ライフサイエンスコーパス: NHE1

1 isoform protein of the Na(+)/H(+) exchanger (NHE1).

2 ed expression of the Na(+)/H(+) exchanger-1 (NHE1).

3 re mediated by the sodium-hydrogen exchanger NHE1.

4 hat are strengthened by protons extruded via NHE1.

5 transporter (NCX1.1) much more potently than NHE1.

6 pression and transport of the Na-H exchanger NHE1.

7 in (CaM) binding to the regulatory domain of NHE1.

8 ignaling pathways, which converge to inhibit NHE1.

9 ts lacking H(+) efflux by the Na-H exchanger NHE1.

10 xyl-terminal 190 amino acids (625 to 815) of NHE1.

11 s imparting partial inhibitor sensitivity to NHE1.

12 is reversible by blockade of sodium channel NHE1.

13 back to cytosolic H+, which is extruded via NHE1.

14 th amiloride or a Na(+)-free bath to inhibit NHE1.

15 erred the ability of mutant SSTR2 to inhibit NHE1.

16 that confer coupling to the Na-H exchanger, NHE1.

17 ation to inhibit the sodium-proton exchanger NHE1.

18 f cell-cell-adhesion by extracellular pH and NHE1.

19 d extrusion on NBC by 40%, without affecting NHE1.

20 f CHP3 are important elements for regulating NHE1.

21 t that CD44 interaction with a ROK-activated NHE1 (a Na(+)-H(+) exchanger) in cholesterol/ganglioside

22 teract with the sodium hydrogen exchanger 1 (NHE1), a major regulator of intracellular pH.

23 ed activity of the sodium/hydrogen exchanger NHE1, a known regulator of skin pH.

24 We conclude that these opposite effects of NHE1 act synergistically during the metastatic cascade.

25 hibiting RSK in cardiomyocytes would prevent NHE1 activation and decrease I/R-mediated injury.

26 However, NHE1 activation by 100 micromol/L H2O2 was significantly

27 tor-alpha (TGFalpha) requires PI3K-dependent NHE1-activation and subsequent pHi alkalization.

28 ipase A(2) and sodium/hydrogen antiporter 1 (NHE1) activities.

29 and activity, and (ii) inhibition of ROK or NHE1 activity (by treating cells with a ROK inhibitor, Y

30 Inhibiting NHE1 activity after TGFalpha stimulation with 10 muM of

31 Inhibition of LC-CoA catabolism reduced NHE1 activity and enhanced apoptosis, whereas inhibition

32 We now show that NHE1 activity and pHi regulate the timing of G2/M entry

33 proximal tubule LC-CoA generation preserved NHE1 activity and protected against apoptosis.

34 cancer cells occurs as a result of increased NHE1 activity and, while much is known about the pathoph

35 summary, RSK is a novel regulator of cardiac NHE1 activity by phosphorylating NHE1 serine 703 and a n

36 These results imply that NHE1 activity disrupts Na+ and Ca2+ homeostasis and cont

37 increased NHE1 phosphorylation, and reduced NHE1 activity following intracellular acidosis.

38 gical inhibition of endogenous PKB increased NHE1 activity following intracellular acidosis.

39 enosine A(1) receptor-mediated regulation of NHE1 activity in ARVM, the mechanism of which appears to

40 NHE1 activity in atRBCs is exceptionally robust in that

41 NHE1 activity is stable with perfusion of nonhydrolyzabl

42 wnstream Akt survival signaling, and dampens NHE1 activity through competitive inhibition and depleti

43 (+) exchange, and blunted apoptosis, whereas NHE1 activity was decreased in cells enriched with PI(3,

44 NHE1 activity was significantly increased during 10-60 m

45 As a result of persistent NHE1 activity, cytosolic free levels of sodium ([Na(+)](

46 with NHE1, necessary for agonist-stimulated NHE1 activity, were increased by I/R and inhibited by 70

47 ing fibronectin expression is independent of NHE1 activity.

48 s-expressing DN-RSK (Ad.DN-RSK) and measured NHE1 activity.

49 703 of NHE1, stimulating 14-3-3 binding and NHE1 activity.

50 e c release were attenuated by inhibition of NHE1 activity.

51 increases sarcolemmal Na(+)/H(+) exchanger (NHE1) activity in cardiac myocytes by an ERK/RSK-depende

52 macrophages by enhancing Na+/H+ exchanger 1 (NHE1) activity.

53 hing medium, and furthermore showed that the NHE1-AE2 mechanism is particularly important when the tr

54 We hypothesized that stimulation of NHE1 after cerebral ischemia contributes to the disrupti

55 Furthermore, genetic ablation of Nhe1 also resulted in Purkinje cell axon degeneration, p

56 did not prevent the interaction of CHP3 with NHE1, although the D123A mutant no longer showed elevate

57 NHE1 and -4 are expressed at the NPE basolateral margin.

58 Immunolocalization studies revealed NHE1 and -4 in native and cultured NPE.

59 ane, which is required for the activation of NHE1 and an increase in submembranous intracellular pH o

60 During myocardial ischemia, low pH activates NHE1 and causes increased intracellular calcium levels a

61 (standard form) and two signaling molecules (NHE1 and Hyal-2) are closely associated in a complex in

62 lished that activation of the Na-H exchanger NHE1 and increases in intracellular pH (pHi) are early a

63 s following in vitro ischemia phosphorylates NHE1 and increases its activity, which subsequently cont

64 , these findings reveal a novel function for NHE1 and NCX1 in membrane blebbing and permeability, and

65 1.1 at </=1muM, while dually inhibiting both NHE1 and NCX1.1 at >/=20muM.

66 and SEA0400 are more selective inhibitors of NHE1 and NCX1.1 than amiloride or DCB, respectively.

67 NHE1 and NHE2 are not regulated by trafficking.

68 Both NHE1 and NHE3 activities are disrupted in giant patches

69 action of two Na(+)/H(+) exchanger isoforms: NHE1 and NHE3.

70 mellitus by interfering with the actions of NHE1 and NHE3.

71 s may act through increased activity of both NHE1 and NHE3.

72 ned, at least in part, by dual inhibition of NHE1 and of Na(+)-dependent calcium efflux by isoform 1.

73 l type-specific differences in regulation of NHE1 and other target genes.

74 with U0126 abolished phosphorylation of both NHE1 and p90(RSK).

75 s and that ROCK1-mediated phosphorylation of NHE1 and pH change is an essential event required for th

76 en cells were subjected to apoptotic stress, NHE1 and phosphorylated ERM physically associated within

77 ultiple drug targets including inhibition of NHE1 and sodium-calcium exchange.

78 was examined in the parotid acinar cells of Nhe1(-/-) and Nhe2(-/-) mice, both of which exhibited im

79 or) interaction with a Na(+)-H(+) exchanger (NHE1) and hyaluronidase-2 (Hyal-2) during HA-induced cel

80 brane acid extrusion by Na(+)/H(+) exchange (NHE1) and Na(+)-HCO3(-) co-transport (NBC) is essential

81 Sodium-proton exchanger 1 (NHE1) and sodium-calcium exchanger 1 (NCX1) are membrane

82 sphorylation of sodium-hydrogen exchanger 1 (NHE1), and inhibition of NHE1 with 5'-N-ethyl-N-isopropy

83 Finally, we confirmed that the keratinocyte NHE1 antiporter is regulated by extracellular pH indepen

84 was enhanced by acidic pH, and abolished by NHE1 Arg/Lys to Ala mutations within two juxtamembrane d

85 ce of melanoma cell-cell adhesion on pHe and NHE1 as a modulator.

86 f Na(+)/H(+) exchange activity and implicate NHE1 as a possible downstream effector contributing to m

87 We uncovered the Na-H exchanger NHE1 as a potential MAPK scaffold, found links between H

88 esults further implicate helix M9 and EL5 of NHE1 as important elements involved in cation transport

89 NHE1-associated Akt activity and cell survival were inhi

90 nsistent with this, membrane localization of NHE1 at axon terminals was greatly reduced in Chp1-defic

91 olog (atNHE1) that is 79% identical to human NHE1 at the amino acid level.

92 present in the sarcolemma, colocalized with NHE1 at the intercalated disc regions, increased NHE1 ph

93 resident plasma membrane isoforms including NHE1 (basolateral) and NHE2 (apical), recycling isoforms

94 Our data fulfill criteria for NHE1 being a bona fide Akt substrate, including direct p

95 with the structurally similar PI(4,5)P2 for NHE1 binding.

96 oforms of CHP1 were defective in stimulating NHE1 biosynthetic maturation.

97 Inactivation of NHE1 blocked IgE-induced macrophage production of inflam

98 ating cells with a ROK inhibitor, Y27632, or NHE1 blocker, S-(N-ethyl-N-isopropyl) amiloride, respect

99 OGD/REOX not only increased the V(max) for NHE1 but also shifted the K(m) toward decreased [H(+)](i

100 changes of hydrophobic mismatch can modulate NHE1 but do not underlie its volume sensitivity.

101 NHE1 (but not NHE3) is reversibly activated by cell shri

102 Ectopic NHE1, but not NHE3, expression rescued NHE1-null cells f

103 reased NGF-induced inhibition of basolateral NHE1 by 45%.

104 he plasma membrane sodium-hydrogen exchanger NHE1 by Akt increases exchanger activity (H(+) efflux).

105 Rapamycin-sensitive inhibition of NHE1 by NGF was associated with an increased level of ph

106 )-antiporter resembling the human antiporter NHE1, by electron crystallography of 2D crystals in a ra

107 ay and surface plasmon resonance assays, the NHE1 C terminus bound phospholipids with low affinity an

108 ein comprising amino acids 516 to 815 of the NHE1 carboxyl-terminal regulatory domain.

109 n was similarly defective in both htt(-) and nhe1(-) cells in a K(+)-based buffer, and the normal loc

110 witch mechanism to selectively stabilize the NHE1.CHP3 complex at the cell surface in a conformation

111 ulate fraction, which contained the cellular NHE1 complement; this effect was abolished by pretreatme

112 d competing LC-CoAs disrupted binding of the NHE1 cytosolic tail to PI(4,5)P2.

113 e normally quiescent Na(+)/H(+) exchanger-1 (NHE1) defends against PTC apoptosis, and is regulated by

114 in intracellular pH, nor is it attenuated in NHE1-deficient cells, indicating fibronectin expression

115 xchanger activity increased nearly 4-fold in Nhe1-deficient mice, despite only minimal or any change

116 Inhibition of NHE1 delayed BR after acute barrier perturbation.

117 ent PI(4,5)P(2) and PI(3,4,5)P(3) effects on NHE1-dependent Na(+)/H(+) exchange and apoptosis were co

118 hypothesize that apoptotic stress activates NHE1-dependent Na(+)/H(+) exchange, and NHE1-ERM interac

119 rotein-mediated translocation of PP2A(c) and NHE1 dephosphorylation.

120 with amiloride and NGF but does not act via NHE1, did not affect cellular F-actin content.

121 ibiting isoform 1 of sodium-proton exchange (NHE1), direct acidification was shown to be cytostatic r

122 LC-CoAs and the cytosolic domain of NHE1 directly interacted, with an affinity comparable to

123 Inhibition of NHE1 disrupts membrane blebbing and decreases changes in

124 ed in cells expressing ERM binding-deficient NHE1, dominant negative ezrin constructs, or ezrin mutan

125 ates NHE1-dependent Na(+)/H(+) exchange, and NHE1-ERM interaction is required for cell survival signa

126 have also been found to be key activators of NHE1 exchanger activity; however, the crosstalk between

127 hat affect phosphorylation; however, whether NHE1 exists in large multi-protein complexes is unknown.

128 , in breast cancer cells, PPARgamma inhibits NHE1 expression and the inflammatory response, and it fu

129 We found that in vivo epidermal NHE1 expression was upregulated within hours of barrier

130 SC barrier break also upregulates NHE1 expression, but this response seems to be mediated

131 e the effects of barrier break in regulating NHE1 expression, suggesting that SC alkalinization is th

132 nization is the major stimulus for increased NHE1 expression.

133 n, is linked to decreased Na+/H+ antiporter (NHE1) expression.

134 K1/2) play a role in stimulation of neuronal NHE1 following in vitro ischemia.

135 ic ablation or pharmacological inhibition of NHE1 following OGD/REOX.

136 egulation of Na(+)/H(+) exchanger isoform 1 (NHE1) following cerebral ischemia are not well understoo

137 We previously cloned NHE1 from Amphiuma tridactylum (AtNHE1) and Pleuronectes

138 Furthermore, these data suggest that NHE1 functions as a metabolic sensor for lipotoxicity.

139 d in vitro a glutathione S-transferase (GST)-NHE1 fusion protein comprising amino acids 516 to 815 of

140 say, purified PP2A(c) dephosphorylated a GST-NHE1 fusion protein containing aa 625-747 of the NHE1 re

141 PKBalpha-mediated phosphorylation of GST-NHE1 fusion proteins containing overlapping segments of

142 rylation analysis of mutated (Ser-->Ala) GST-NHE1 fusion proteins revealed that PKBalpha-mediated pho

143 in, tropomyosin, ICAM-4, GLUT4, Na/K-ATPase, NHE1, GPA, CD47, Duffy, and Kell were reduced.

144 al signaling cascade involving TGFalpha>PI3K>NHE1>pHi alkalization, which leads to a permissible envi

145 s and a similar relationship between Htt and Nhe1 have not been reported for mammalian neurons and de

146 ary flow were significantly less impaired in Nhe1-/- hearts relative to wild-type hearts, and release

147 NHE1(+/+) mice treated with HOE 642 or NHE1 heterozygous mice exhibited a approximately 33% dec

148 us to the amiloride- and HOE-sensitive human NHE1 (hNHE1), AtNHE1 is insensitive to HOE-type and PaNH

149 +)/H(+) exchange in atRBCs is mediated by an NHE1 homolog (atNHE1) that is 79% identical to human NHE

150 nging the extracellular loops (ECL) of human NHE1 (huNHE1) and chNHE1 and by ECL replacement with a h

151 alated discs are commonly located, and where NHE1 immunostaining is prominent.

152 ced apoptosis, indicating the involvement of NHE1 in apoptosis.

153 y may play in the disrupted functionality of NHE1 in breast cancer metastasis.

154 rovide direct genetic evidence of a role for NHE1 in Ca2+ homeostasis and important insight into how

155 ally, our results obtained by expressing rat NHE1 in Caenorhabditis elegans suggest that a conserved

156 The role of NHE1 in cardiac injury has prompted interest in the deve

157 NHE1 in Chinese hamster ovary fibroblasts (but not NHE3

158 (JH+) are equivalent to currents >20 pA for NHE1 in Chinese hamster ovary fibroblasts, >200 pA for N

159 inese hamster ovary fibroblasts, >200 pA for NHE1 in guinea pig ventricular myocytes, and 5-10 pA for

160 mutant no longer showed elevated binding to NHE1 in the presence of Ca(2+) when assessed using in vi

161 is known about the pathophysiologic role of NHE1 in tumor progression with regard to ion flux, the r

162 d significant co-localization of PP2A(c) and NHE1, in intercalated disc regions.

163 I(4,5)P2], but pathophysiologic triggers for NHE1 inactivation are unknown.

164 edict that other functions shared by Akt and NHE1, including cell growth and survival, might be regul

165 ll blebbing; cells become swollen because of NHE1 induced intracellular sodium accumulation.

166 Our study found that NHE1 induced sodium influx is a driving force for membra

167 vation of RSK1, which via phosphorylation of NHE1 induces cardiomyocyte apoptosis.

168 rug-drug interaction potential starting from NHE1 inhibitor sabiporide.

169 covery was eliminated in the presence of the NHE1 inhibitor zoniporide.

170 ults were recapitulated by treatment with an NHE1 inhibitor, 5-(N,N-hexamethylene) amiloride (HMA).

171 re also inhibited by the Na+-H+ exchanger-1 (NHE1) inhibitor dimethylamiloride, but not by the NHE3 i

172 has prompted interest in the development of NHE1 inhibitors for the treatment of heart failure.

173 affinity comparable to that of the PI(4,5)P2-NHE1 interaction, and competing LC-CoAs disrupted bindin

174 addition to mediating Na(+)/H(+) transport, NHE1 interacts with ezrin/radixin/moesin (ERM), which te

175 NHE1 interacts with multiple regulatory proteins that af

176 Our data suggest that NHE1 is a novel PKB substrate and that its PKB-mediated

177 cs and transverse tubules (t-tubules), while NHE1 is absent from t-tubules.

178 In human melanoma, the Na(+)/H(+) exchanger NHE1 is an important modifier of the tumour nanoenvironm

179 NHE1 is constitutively active in a neoplastic microenvir

180 Expressed in AP-1 cells, however, NHE1 is insensitive to these agents but remains sensitiv

181 expressing NHE1-KRA2 because scaffolding by NHE1 is mislocalized.

182 t NHE1 that lacks H(+) efflux, and wild-type NHE1 is not activated in fibroblasts expressing mutation

183 H(+) efflux by NHE1 is not necessary for release of Cdc42-guanosine dip

184 Our objectives were to determine whether NHE1 is phosphorylated by protein kinase B (PKB), identi

185 These data suggest that the keratinocyte NHE1 is regulated by extracellular pH.

186 In response to apoptotic stress, NHE1 is stimulated by PI(4,5)P(2), which leads to PI 3-k

187 The membrane domain of NHE1 is sufficient for ion exchange.

188 The Na(+)/H(+)Exchanger isoform 1 (NHE1) is a highly versatile, broadly distributed and pre

189 Na+/H+ exchanger isoform 1 (NHE1) is a major acid extrusion mechanism after intracel

190 Sodium-hydrogen exchanger isoform 1 (NHE1) is a ubiquitously expressed transmembrane ion chan

191 previously shown that the Na+/H+ antiporter (NHE1) is an essential endogenous pathway responsible for

192 NHE3 (but not NHE1) is reversibly activated by phosphatidylinositol 3,

193 n that regulates the Na(+)/H(+) exchanger 1 (NHE1), is highly expressed in various mouse tissues such

194 We conclude that functional NHE2, but not NHE1, is essential for mouse gastric epithelial restitut

195 ulates the plasmalemmal Na(+)/H(+) exchanger NHE1 isoform by enhancing its rate of oligosaccharide ma

196 Molecular manipulations of the prototypical NHE1 isoform have implicated several predicted membrane-

197 ogen exchanger in the heart and vasculature (NHE1 isoform) and the kidneys (NHE3 isoform) may serve a

198 However, aside from the ubiquitous NHE1 isoform, their relative contributions are poorly un

199 tion of phosphorylation of p90(RSK), a known NHE1 kinase.

200 in) intracellular acidosis activated several NHE1 kinases in NRVM, in an in-gel kinase assay using as

201 These changes in NHE1 kinetics were absent when MAPK/ERK kinase (MEK) was

202 duction is nearly absent in cells expressing NHE1-KRA2 because scaffolding by NHE1 is mislocalized.

203 d TGF-beta activation, and they suggest that NHE1-KRA2 can be used for obtaining a mechanistic unders

204 Our data indicate that scaffolding by NHE1-KRA2 dominantly suppresses fibronectin synthesis an

205 ane protrusions or lamellipodia but a mutant NHE1-KRA2 lacking binding sites for PI(4,5)P2 and the ER

206 Decreased NHE1 levels lead to increased SC pH, which results in de

207 In fibroblasts, wild-type NHE1 localizes to the distal margin of membrane protrusi

208 and activate an Na(+)/H(+) exchanger type-1 (NHE1), may underlie tyrosine kinase inhibitor resistance

209 plasma membrane lipids, we hypothesized that NHE1-mediated cell survival is dynamically regulated by

210 ronal axons and that selective disruption of NHE1-mediated proton homeostasis in axons can lead to de

211 NHE1(+/+) mice treated with HOE 642 or NHE1 heterozygous

212 usion induced 84.8 +/- 8.0 mm3 infarction in NHE1(+/+) mice.

213 Indeed, the parotid glands of Nhe1(-/-) mice expressed higher levels of carbonic anhyd

214 ory changes in the exocrine parotid gland of Nhe1(-/-) mice that together attenuate the severity of i

215 94) slows restitution 72-83% in wild-type or NHE1(-/-) mice.

216 complexes in the parotid plasma membranes of Nhe1(-/-) mice.

217 ding limb (MTAL), inhibiting the basolateral NHE1 Na(+)/H(+) exchanger with amiloride or nerve growth

218 k ascending limb, inhibiting the basolateral NHE1 Na(+)/H(+) exchanger with nerve growth factor (NGF)

219 cesses opposed by the ubiquitously expressed NHE1 Na(+)/H(+) exchanger.

220 ial for the ROCK1-induced phosphorylation of NHE1 (Na(+)/H(+)exchanger 1), which is involved in the r

221 vation of RSK and interaction of 14-3-3 with NHE1, necessary for agonist-stimulated NHE1 activity, we

222 In NHE1(+/+) neurons, OGD caused a twofold increase in [Na+

223 EOX evoked a 1.5-fold increase in [Ca2+]i in NHE1(+/+) neurons, which was abolished by inhibition of

224 ding AE3, AQP4, AQP5, CFTR, ClC2gamma, KCC1, NHE1, NKAalpha1, NKAbeta1, NKAbeta2, NKAbeta3, and NKCC1

225 topic NHE1, but not NHE3, expression rescued NHE1-null cells from apoptosis induced by staurosporine

226 ase in Cl(-)/HCO(3)(-) exchanger activity in Nhe1-null mice suggesting that increased anion exchange

227 -kinase, and Akt inhibition in wild-type and NHE1-null PTCs.

228 ed that PKBalpha-mediated phosphorylation of NHE1 occurred principally at Ser648.

229 s 364-415) of a cysteine-less variant of rat NHE1 on its kinetic and pharmacological properties.

230 Genetic ablation of NHE1 or HOE 642 treatment had no effects on the OGD-medi

231 Despite this evidence, a specific role for NHE1 or pHi in cell cycle progression remains undetermin

232 which was abolished by inhibition of either NHE1 or reverse-mode operation of Na+/Ca2+ exchange.

233 ed in mammalian cells lacking H(+) efflux by NHE1, our current data suggest that full-length Aip1 fac

234 Acidification and NHE1 overexpression both reduce cell-cell adhesion stren

235 are strongly impaired under acidification or NHE1 overexpression.

236 In addition to Na-H exchanger isoform-1 (NHE1), pHi acidification is regulated by a HCO3-dependen

237 mation about the pathogenetic role of a TESC-NHE1-pHi axis in mediating sorafenib resistance in AML.

238 NHE1-phosphoinositide binding was enhanced by acidic pH,

239 y, the authors reported ERK1/2, p90(RSK) and NHE1 phosphorylation after 2 hours.

240 enuate the phenylephrine-induced increase in NHE1 phosphorylation and activity was lost in the presen

241 HA/CD44-activated Rho kinase (ROK) mediates NHE1 phosphorylation and activity, and (ii) inhibition o

242 NHE1 phosphorylation contributes to Na(+)/H(+) exchange

243 We examined the role of NHE1 phosphorylation during activation by OCS, using an

244 is the first reported evidence of increased NHE1 phosphorylation during OCS in any vertebrate cell t

245 tyladenosine (CPA) inhibited the increase in NHE1 phosphorylation induced by the alpha(1)-adrenorecep

246 at the intercalated disc regions, increased NHE1 phosphorylation, and reduced NHE1 activity followin

247 N-isopropyl) amiloride, respectively) blocks NHE1 phosphorylation/Na(+)-H(+) exchange activity, reduc

248 ntributes to tubular atrophy by severing the NHE1-PI(4,5)P2 interaction, thereby lowering the apoptot

249 es indicate that Na+-H+ exchanger isoform 1 (NHE1) plays a central role in myocardial ischemia-reperf

250 icate that the (Na+)-H+ exchanger isoform 1 (NHE1) plays a critical role in myocardial ischemia and r

251 myocytes, suggesting that, by guarding pHi, NHE1 preferentially protects gap junctional communicatio

252 uggesting a mechanism for how H(+) efflux by NHE1 promotes Cdc42 activity to generate a positive feed

253 We conclude that NHE1 promotes cell survival by dual mechanisms: by defen

254 apical membranes of surface epithelium, and NHE1 protein amount or localization is unchanged.

255 cariporide (HOE 642) or genetic ablation of NHE1 reduced OGD-induced cell death by approximately 40-

256 to PaNHE1, and we thereby identified several NHE1 regions involved in inhibitor interaction.

257 to apical and lateral PTC domains, increased NHE1-regulated Na(+)/H(+) exchange, and blunted apoptosi

258 Apoptotic stimuli induced NHE1-regulated Na(+)/H(+) transport, as demonstrated by

259 These results indicate that basolateral NHE1 regulates apical NHE3 and HCO3- absorption in the M

260 Although NHE1 regulates intracellular pH homeostasis, fibronectin

261 The Na+/H+ exchanger NHE1 regulates proximal tubule cell survival through int

262 fusion protein containing aa 625-747 of the NHE1 regulatory domain, which had been pre-phosphorylate

263 kely via RSK-mediated phosphorylation of the NHE1 regulatory domain.

264 tathione S-transferase fusion protein of the NHE1 regulatory domain.

265 hieved via kinase-mediated modulation of the NHE1 regulatory domain.

266 th factor in fibroblasts expressing a mutant NHE1-S648A.

267 dium are inhibited in fibroblasts expressing NHE1-S648A.

268 of cardiac NHE1 activity by phosphorylating NHE1 serine 703 and a new pathological mediator of I/R i

269 elicited responses in cells transfected with NHE1 siRNA but not in those transfected with ENaCalpha o

270 fter TGFalpha stimulation with 10 muM of the NHE1-specific inhibitor N-Methyl-N-isobutyl Amiloride (M

271 S6 kinase (RSK) phosphorylated serine 703 of NHE1, stimulating 14-3-3 binding and NHE1 activity.

272 uniform pHi recovery from acidosis, whereas NHE1 stimulation induces pHi non-uniformity during recov

273 olding by the plasma membrane Na-H exchanger NHE1 suppresses fibronectin expression, secretion, and a

274 at CHP1 assists in the full glycosylation of NHE1 that is necessary for the membrane localization of

275 activated in fibroblasts expressing a mutant NHE1 that lacks H(+) efflux, and wild-type NHE1 is not a

276 -life and near maximal transport velocity of NHE1 to a similar extent.

277 th ezrin/radixin/moesin (ERM), which tethers NHE1 to cortical actin cytoskeleton to regulate cell sha

278 phosphorylation mediates the recruitment of NHE1 to the invadopodium compartment, where it locally i

279 e biosynthetic processing and trafficking of NHE1 to the plasma membrane nor did it affect the H(+) s

280 sults reveal an on-off switch model, whereby NHE1 toggles between weak interactions with PI(4,5)P(2)

281 diffusion distances, particularly to surface NHE1 transporters mediating high membrane flux.

282 We have studied two mammalian isoforms, NHE1 (ubiquitous) and NHE3 (epithelial-specific), by mea

283 In the present study, expression of NHE1 was detected in cultured mouse cortical neurons.

284 based buffer, and the normal localization of Nhe1 was disrupted in the htt(-) mutant.

285 At 10 min REOX, phosphorylated NHE1 was increased with a concurrent elevation of phosph

286 We next asked whether NHE1 was regulated by barrier status per se, or by the S

287 NHE1 was upregulated by alkalinizing SC pH, whereas this

288 ent of barrier status, by demonstrating that NHE1 was upregulated in cultured keratinocytes exposed t

289 barrier perturbations, we asked whether the NHE1 was, in turn, regulated by changes in barrier statu

290 Na+/H+-exchanger isoform 1 (NHE1) was present on hair-cell soma membranes and was li

291 lcineurin Abeta and the Na(+)/H(+) exchanger NHE1 were observed in VSMCs.

292 ity, and H(+) efflux by Na-H(+) exchanger 1 (NHE1), which is necessary at the front of migrating cell

293 (NHE) activity is mediated by NHE isoform 1 (NHE1), which is subject to regulation by protein kinases

294 contrast, when sodium/hydrogen antiporter-1 (NHE1), which predominantly acidifies membrane domains at

295 biquitous plasma membrane Na+/H+exchanger-1 (NHE1), which uses a highly conserved process to transfer

296 two endogenous mechanisms, namely, sPLA2 and NHE1, which are known to be important for acidification

297 mma activates expression of the pH regulator NHE1, which is associated with tumor progression.

298 drogen exchanger 1 (NHE1), and inhibition of NHE1 with 5'-N-ethyl-N-isopropyl-amiloride blocks H/R in

299 Inhibition of NHE1 with the potent inhibitor cariporide (HOE 642) or g

300 tion of the ubiquitous Na(+)/H(+) exchanger, NHE1, with its commonly used inhibitors, amiloride- and