ライフサイエンスコーパス: NHE

1 NHE activity was inhibited significantly (approximately

2 NHE inhibition involved a decrease of both NHE2 and NHE3

3 NHE-1 activation preceding TRPV1 stimulation suggests th

4 NHE-1 inhibition also reduced plasma levels alanine amin

5 NHE-1 inhibition also resulted in reduced plasma levels

6 NHE-1 inhibition facilitated the hemodynamic response to

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

8 NHE-1 inhibition, however, replicated previously reporte

9 NHE-1 may be an important pathway for Na(+) entry during

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

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

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

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

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

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

16 olemmal sodium-hydrogen exchanger isoform-1 (NHE-1) in response to the intense intracellular acidosis

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

18 olemmal sodium-hydrogen exchanger isoform-1 (NHE-1) is emerging as a promising novel strategy for ame

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

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

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

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

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

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

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

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

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

28 5-HT and Ang II rapidly activated NHE-1 via their G protein-coupled receptors (5-HT(2A) an

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

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

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

32 Although NHE inhibitors are known to lower intraocular pressure (

33 ethylsulfonyl-4piperidonbenzoylguanidine, an NHE-1 and NHE-2 isoform inhibitor.

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

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

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

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

38 nyl-4piperidonbenzoylguanidine, an NHE-1 and NHE-2 isoform inhibitor.

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

40 oxytryptamine (5-HT) stimulated both ERK and NHE-1 activities, with activation of NHE-1 preceding tha

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

42 gnaling complex that includes CaM, Jak2, and NHE-1.

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

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

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

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

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

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

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

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

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

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

53 This suggests that SNP causes NHE inhibition.

54 Depriving NHEs of intracellular protons by buffering HC cytosol wi

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

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

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

58 489 mV versus the normal hydrogen electrode (NHE), were used to immobilize and "wire" GcGDH to the sp

59 +/- 0.2 V vs. the normal hydrogen electrode (NHE).

60 +0.6 V versus the normal hydrogen electrode (NHE).

61 .95 and 0.28 V vs normal hydrogen electrode (NHE)], respectively.

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

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

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

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

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

67 human disorders linked to loss of endosomal NHE function.

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

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

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

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

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

73 region are identical to Na(+)-H(+) exchange (NHE)-1 isoform with the remaining 63 amino acids compris

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

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

76 al acid-extrusion proteins, Na+-H+ exchange (NHE) and Na+-HCO3- co-transport (NBC) in guinea-pig isol

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

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

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

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

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

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

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

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

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

86 ion of the sarcolemmal Na(+)/H(+) exchanger (NHE) affords significant protection to myocardium subjec

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

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

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

90 with the activity of a Na(+)-H(+) exchanger (NHE).

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

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

93 Activity of the Na+/H+ exchanger (NHE) isoform 1 (NHE1) is increased by intracellular acid

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 um, at a concentration sufficient to inhibit NHE activity, before (or as soon as possible after) the

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

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

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

115 ll other known Na(+)-H(+) exchange isoforms, NHE-deficient PS120 fibroblasts stably transfected with

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

117 nserved in AtNHX1 and prototypical mammalian NHE Na+/H+ exchangers led to the identification of five

118 unctionally characterized in plasma membrane NHE null fibroblasts.

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

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

121 Likewise, J(ms)(NHE) and cell volume were unaffected by intracellular cy

122 induced by hypertonic medium inhibited J(ms)(NHE) in both CFTR(+) and CFTR(-) mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

136 Thus, mitogen-induced activation of NHE-1 in VSMC is dependent upon elevated intracellular C

137 ERK and NHE-1 activities, with activation of NHE-1 preceding that of ERK.

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

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

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

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

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

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

147 Inhibition of NHE activity by amiloride inhibits regeneration of alkal

148 5-HT-mediated inhibition of NHE activity was dependent on phosphorylation of phospho

149 culin A also prevented hypoxic inhibition of NHE activity.

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

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

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

153 Inhibition of NHE-1 with pharmacological agents or by isotonic replace

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 stigations continue to test the potential of NHE inhibitors in the treatment of other cardiovascular

162 to NH4Cl and its washout in the presence of NHE inhibition (by zero [Na+]o or the NHE1 inhibitor car

163 hanisms underlying the osmotic regulation of NHE-1 are poorly understood.

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

165 We have examined the regulation of NHE-1 by two potent mitogens, serotonin (5-HT, 5-hydroxy

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 Similar NHE stimulatory effects of sustained acidosis were obser

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

185 is was sustained for > or =3 min, subsequent NHE activity was significantly increased (>4-fold).

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

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

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

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

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

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

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

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

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

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

196 ain maximum cardioprotective benefit, 1) the NHE inhibitor must be present in jeopardized myocardium,

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

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

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

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

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

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

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

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

205 One binding partner of the NHE family is calcineurin homologous protein (CHP).

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

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

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

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

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

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

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

213 n contrast, recent clinical studies with the NHE inhibitors cariporide and eniporide in patients with

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

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

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

217 M and subsequent increased binding of CaM to NHE-1, similar to the pathway previously described for t

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

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

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

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

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

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

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

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

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

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

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

229 V for Mn(III)TE-2-PyP(5+) and +219 mV versus NHE for Mn(III)Br(8)T-2-PyP(+).

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

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

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

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

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

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

236 ion potential of approximately 800 mV versus NHE.

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

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

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

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

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

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

243 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

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

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

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

247 se of F61I/F65Y/R106L (DeltaE(m) = 158 mV vs NHE), increased solvent exposure of the heme as a result

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

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

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

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

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

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

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

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

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

261 0 nmol Co ions/cm(2)) deposited at 1.25 V vs NHE than in an extremely thin film ( approximately 3 nmo

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

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

264 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

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

266 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

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

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

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

270 l region studied (0.0 V <or= E <or= 1.2 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 V,V) complex in organic solvents at 1.9 V vs NHE.

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

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

278 ontrolled potential electrolyses at 1.3 V vs NHE.

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

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

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

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

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

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

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

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

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

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

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

290 oing clinical studies will determine whether NHE inhibition will find therapeutic application in the

291 t models of ventricular fibrillation whether NHE-1 inhibition, by using the selective inhibitor carip

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