ライフサイエンスコーパス: Na K ATPase

1 low molar stoichiometry (1:15-30 caveolin 1/Na,K-ATPase).

2 ) was found to be in direct interaction with Na,K-ATPase.

3 display selectivity of interaction with the Na,K-ATPase.

4 ell surface substantially faster than is the Na,K-ATPase.

5 ls express mainly the alpha2beta3 isoform of Na,K-ATPase.

6 aC) and is extruded into the interstitium by Na,K-ATPase.

7 nhibiting p38 kinase-mediated endocytosis of Na,K-ATPase.

8 proteins with the size and complexity of the Na,K-ATPase.

9 or phosphatidylethanolamine destabilizes the Na,K-ATPase.

10 K0.5K(+) and lower K0.5Na(+) for activating Na,K-ATPase.

11 s tissue-specific regulatory subunits of the Na,K-ATPase.

12 crucial for addressing physiological role of Na/K-ATPase.

13 th pumping and signaling functions of alpha1 Na/K-ATPase.

14 lized/inactivated Na(+)-H(+) exchanger-3 and Na(+)/K(+)ATPase.

15 a(+) transporters Na(+)-H(+)-exchanger-3 and Na(+)/K(+)ATPase.

16 eased membrane E-cadherin, beta-catenin, and Na(+)K(+) ATPase.

17 ct as part of the catalytic mechanism of the Na(+),K(+)-ATPase.

18 nnel is a major electrogenic reaction of the Na(+),K(+)-ATPase.

19 d stimulation of apical ENaC and basolateral Na(+),K(+)-ATPase.

20 id (+)-cassaine, a nonsteroidal inhibitor of Na(+)-K(+)-ATPase.

21 nd regulation, and Na(+)/Ca(2+) exchange and Na(+)/K(+) ATPase.

22 etween the cardiac glycoside bufalin and the Na(+)/K(+)-ATPase.

23 ing residues in E1P and E2P conformations of Na(+)/K(+)-ATPase.

24 olved in cellular Na(+) homeostasis, such as Na(+)/K(+)-ATPase.

25 ations to the Na(+) driving force created by Na(+)/K(+)-ATPase.

26 lycoside that inhibits the ubiquitous enzyme Na(+)/K(+)-ATPase.

27 oplasmic reticulum Ca(2+)-ATPase (SERCA) and Na(+), K(+)-ATPase.

28 nt for this exchange activity is provided by Na,K-ATPase, a hetero-oligomer consisting of a catalytic

29 in (10 mumol l(-1)), a specific inhibitor of Na/K-ATPase, abolished dopamine-induced salivary secreti

30 urements of the current, Ip, produced by the Na(+),K(+)-ATPase across the plasma membrane of rabbit c

31 However, KIR channels, NO, PGs and Na(+) /K(+) -ATPase activity are not obligatory to obser

32 le would be independent of KIR , NO, PGs and Na(+) /K(+) -ATPase activity.

33 ediated phosphorylation of Ser-938 regulates Na(+),K(+)-ATPase activity in vivo Ser-938 is located in

34 entry per se induce a coordinated change in Na(+),K(+)-ATPase activity through the signaling of prot

35 or functions such as phagocytosis, motility, Na(+)/K(+)-ATPase activity, and metastatic activity.

36 >sarcoplasm-->ECF that ultimately depends on Na(+)/K(+)-ATPase activity.

37 acological inhibition of AKT restored normal Na+/K+-ATPase activity in primary cultured lens cells an

38 sport through an AKT-dependent modulation of Na+/K+-ATPase activity, and provide a new animal model t

39 acellular sodium concentrations, and reduced Na+/K+-ATPase activity.

40 Structural selectivity for stimulation of Na,K-ATPase activity and destabilization by neutral phos

41 gests a possible mechanism of stimulation of Na,K-ATPase activity by the neutral phospholipid.

42 Furthermore, Na,K-ATPase activity depends on phosphatidylserine (PS)

43 This paper describes stimulation of Na,K-ATPase activity of the purified human alpha1beta1 o

44 Binding of FXYD1 reduces Na,K-ATPase activity, and phosphorylation at Ser-68 or S

45 op destabilize the protein but do not affect Na,K-ATPase activity, whereas mutations in transmembrane

46 hatidylethanolamine (PE), known to stimulate Na,K-ATPase activity.

47 We traced the regulation of Na/K ATPase activity back to either TRPV4, which sensed

48 harmacological agent digoxin, which inhibits Na/K ATPase activity, protected motor neurons from mutan

49 Na/K-ATPase activity was measured as Pi from cellular ho

50 The alpha1 isoform of Na(+)/K(+)-ATPase acts as a direct regulatory partner of

51 f sodium potassium adenosine triphosphatase (Na/K-ATPase), acts as a receptor and an amplifier for re

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

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

54 ings define chronic activation of the alpha2-Na/K ATPase/alpha-adducin complex as a critical glial ce

55 tic mutations in either ATP1A1, encoding the Na(+)/K(+) ATPase alpha1 subunit, or CACNA1D, encoding C

56 Increasing Na,K-ATPase alpha1 content cannot fully compensate for t

57 h most other cells, which express mainly the Na,K-ATPase alpha1 isoform, but its functional significa

58 ocalization and interaction of LMO7b and the Na,K-ATPase alpha1 subunit at the plasma membrane, which

59 defective in Src regulation, we transfected Na/K-ATPase alpha1 knockdown PY-17 cells with expression

60 icate that carbonylation modification of the Na/K-ATPase alpha1 subunit is involved in a feed-forward

61 acid residues in the actuator domain of the Na/K-ATPase alpha1 subunit.

62 blocking Na(+) current, suggesting that the Na(+)/K(+)-ATPase-alpha1 isoform is specifically involve

63 mentary approach, we utilized purified human Na,K-ATPase (alpha1beta1 and alpha2beta1) reconstituted

64 4 PC can bind specifically to purified human Na,K-ATPase (alpha1beta1).

65 arkinsonism (RDP) are caused by mutations of Na(+),K(+)-ATPase alpha2 and alpha3 isoforms, expressed

66 Indeed, Atp1a2(+/-) (encoding Na(+)-K(+) ATPase alpha2) mice, which have reduced Na(+)

67 The Na,K-ATPase alpha2 subunit plays a key role in cardiac m

68 Na(+)/K(+)-ATPase alpha3 does not reside within the core

69 ssociated behavioral characterization of the Na(+)/K(+)-ATPase alpha3 Myshkin (Myk/+) mouse model of

70 Mutations in the Na(+)/K(+)-ATPase alpha3 subunit gene (ATP1A3) cause rap

71 It relies on the Na(+)/K(+) ATPase (also referred to as the Na pump), whi

72 In the related ion pumps Na(+),K(+)-ATPase and Ca(2+)-ATPase, M4 moves during the

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

74 nd-site mutation is unique in the history of Na(+),K(+)-ATPase and points to new possibilities for tr

75 ogical mechanism in which miR-192 suppresses Na(+)/K(+)-ATPase and contributes to renal handling of f

76 rdly rectifying potassium (KIR) channels and Na(+)/K(+)-ATPase and is largely independent of the comb

77 teins, FXYD5 specifically interacts with the Na,K-ATPase and alters its kinetics by increasing Vmax H

78 In most polarized epithelial cells, both the Na,K-ATPase and E-cadherin are localized to the basolate

79 the itineraries pursued by newly synthesized Na,K-ATPase and E-cadherin in polarized MDCK epithelial

80 a direct interaction between purified human Na,K-ATPase and human caveolin was obtained, albeit with

81 is driven mostly by the alveolar epithelial Na,K-ATPase and is crucial for survival of patients with

82 ells that express the alpha1beta1 isoform of Na,K-ATPase and nonpigmented epithelial cells that expre

83 no stable interactions were detected between Na,K-ATPase and purified Src kinase.

84 s postulates direct interactions between the Na,K-ATPase and Src kinase (non-receptor tyrosine kinase

85 We found that a protein complex of alpha2-Na/K ATPase and alpha-adducin was enriched in astrocytes

86 Notably, alpha2-Na/K ATPase and alpha-adducin were upregulated in spinal

87 f the FXYD family (FXYD1-12), which regulate Na(+) ,K(+) -ATPase, and phospholamban, sarcolipin, myor

88 proteins such as FXYDs, which interact with Na(+) ,K(+) -ATPase, and the micropeptides that interact

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

90 in derivative that displaces 3H-ouabain from Na+, K+ -ATPase, and attenuates some forms of hypertensi

91 Na(+)/K(+)-ATPases are transmembrane ion pumps that main

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

93 In this study, we investigated Na/K-ATPase as an important component of the secretory p

94 ification of ATP1A1, the alpha1-chain of the Na/K-ATPase, as a factor required for efficient secretio

95 ch facilitates the interaction of LMO7b with Na,K-ATPase at the plasma membrane promoting the endocyt

96 Here, we report that targeting the Na(+)/K(+)-ATPase (ATP1A1) is synthetic lethal with STK1

97 d its predicted target the beta-1 subunit of Na(+)/K(+)-ATPase (Atp1b1), an enzyme providing the driv

98 eral localized protein, the alpha subunit of Na(+)-K(+) ATPase (ATPalpha).

99 channels alone or combined with NO, PGs and Na(+) /K(+) -ATPase, attenuated ATP-mediated vasodilatat

100 dly rectifying potassium (KIR ) channels and Na(+) /K(+) -ATPase (BaCl2 + ouabain).

101 ulations of newly synthesized E-cadherin and Na,K-ATPase become separated from one another within the

102 similar to multiply spin-labeled membranous Na,K-ATPase below 200 K.

103 tions were found for chicken BetaM and human Na,K-ATPase beta1, beta2 and beta3 isoforms, indicating

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

105 is confirmed, the lack of direct Src kinase/Na,K-ATPase binding requires reassessment of the mechani

106 The Na(+),K(+)-ATPase binds Na(+) at three transport sites d

107 e steroid, marinobufagenin, is an endogenous Na/K-ATPase bufadienolide inhibitor that is synthesized

108 ta-intercalated cells was independent of the Na(+)/K(+)-ATPase but critically relied on the presence

109 d the basolateral cell surface expression of Na,K-ATPase by inhibiting p38 kinase-mediated endocytosi

110 ecretion of TRAIL that causes endocytosis of Na,K-ATPase by the alveolar epithelium.

111 Disruption of the Na/K-ATPase.c-Src signaling complex attenuated ouabain-s

112 ported that missense mutations affecting the Na(+)/K(+) ATPase can elicit ionic leakage.

113 e sodium potassium adenosine triphosphatase (Na/K-ATPase) can effect the amplification of reactive ox

114 1A3, the gene encoding the alpha3 subunit of Na(+)/K(+)-ATPase, cause both rapid-onset dystonia parki

115 d within caveolae by a complex consisting of Na,K-ATPase, caveolin, and Src kinase.

116 ximately 30%, inhibition of KIR channels and Na(+) /K(+) -ATPase, combined with inhibition of NO and

117 to the very slow dissociation of the ouabain.Na(+)/K(+)-ATPase complex.

118 embrane potential-generating function of the Na/K-ATPase complex but rather a so far unidentified rol

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

120 h have a considerably lower affinity for the Na,K-ATPase, confirm these results.

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

122 rmonal stimulus, cross-talk between ENaC and Na,K-ATPase coordinates Na(+) transport across apical an

123 ionization state of coordinating residues in Na,K-ATPase could contribute to altering face-specific i

124 ac glycoside neriifolin, an inhibitor of the Na(+), K(+)-ATPase, delays the onset and reduces the cli

125 ting motifs of a protein, as are evident for Na,K-ATPase, demonstrate a remarkable capacity to adapt

126 < PK(s) and N(t) < N(s) [P, permeability; N, Na(+)/K(+)-ATPase density; (t), t-system membrane; (s),

127 secretion that were again CFTR-, NKCC-, and Na(+)-K(+)-ATPase-dependent.

128 The charge-transporting activity of the Na(+),K(+)-ATPase depends on its surrounding electric fi

129 and beta3-chains (ATP1B1 and ATP1B3) of the Na/K-ATPase did not affect FGF2 secretion, suggesting th

130 It has been an enigma how Na,K-ATPase discriminates between Na(+) and K(+), despit

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

132 required for high CO2 (hypercapnia)-induced Na,K-ATPase endocytosis in alveolar epithelial cells.

133 phosphorylation and the hypercapnia-induced Na,K-ATPase endocytosis.

134 a single-transmembrane protein regulator of Na,K-ATPase, expressed strongly in heart, skeletal muscl

135 ntry invariably led to increased basolateral Na,K-ATPase expression and activity.

136 re investigated whether IAV infection alters Na,K-ATPase expression and function in alveolar epitheli

137 This reduction of Na,K-ATPase expression decreases alveolar fluid clearanc

138 doneurial location, given that the axolemmal Na(+)-K(+)-ATPase extrudes these ions into the periaxona

139 Na(+),K(+)-ATPase frequently assembles with other membra

140 substitution of Arg-1005 was compatible with Na(+),K(+)-ATPase function, and the Na(+) affinity of th

141 that leads to decreased alveolar epithelial Na,K-ATPase function and plasma membrane abundance and i

142 We show a tipping point of Na(+)/K(+)-ATPase functioning, where below cell volume r

143 f a small, single-span regulatory subunit of Na,K-ATPase, FXYD2, alters glucose control.

144 Heterozygous disruption of the alpha2-Na/K ATPase gene suppressed degeneration in vivo and inc

145 ts of 2 of the 12 amino acids comprising the Na(+)/K(+)-ATPase H1-H2 extracellular domain that consti

146 ctively penetrate the cornea and inhibit the Na,K-ATPase, hence reducing aqueous humor production.

147 interactions utilizing purified recombinant Na,K-ATPase (human alpha1beta1FXYD1 or porcine alpha1D36

148 Moreover, induced Na,K-ATPase improved alveolar fluid clearance (AFC) in I

149 ays independent of KIR channels, NO, PGs and Na(+) /K(+) -ATPase in humans, consistent with a role fo

150 renal outer medullary potassium channel, and Na(+), K(+)-ATPase in the CD, which probably contributed

151 l structure of the phosphorylated pig kidney Na(+),K(+)-ATPase in complex with the CTS representative

152 We report crystal structures of the Na(+),K(+)-ATPase in the E2P form in complex with bufali

153 m channel (ENaC) and basolaterally localized Na(+)-K(+)-ATPase in type II alveolar epithelial cells.

154 growth in metabolic cost and activity of the Na(+)-K(+)-ATPase in white skeletal muscle from crustace

155 is thought to be exclusively mediated by the Na(+)/K(+)-ATPase in animal cells.

156 n which GlyT2.PMCA2-3.NCX complex would help Na(+)/K(+)-ATPase in controlling local Na(+) increases d

157 ro and animal model systems, and the role of Na(+)/K(+)-ATPases in the brain.

158 plasma membrane promoting the endocytosis of Na,K-ATPase in alveolar epithelial cells.

159 the energy depletion-induced accumulation of Na,K-ATPase in intracellular compartments.

160 e membrane transport of Rb and K ions by the Na,K-ATPase in mouse skeletal muscles and human red bloo

161 Much evidence points to a role of Na,K-ATPase in ouabain-dependent signal transduction.

162 IAV infection reduced Na,K-ATPase in the plasma membrane of human and murine A

163 eference to the recent crystal structures of Na,K-ATPase in the unbound and ouabain-bound states.

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

165 also inhibits an ion resorptive function of Na/K-ATPase in the type I acini.

166 dopamine-independent resorptive function of Na/K-ATPase in type I acini located in the proximal end

167 endent primary saliva formation, mediated by Na/K-ATPase in type III and type II acini, is followed b

168 Previous studies proposed a role for the Na/K-ATPase in unconventional secretion of fibroblast gr

169 ecular changes to the sodium-potassium-pump (Na(+)/K(+)-ATPase) in insects, amphibians, reptiles, and

170 The sodium pump (Na,K-ATPase) in animal cells is vital for actively maint

171 study the pumping and signaling functions of Na/K-ATPase independently in live cells.

172 occurring on the external side of functional Na+/K+-ATPases induced by the binding of ouabain.

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

174 nternalization of Na(+)-H(+) exchanger-3 and Na(+)/K(+)ATPase, inducing natriuresis in a bradykinin-n

175 aled that cardiac glycosides, antagonists of Na(+),K(+)-ATPase, inhibit autotic cell death in vitro a

176 ntrol (saline), and combined KIR channel and Na(+) /K(+) -ATPase inhibition.

177 constriction during combined KIR channel and Na(+) /K(+) -ATPase inhibition.

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

179 NCX1 TG mice, similar to treatment with the Na(+)-K(+) ATPase inhibitor digoxin.

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

181 In principle, a Na,K-ATPase inhibitor with selectivity for alpha2 could

182 In principle, a Na,K-ATPase inhibitor with selectivity for alpha2beta3 t

183 its activity, whereas ouabain, the specific Na,K-ATPase inhibitor, binds and stabilizes the E2 confo

184 Therefore, the endogenous steroidal Na/K-ATPase inhibitor, marinobufagenin, is synthesized i

185 rred in axons treated with sodium channel or Na(+)-K(+)-ATPase inhibitors.

186 Marinobufagenin binding to Na/K-ATPase initiates profibrotic cell signaling, and he

187 Thus, overall, whereas a direct caveolin 1/Na,K-ATPase interaction is confirmed, the lack of direct

188 Hypoxia causes a reduction in levels of the Na(+)/K(+) ATPase ion transporter in both cultured prima

189 A reduction of Na(+)/K(+) ATPase ion transporter levels likely contribu

190 These results suggest that hypoxia and the Na(+)/K(+) ATPase ion transporter may be a novel mechani

191 e properties as well as ion channels and the Na/K-ATPase ion pump.

192 Signaling via the ouabain/Na,K-ATPase/IP3R/NF-kappaB pathway increases expression

193 The Na(+),K(+)-ATPase is a plasma membrane ion transporter o

194 is concluded that the Na(+) affinity of the Na(+),K(+)-ATPase is an important determinant of [Na(+)]

195 The Na(+),K(+)-ATPase is essential for ionic homeostasis in

196 eported that the subcellular distribution of Na(+),K(+)-ATPase is modulated by direct binding to Akt

197 the use of the energy of ATP hydrolysis, the Na+/K+-ATPase is able to transport across the cell membr

198 e-examination of electron densities of shark Na,K-ATPase is consistent with two bound phospholipids l

199 n of spin-labeled lipid chains in membranous Na,K-ATPase is investigated by spin-echo electron parama

200 determined that the IAV-induced reduction of Na,K-ATPase is mediated by a host signaling pathway that

201 Na,K-ATPase is proposed to bind Src kinase and inhibit i

202 The Na,K-ATPase is specifically inhibited by cardiotonic ste

203 The affinity of ionized fatty acids for the Na,K-ATPase is used to determine the transmembrane profi

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

205 ined inhibition of NO, PGs, KIR channels and Na(+) /K(+) -ATPase (l-NMMA + ketorolac + BaCl2 + ouabai

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

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

208 Na/K-ATPase-regulated signaling cascades and Na/K-ATPase localization.

209 extruded into the interstitial space by the Na(+),K(+)-ATPase located along the basolateral membrane

210 The Na(+),K(+)-ATPase maintains electrochemical gradients fo

211 er, the new findings suggest that the alpha1 Na/K-ATPase may be a key player in dynamic regulation of

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

213 In both native Na,K-ATPase membranes from shark salt gland and bilayers

214 egion in the range n = 6 to 10 is found with Na,K-ATPase membranes.

215 ing purified enzyme we found that the alpha1 Na/K-ATPase might interact with and regulate Src activit

216 a conformational change of the ouabain-bound Na(+)/K(+)-ATPase molecule or more generally by the disr

217 inferred that a small fraction of the renal Na,K-ATPase molecules is in a approximately 1:1 complex

218 The activity of ENaC and Na,K-ATPase must be highly coordinated to accommodate va

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

220 Two Na(+),K(+)-ATPase mutations, extending the C terminus by

221 treatment of neurological patients carrying Na(+),K(+)-ATPase mutations.

222 owing to their potent inhibition of cardiac Na(+), K(+)-ATPase (NKA).

223 The Na(+),K(+)-ATPase (NKA or Na/K pump) hydrolyzes one ATP

224 The Na(+)/K(+) ATPase (NKA) is an essential membrane protein

225 The Na(+)/K(+) ATPase (NKA) plays a critical role in maintai

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

227 In the context of Na(+)/K(+)-ATPase (NKA) regulation, pSer-68-PLM is depho

228 s on cardiac Na(+)/Ca(2+) exchange (NCX) and Na(+)/K(+)-ATPase (NKA).

229 Low Ko reduced Na+,K+-ATPase (NKA) currents, increased cytosolic Na+ co

230 ochemical gradient actively generated by the Na+/K+-ATPase (NKA).

231 c cells express more than one isoform of the Na, K-ATPase (NKA), the heteromeric enzyme that creates

232 driven by the sodium gradient implemented by Na(+)/K(+)-ATPases (NKAs) and the alpha2 subunit of NKA

233 m a basal level to 32.5% of the housekeeping Na(+)/K(+) ATPase on the cell surface, thereby providing

234 Knockdown of alpha2-Na/K ATPase or alpha-adducin in mutant SOD1 astrocytes p

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

236 trafficking of most proteins, including the Na,K-ATPase, out of the trans-Golgi network.

237 Attenuation of Na/K-ATPase oxidant amplification may be a potential str

238 tenuation of oxidant stress by antagonism of Na/K-ATPase oxidant amplification might ameliorate exper

239 Both inhibition of Na/K-ATPase oxidant amplification with pNaKtide and indu

240 The alpha1 Na/K-ATPase possesses both pumping and signaling functio

241 lizes/inactivates Na(+)-H(+)-exchanger-3 and Na(+)/K(+)ATPase, prevents Na(+) retention resulting in

242 The Na(+),K(+)-ATPase pump constitutes a molecular receptor

243 factors, including the neuron and astrocyte Na(+)-K(+) ATPase pump strengths.

244 We observed that the Na(+)/K(+)-ATPase pump (NKA) was less abundant in the ba

245 pithelial sodium channel and the basolateral Na(+)/K(+)ATPase pump.

246 n in atp1b1a, encoding the beta subunit of a Na,K-ATPase pump, causes edema and epidermal malignancy.

247 identified an influence of retinoschisin on Na/K-ATPase-regulated signaling cascades and Na/K-ATPase

248 nsport and the concomitant activation of the Na(+)/K(+)-ATPase represent a substantial energetic dema

249 The Na(+)/K(+)-ATPase restores sodium (Na(+)) and potassium

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

251 Immunoreactivity for Na/K-ATPase revealed basal infolding of lamellate cells

252 The Na(+)/K(+)-ATPase role was investigated using patch-clam

253 llectively, this study demonstrates that the Na/K-ATPase/ROS amplification loop contributes significa

254 h binds from the extracellular medium to the Na(+),K(+)-ATPase's transport sites in competition with

255 on of ouabain-mediated renal proximal tubule Na/K-ATPase signal transduction and subsequent sodium tr

256 activation of Src, an initial transmitter in Na/K-ATPase signal transduction, and of Ca(2+) signaling

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

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

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

260 responding to the Na(+)-specific site of the Na(+),K(+)-ATPase (site III).

261 We have identified the beta1 subunit of Na(+),K(+)-ATPase (sodium pump) as a binding partner for

262 ction mutations in the alpha3 isoform of the Na(+)/K(+) ATPase (sodium pump) are responsible for rapi

263 aglycones at different pH values using shark Na,K-ATPase stabilized in the E2MgPi or in the E2BeFx co

264 Na(+),K(+)-ATPase structures revealed a previously undes

265 he encoded BetaM proteins, which function as Na,K-ATPase subunits in lower vertebrates and birds.

266 quired for the intracellular accumulation of Na(+),K(+)-ATPase that occurs in response to energy depl

267 rformed with two transmembrane proteins; the Na(+)/K(+)ATPase that contains transmembrane as well as

268 from the nucleotide binding domain of alpha1 Na/K-ATPase that binds and inhibits Src in vitro.

269 Internalization of the Na(+)/K(+)-ATPase (the Na(+) pump) has been studied in t

270 h as digoxin and ouabain selectively inhibit Na+, K+ -ATPase (the Na+ pump) and, via Na+ / Ca2+ excha

271 In multiply spin-labeled membranous Na,K-ATPase, this heterogeneous population of conformati

272 e lung interstitium by basolaterally located Na/K-ATPase, thus creating a local osmotic gradient to r

273 ormal 3Na(+):2K(+):1ATP stoichiometry of the Na(+),K(+)-ATPase to electroneutral 2Na(+):2K(+):1ATP st

274 a direct role in linking the trafficking of Na(+),K(+)-ATPase to the energy state of renal epithelia

275 currents that drive active transport by the Na(+)/K(+) ATPase to maintain the Na(+) and K(+) ion con

276 endence of the L-type Ca(2+) channel and the Na-K ATPase to better fit experiment, appropriate depend

277 Here, we investigated the effect of AS160 on Na(+),K(+)-ATPase trafficking in response to energy depl

278 To derive robust conclusions about the Na(+)/K(+)-ATPase transport mechanism, we did not rely o

279 Na(+)/K(+)-ATPase transports Na(+) and K(+) ions across

280 erine, soy phosphatidylcholine increases the Na,K-ATPase turnover rate from 5483 +/- 144 to 7552 +/-

281 peptide directly activates ENaC, but not the Na(+)-K(+)-ATPase, upon binding to the carboxy-terminal

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

283 the expression of the alpha1 isoform of the Na(+), K(+)-ATPase was increased.

284 hanism underlying PKA-mediated regulation of Na(+),K(+)-ATPase was explored in mutagenesis studies of

285 Na,K-ATPase was found to be a substrate for Src kinase p

286 cts of renal ischemia on the distribution of Na(+),K(+)-ATPase were substantially reduced in the epit

287 the alpha1-, alpha2-, and alpha3-isoforms of Na(+),K(+)-ATPase, whereas other substitutions of this a

288 ted cells express the alpha1beta1 isoform of Na,K-ATPase, whereas the non-pigmented cells express mai

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

290 Na(+),K(+)-ATPase, which is normally found at the basola

291 acellular domain of the beta1-subunit of the Na(+)/K(+)-ATPase, which also resides in adherens juncti

292 sis-regulating proteins in CMs were reduced: Na(+)/K(+)-ATPase, which is vital for effective action p

293 entry via ENaC and its basolateral exit via Na,K-ATPase, which may allow principal cells to maintain

294 t all feedback went through transport by the Na/K ATPase, which adjusted surface cell osmolarity such

295 ion of established interaction motifs of the Na(+),K(+)-ATPase with ankyrin B and caveolin-1 are expe

296 e cysteine C932 in transmembrane helix M8 of Na(+),K(+)-ATPase with arginine, present in the H(+),K(+

297 mbined with stimulation of ATP hydrolysis by Na(+),K(+)-ATPase with subtoxic doses of gramicidin A or

298 s) are specific and potent inhibitors of the Na(+),K(+)-ATPase, with highest affinity to the phosphoe

299 A recent structure of Na,K-ATPase, with bound digoxin, shows the third digitox

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