 gy, structural information for the mammalian NHE was lacking.

121 unctionally characterized in plasma membrane NHE null fibroblasts.

122 nd 4.1 ERM (FERM) domain to recruit a moesin-NHE-1 complex to invadopodia.

123 n CFTR(+) jejunum but had no effect on J(ms)(NHE) across CFTR(-) jejunum.

124 ) exchanger-mediated Na(+) absorption (J(ms)(NHE)) in CFTR(+) jejunum but had no effect on J(ms)(NHE)

125 ium and recovered approximately 40% of J(ms)(NHE).

126 port process, and with an E(1/2) of -158 mV (NHE), FeFbpA-SO4 is the most easily reduced of all FeFbp

127 The major G-quadruplex formed in c-Myc NHE III(1) is a mixture of four loop isomers, which have

128 p isomer formed in the single-stranded c-MYC NHE III(1) oligonucleotide, the Myc2345 G-quadruplex.

129 tic thermodynamic analysis of modified c-MYC NHE III(1) sequences, which provided quantitative measur

130 in the transport of Cu (CTR1 and ATP7A), Na (NHE-2), Ca (ECaC), divalent metals (DMT1), and Zn (ZIP8)

131 We find that NBC, but not NHE flux is enhanced by catalytic CA activity, with faci

132 blockade attenuated ERK activation, but not NHE-1 activation by 5-HT and Ang II, suggesting that the

133 urrent study demonstrates that activation of NHE-1 (Na(+)/H(+) exchanger isoform 1) in dendrites pres

134 Receptor-independent activation of NHE-1 by acute acid loading of RASM cells resulted in th

135 ose that hypertonicity induces activation of NHE-1 in CHO-K1 cells in large part through the followin

136 olved in hypertonicity-induced activation of NHE-1 in CHO-K1 cells.

137 Activation of NHE-1 was blocked by inhibitors of phospholipase C, CaM,

138 inotropic response to stretch: activation of NHE; and of activation of SACs.

139 h hetastarch infusion alone, the addition of NHE-1 inhibitor improved the hemodynamic response to flu

140 putative transmembrane region, subunit C of NHE initiates binding to the plasma membrane, leading to

141 ruplex structure of the G-rich strand DNA of NHE was identified by CD and dimethyl sulfate (DMS) foot

142 The efficacy of NHE inhibitors on the risk of cardiovascular events may

143 ely linking the proton transport function of NHE-1 to ERK activation.

144 ubule cells, internalization/inactivation of NHE-3 (sodium-hydrogen exchanger-3) and Na(+)/K(+)ATPase

145 f pHi (dpHi/dt) was measured as the index of NHE activity.

146 cation, an effect mediated via inhibition of NHE activity (likely through acid extrusion by NHE isofo

147 Hypoxic inhibition of NHE activity and the reduction in ROS levels were revers

148 Inhibition of NHE activity by amiloride inhibits regeneration of alkal

149 5-HT-mediated inhibition of NHE activity was dependent on phosphorylation of phospho

150 culin A also prevented hypoxic inhibition of NHE activity.

151 synaptic acidification because inhibition of NHE by amiloride or lithium under physiological or weak

152 Inhibition of NHE with HOE 642 (5 microm) significantly reduced (P < 0

153 Inhibition of NHE-1 or the reverse mode of Na(+)/Ca(2+) exchange preve

154 aC) and Na-H exchangers (NHE), inhibition of NHE-mediated Na(+) absorption is the primary cause of di

155 hose normally experienced, via inhibition of NHE.

156 be blocked by pharmacological inhibitors of NHE-1 or by isotonic replacement of sodium, closely link

157 The CAi insensitivity of NHE flux suggests that, in the native cell, intrinsic mo

158 at the polarized presynaptic localization of NHE/CHP1 is an important feature of neuronal axons and t

159 egulating intracellular pH via modulation of NHE activity.

160 enforced alkalinization or overexpression of NHE-1, leading to a restoration of apoptosis.

161 mental mechanism for the rapid regulation of NHE-1 by G(q/11) protein-coupled receptors in multiple c

162 E, NO could act as an autocrine regulator of NHE activity.

163 and p90RSK and abolished the stimulation of NHE activity by sustained (3 min) intracellular acidosis

164 Moreover, stimulation of NHE-1 caused dendritic Na(+)(i) accumulation, swelling,

165 e cryogenic electron microscopy structure of NHE isoform 9 (SLC9A9) from Equus caballus at 3.2 angstr

166 ng intermediates in 5-HT-mediated effects on NHE activity was elucidated using pharmacologic inhibito

167 The effects of 5-HT on NHE activity were not cell-line specific because T84 cel

168 ute effects of 5-hydroxytryptamine (5-HT) on NHE activity using Caco-2 cells as an in vitro model.

169 ere are conflicting observations reported on NHE expression in human UC, the present study was initia

170 Drugs previously classified as NCX or NHE inhibitors are shown to also inhibit hASIC-1.

171 cutive 5' runs of guanines of c-MYC promoter NHE III(1,) which have recently been shown to form in a

172 eted disruption of the Puralpha gene reduced NHE activity and PDGF-A mRNA expression in mouse embryo

173 how for the first time that the pH regulator NHE-1 can be silenced in a human cancer and also suggest

174 glucose deprivation and a 1-h reoxygenation, NHE-1 activity was increased by approximately 70-200% in

175 E-1/Bcl-xL deamidation pathway by repressing NHE-1 upregulation in response to DNA damage.

176 to that of the wild-type 27-mer purine-rich NHE III(1) sequence of the c-MYC promoter.

177 osphorylation at Ser648 inhibits sarcolemmal NHE activity during intracellular acidosis, most likely

178 es have confirmed that, in certain settings, NHE inhibition does indeed protect human myocardium.

179 -line specific because T84 cells also showed NHE inhibition.

180 Similar NHE stimulatory effects of sustained acidosis were obser

181 pH(i) reversibly and zoniporide, a specific NHE-1 blocker, inhibited the Na(+)-induced changes in pH

182 Our findings indicate that targeting NHEs could be a novel strategy to combat human-pathogeni

183 cally during GABAergic transmission and that NHE plays a critical role in generating the acidic nano-

184 Taken together, our study demonstrates that NHE-1-mediated Na(+) entry and subsequent Na(+)/Ca(2+) e

185 We found that NHE-1 on 1p is silenced in oligodendrogliomas secondary

186 These data indicate that NHE and HBL operate synergistically to induce inflammati

187 The data indicate that NHE, probably in combination with Cl(-)-HCO(3)(-) exchan

188 Taken together, our study shows that NHE-1 protein is abundantly expressed in microglial lame

189 Furthermore, pre-clinical work suggests that NHE inhibition may provide therapeutic benefit in heart

190 Thus, our findings demonstrated that NHEs play important roles in normal hearing in the mamma

191 Together, these results suggest that NHEs are the primary source of extracellular protons in

192 The NHE gene family is comprised of nine members that are ca

193 The NHE response does not appear to be the consequence of NO

194 The regulation of MYC is complex, and the NHE III1 and FUSE elements rely upon noncanonical DNA st

195 ocked by the AMPK antagonist compound C, the NHE inhibitor HOE694, and mutation of a predicted AMPK r

196 n cells expressing JAK2V617F compromises the NHE-1/Bcl-xL deamidation pathway by repressing NHE-1 upr

197 Together, these experiments identify the NHE isoforms involved in regulating oocyte pH(i), indica

198 In the NHE III1 only the G-quadruplex has been extensively stud

199 her order G-quadruplex (G4) structure in the NHE III1 region.

200 tructure formed within the duplex DNA of the NHE at temperatures up to 100 degrees C.

201 ssay has shown that the G-rich strand of the NHE can form two major G-quadruplex structures, which ar

202 The purine-rich strand of the NHE III(1) element has been shown to be a silencer eleme

203 we reveal the conserved architecture of the NHE ion-binding site, their elevator-like structural tra

204 on, which requires detailed knowledge of the NHE structure.

205 otprinting in the double-stranded DNA of the NHE.

206 nd light-emitting diode devices based on the NHE-FAPbI(3) showed efficiencies and stabilities superio

207 ght pigs each were randomized to receive the NHE-1 inhibitor zoniporide (3 mg.kg-1) or vehicle contro

208 The findings suggest the NHE is inhibited by NO which acts via a cGMP and protein

209 MYC mRNA and altered protein binding to the NHE III(1) region, in agreement with a G4 stabilizing co

210 Here we show that treatment with the NHE inhibitor 5-(N-ethyl-N-isopropyl) amiloride (EIPA) r

211 By contrast, clinical studies with the NHE inhibitors cariporide, eniporide and zoniporide, in

212 n between nucleotides -91 and -77 within the NHE element, which contains binding sites for the double

213 This NHE is readily applicable to various substrates used for

214 Acid-extrusion (Je) through NHE was approximately 50% slower than at 37 degrees C, c

215 s restored earlier in more rats subjected to NHE-1 inhibition, the differences were statistically ins

216 presence of HCO(3)(-), HCO(3)(-) transport, NHE and CA activity.

217 Nhx1, an endosomal member of the ubiquitous NHE family of Na+/H+ exchangers, regulates luminal and c

218 der static anodic potentials (+2.2 or +3.0 V NHE) using domestic wastewater samples, with added chlor

219 radicals (Cl., Cl2(-).) generation at +3.0 V NHE.

220 density of more than 300 mA cm(-2) at 1.7 V(NHE) were obtained in 1 m KOH.

221 ncies of around 40% were obtained at -0.45 V/NHE across the entire visible spectral region.

222 anced to 5 mA/cm(2) at a potential of -0.5 V/NHE under visible light irradiation of approximately 40

223 dation of NO2YO(-)122 occurs near 1.1 versus NHE; oxidation of NO2YO(-)109 is near 1.2 V.

224 potential of +36 +/- 15 mV at pH 7.8 (versus NHE).

225 A DNA-bound potential of +200 mV versus NHE (normal hydrogen electrode) is found for SoxR isolat

226 h have redox potentials close to 0 mV versus NHE (this result is in partial disagreement with an exis

227 ate-free heme iron potential (-268 mV versus NHE) is positive for a low spin P450, and the elevated p

228 PVI)Cl](+) had a potential of +309 mV versus NHE, and the optimum GcGDH/Os polymer ratio was 1:2 yiel

229 or Endo III and AfUDG of 58 and 95 mV versus NHE, respectively, comparable to 90 mV for MutY bound to

230 NA-bound MutY is approximately 275 mV versus NHE, which is characteristic of HiPiP iron proteins.

231 a DNA-bound redox potential of ~80 mV versus NHE.

232 ion potential of approximately 800 mV versus NHE.

233 a midpoint potential of 113 +/- 5 mV versus NHE.

234 O2 reduction at a potential of -1.3 V versus NHE.

235 ent with an onset potential of ~0.8 V versus NHE.

236 rate approximately 25% of that mediated via NHE, and consistent with an apparent NBC stoichiometry b

237 follows: E(0')(Comp-I) = 1.22 V (at pH 7, vs NHE) with D(O-H)(Comp-II) = 95 kcal/mol and E(0')(Comp-I

238 mol and E(0')(Comp-II) = 0.99 V (at pH 7, vs NHE) with D(O-H)(Ferric) = 90 kcal/mol.

239 E degrees (2NO, H+/ONNOH) = -0.06 V, all vs NHE.

240 e to be approximately 155 mV (-15 kJ/mol) vs NHE which, like the reduction potential for the native s

241 chieves an H(2) evolution onset of 520 mV vs NHE and a Tafel slope of 30 mV when illuminated by the r

242 trolysis of [Ru(II)-OH(2)](2+) at 1260 mV vs NHE at pH 1 (0.1 M triflic acid) and 1150 mV at pH 6 (10

243 with the redox potential at around -79 mV vs NHE in 0.1 M phosphate buffer pH 7.4.

244 otentials in the range of +700 to +540 mV vs NHE over a pH range of 4-6.

245 termined and varied from -228 to +1111 mV vs NHE under similar solution conditions, allowing direct c

246 mplies a "rack" mechanism for the 290 mV (vs NHE) reduction potential measured at neutral pH.

247 locenter to an optimum value near 300 mV (vs NHE), to provide a source of protons for catalysis, and

248 ial for the 30% portion (perhaps <-800 mV vs NHE).

249 izontal lineO](2+) takes place at 1420 mV vs NHE, bulk electrolysis of [Ru(II)-OH(2)](2+) at 1260 mV

250 e heme reduction potentials (77 and 80 mV vs NHE, respectively, in the absence and in the presence of

251 redox potential range of -470 to +130 mV vs NHE, which includes the redox potential range occupied b

252 phite exhibits an onset current at 560 mV vs NHE.

253 h a DNA-bound midpoint potential of 90 mV vs NHE.

254 omplex can be reduced with E1/2 = -641 mV vs NHE.

255 eme reduction potential from -85 to 49 mV vs NHE.

256 O intermediate at potentials above 1.34 V vs NHE at pH 1, which is characterized by electron paramagn

257 ntrolled-potential electrolysis at 1.61 V vs NHE at pH 7.2 resulted in sustained water oxidation cata

258 y offer highly oxidizing potentials (>1 V vs NHE in aqueous solution) that are sufficient to drive a

259 ed by a single electron (E(1/2) = -0.57 V vs NHE in CH(3)CN) when confined within the fully reduced m

260 single four-electron step (E(p) = +0.77 V vs NHE in CH(3)CN); one of the ligand-based electrons is in

261 and modest reduction potential of 0.99 V vs NHE is in part attributed to complete charge delocalizat

262 0 nmol Co ions/cm(2)) deposited at 1.25 V vs NHE than in an extremely thin film ( approximately 3 nmo

263 on potential E degrees (Cl(*/-)) = 1.87 V vs NHE that is at least 300 meV more favorable than the acc

264 nd-based, oxidations at +0.21 and +0.63 V vs NHE to yield [L(Delta)Zn] and [L(Delta Delta)Zn](2+), wh

265 ial values of 1.79 V vs Ag/Ag+ (or 1.98 V vs NHE) and 1.82 V vs Ag/Ag+ (or 2.01 V vs NHE) were estima

266 d-state potentials ( approximately -1.2 V vs NHE) sufficient to inject into TiO2.

267 V vs NHE) and 1.82 V vs Ag/Ag+ (or 2.01 V vs NHE) were estimated for Ag(II)/Ag(I) and NO3*/NO3(-) cou

268 (OEC) tetramanganese cluster (Em = 0.2 V vs NHE), quinones (Em = -0.29 V), and pheophytin (Em = -0.7

269 nocarboxylate ligated Eu(II) (E(m) -1.1 V vs NHE).

270 es (E degrees ranging from 0.59 to 1.38 V vs NHE).

271 O2 reduction at FTO occurs at -0.33 V vs NHE, allowing for in situ detection of oxygen as it is f

272 5,4](4+) and [5,5](5+), 1.875 and 2.032 V vs NHE, respectively, exclude the otherwise plausible possi

273 ction to CO in tetrahydrofuran at -0.48 V vs NHE, the least negative potential reported for a molecul

274 with E(fb) extrapolated at pH 0 of 0.08 V vs NHE.

275 on potentials ranging from -2.3 to -3.9 V vs NHE.

276 urrent densities of 1 mA cm(-2) at 1.07 V vs NHE.

277 V,V) complex in organic solvents at 1.9 V vs NHE.

278 O4(aq)) to be tuned from -0.69 to -1.03 V vs NHE.

279 reduction potential, E(Ir(+*/0)) = 1.76 V vs NHE.

280 ontrolled potential electrolyses at 1.3 V vs NHE.

281 nt [E degrees (DTV*(2+)/DTV(*+)) = 0.09 V vs NHE]).

282 Ce(NH4)2(NO3)6 [E1/2(Ce(3+/4+)) = 1.61 V vs NHE], a strong and versatile ground-state oxidant common

283 nerated with an onset potential of 0.05V vs. NHE.

284 hodic oxygen reduction starting at 0.71V vs. NHE.

285 e of the enzyme was measured to be 75 mV vs. NHE, (ii) the surface coverage of CtCDH was found to be

286 mbers (TNs) at pH 7 with an Eapp =1.45 V vs. NHE without any sign of degradation.

287 for human eumelanosomes (-0.2 +/- 0.2 V vs. NHE), despite the presence of a significant fraction of

288 potential of +1.50 V vs. ferrocene (>2 V vs. NHE), the highest value thus far determined electrochemi

289 gher oxidation potential (+0.5 +/- 0.2 V vs. NHE).

290 to the physiologically accessible +0.1 V vs. NHE.

291 However, the mechanism whereby NHE-1 expression is inhibited by JAK2V617F is unknown.

292 sent study was initiated to identify whether NHE isoforms (NHE2 and NHE3) expression is altered and h

293 We investigated whether NHE-1 inhibition (with cariporide) could minimize mechan

294 V in HeLa cells, but the mechanisms by which NHE activity contributed to the life cycle of LCMV remai

295 etabolons consisting of CAII associated with NHE or NBC, respectively.

296 orylation of CaM --> association of CaM with NHE-1 --> NHE-1 activation.

297 oexist and may be attenuated when drugs with NHE inhibitory actions are given concomitantly.

298 ticoid-induced kinase (SGK) 1 interacts with NHE regulatory factor 2 (NHERF2) and mediates activation

299 ell as protein associated predominantly with NHE in the perikaryon and predominantly with NBC in the

300 erior to those of devices fabricated without NHE.

301 that rapid tumor growth cannot occur without NHE-1-mediated neutralization of the acidosis generated