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1 0.9 versus 1.6 +/- 0.5 mmHg with intravenous ouabain).
2  /K(+) -ATPase (l-NMMA + ketorolac + BaCl2 + ouabain).
3  ) channels and Na(+) /K(+) -ATPase (BaCl2 + ouabain).
4 before or after administration of BaCl2 plus ouabain.
5 ively inhibiting alpha2 enzyme activity with ouabain.
6 e measured with and without NKA inhibited by ouabain.
7 ensitive to the Na+/K+-ATPase pump inhibitor ouabain.
8 of Na/K-ATPase, like the pumping pump, binds ouabain.
9 umps were silenced by continuous exposure to ouabain.
10 /K pump and the site of its interaction with ouabain.
11 ent arteriole to contract in the presence of ouabain.
12 n ADPKD cells exhibits a higher affinity for ouabain.
13 ked by a saturating concentration of dihydro-ouabain.
14 nal Na+/K+-ATPases induced by the binding of ouabain.
15 ibition of FGF2 secretion in the presence of ouabain.
16  of action potential fall in the presence of ouabain.
17 zation of the pump or affect the response to ouabain.
18 TPase with subtoxic doses of gramicidin A or ouabain.
19  by comparison with digoxin, digoxigenin, or ouabain.
20 c; and L-NMMA plus ketorolac plus BaCl2 plus ouabain.
21 podocyte primary cell cultures with low-dose ouabain.
22 s of these experiments showed that 20 microM ouabain, 0.3 microM ionomycin, or their combination incr
23                                              Ouabain (10 mumol l(-1)), a specific inhibitor of Na/K-A
24                                              Ouabain (3 nm) also increased ER Ca(2+) release and enha
25                                              Ouabain (3 nm) pre-incubation also augmented 10 muM cycl
26 urve) was attenuated by BaCl2 (-61+/-3%) and ouabain (-44+/-12%) alone, and this effect was enhanced
27 unction of Na(+),K(+)-ATPase is activated by ouabain, a mammalian steroid hormone, at far lower conce
28 sistance in other species to the cardenolide ouabain, a plant toxin capable of blocking ATPases.
29 2V vs. Ag/AgCl in the presence or absence of ouabain, a specific NKA inhibitor.
30                                              Ouabain, a steroid present in the circulation and in var
31 bition of the NKA alpha2 isoform by low dose ouabain abolished the ability of low Ko to reduce NKA cu
32                                              Ouabain, acting from the basolateral side of the cells,
33                                              Ouabain activated the NF-kappaB antiapoptotic subunit p6
34 two mutants caused significant inhibition of ouabain-activated signal transduction and cell growth.
35                           We have shown that ouabain activates Src, resulting in subsequent tyrosine
36 ptor function as evidenced by the failure of ouabain administration to induce the activation of Src a
37                                The increased ouabain affinity of ADPKD cells was not due to differenc
38  loop, known to make a major contribution to ouabain affinity, strongly influenced conductance of sin
39 d astrocytes express Na(+) pumps with a high-ouabain-affinity catalytic subunit (alpha3 and alpha2, r
40 brain as a result of its actions on the high-ouabain-affinity Na(+) pumps in both neurones and astroc
41    Treatment of hTMC with sodium fluoride or ouabain, agents shown to cause morphological changes to
42                                              Ouabain alone reduced pH(i) recovery, but SNP+ouabain ca
43                     Treatment with 20 microM ouabain also increased the ultimate tensile strength of
44               By binding to the Na,K-ATPase, ouabain also induces proliferation in some cell types.
45                           This suggests that ouabain also inhibits an ion resorptive function of Na/K
46 ns, resulting from intravitreal injection of ouabain, also exhibited increased TNFalpha expression th
47 at inhibit Na,K-ATPases, such as digoxin and ouabain, alter cardiac myocyte contractility.
48 ibitor of cytochrome-P450 enzymes or dihydro-ouabain, an inhibitor of Na+,K+-ATPase blocked the effec
49 was phenocopied by treatment of embryos with ouabain, an inhibitor of Na,K-ATPase activity.
50 onensin, a Na(+) ionophore, with and without ouabain, an NKA inhibitor, in suspensions of human eryth
51 vity to the electrolyte transport inhibitors ouabain and bumetanide, as well as bath Cl(-) and HCO(3)
52                     We further characterized ouabain and demonstrated that it inhibits sFlt1 mRNA and
53 ied a group of cardiac glycosides, including ouabain and digoxin, as potent inhibitors of NMD.
54 veral cardiotonic steroids (CTSs), including ouabain and digoxin, increased RGS2 but not RGS4 protein
55 extracellular K(+) did not reduce p53 as did ouabain and digoxin, it did potentiate both digoxin- and
56 CX) blocker, antagonized the effects of both ouabain and digoxin.
57 mally sensitive to the Na+/K+ pump inhibitor ouabain and exhibited age-dependent changes, including d
58                                 In contrast, ouabain and extracellular K(+) failed to produce detecta
59 ies, we used the Na(+)/K(+) ATPase inhibitor ouabain and found conditions in which SD was always prev
60            Fluid absorption was sensitive to ouabain and gadolinium but insensitive to benzamil, bafi
61                                              Ouabain and ionomycin may be useful pharmacologic agents
62          The enzyme is strongly inhibited by ouabain and its derivatives, some that are therapeutical
63 reduced peak FBF (-50+/-6%; P<0.05), whereas ouabain and L-NMMA plus ketorolac did not.
64                               The effects of ouabain and low-Na(+) solutions were determined under op
65       We have also determined the effects of ouabain and reduced bath [Na(+)].
66  demonstrated by reduction of the current by ouabain and the K(+) channel blockers Ba(2+), XE991, and
67 d by the beta-surface of the steroid core of ouabain and the side chains of alphaM1, alphaM2, and alp
68 e, or combined NO, PGs, Na(+) /K(+) -ATPase (ouabain) and KIR channel inhibition (n = 6; Protocol 2).
69  were cardiac glycosides, including digoxin, ouabain, and proscillaridin A, which inhibited HIF-1alph
70 n carbonylation is reversed after removal of ouabain, and this reversibility is largely independent o
71 -interacting pool of Src and act as a potent ouabain antagonist in cultured cells: 1) pNaKtide, unlik
72                                              Ouabain antagonists (PST 2238 and canrenone) and NCX blo
73  that intraperitoneal administration of anti-ouabain antibodies to pregnant mice resulted in a >80% d
74    Consistently, exposure of intact cells to ouabain apparently increased the distance between the Na
75                Cardiotonic steroids, such as ouabain, are specific inhibitors of the Na/K pump.
76 bule of the E2P model explains high-affinity ouabain binding in a mutant of the H,K ATPase.
77 and ouabain-resistant mutation of the alpha2 ouabain binding site (alpha2(R/R) mice) confers resistan
78 he CTS binding pocket of [Mg]E2P allows deep ouabain binding with possible long-range interactions be
79 d the cation site and thereby hindering deep ouabain binding.
80 ypes of cells, may function as non-canonical ouabain-binding receptors.
81  cardiotonic steroids, which act through the ouabain-binding site and are important in cardiovascular
82          The amino acids that constitute the ouabain-binding site are highly conserved across the evo
83                  These data suggest that the ouabain-binding site of the alpha1 Na,K-ATPase can parti
84 is important to characterize the role of the ouabain-binding sites in this context.
85 lute and water transport in ADPKD cells, and ouabain blocks fluid secretion in these cells.
86  triggered by a conformational change of the ouabain-bound Na(+)/K(+)-ATPase molecule or more general
87 structures of Na,K-ATPase in the unbound and ouabain-bound states.
88 T inhibitors and the Na+/K+-ATPase inhibitor ouabain, but not 5-HT2 and 5-HT1B/1D receptor inhibitors
89 ht: prolonged subcutaneous administration of ouabain, but not digoxin, induces hypertension, and digo
90  of hypertension, antagonized the effects of ouabain, but not digoxin.
91   Taken together, these results suggest that ouabain can protect the kidney from the apoptotic effect
92 uabain alone reduced pH(i) recovery, but SNP+ouabain caused significant further reduction.
93                           On the other hand, ouabain causes a gradual depletion of Na/K-ATPase and an
94 iotonic steroids, most notably the digitalis/ouabain class of compounds, which have been used for cen
95 g kinetics with the previously described E2P-ouabain complex to derive specific details and the gener
96 g(2+) is bound in site II of the digoxin and ouabain complexes, whereas both sites are occupied by K(
97 sh retina by intravitreal injection of a low ouabain concentration to rapidly damage the ganglion cel
98                         Although much higher ouabain concentration was required to stimulate Src in I
99  of the sensitivity of the alpha2 isoform to ouabain, conferring ouabain sensitivity to alpha1 augmen
100 resistant mice were inhibited by intravenous ouabain (control stop-flow pressure = 9.7 +/- 0.9 versus
101 nse light and recovered for up to 8 weeks or ouabain-damaged retinas that recovered for up to 3 weeks
102 rate at detecting the inner nuclear layer in ouabain-damaged retinas, but accurately detected the und
103                                              Ouabain decreased glycolysis by 25% and decreased (14)CO
104 ents, loop of Henle perfusion with 50 microM ouabain decreased TGF responses (control stop-flow press
105  evidence points to a role of Na,K-ATPase in ouabain-dependent signal transduction.
106                                              Ouabain-dependent signaling is thought to be mediated wi
107 ng requires reassessment of the mechanism of ouabain-dependent signaling.
108 ing various cardiac glycoside compounds like ouabain, digoxin, digitoxin, and gitoxin with their agly
109  eyes that were injected intracamerally with ouabain, disodium 4,4'-diisothiocyanatostilbene-2,2'-dis
110                                              Ouabain down-regulated sFlt1 production by inhibiting hy
111     Pre-incubation (0.5-10 min) with 1-10 nm ouabain (EC50 < 1 nm) augmented Glu- and CCh-evoked sign
112 tion and cell proliferation, suggesting that ouabain effect is mediated through the MEK-ERK pathway.
113 rd E2 species reduced glutathionylation, and ouabain eliminated a ONOO(-)-induced increase.
114 reased by inhibition of the Na(+)/K(+) pump (ouabain), ENaC (amiloride), CF transmembrane conductance
115 ted by both brain and circulating endogenous ouabain (EO).
116 one another in both assays: For example, the ouabain-evoked (3 nm) increases in MT70 and neuronal Ca2
117 TPase in complex with the CTS representative ouabain, extending to 3.4 A resolution.
118 NaKtide may be used as a novel antagonist of ouabain for probing the physiological and pathological s
119 , a digoxigenin derivative that displaces 3H-ouabain from Na+, K+ -ATPase, and attenuates some forms
120                                              Ouabain further reduced glutathionylation in E2 and elim
121 3 compounds in the cardiac glycoside family, ouabain, gitoxigenin, and digitoxin, that inhibit placen
122                                              Ouabain had similar effects to those of MBG, suggesting
123 somer of the plant-derived cardiac glycoside ouabain, if not ouabain itself.
124 inding abolished the antiapoptotic effect of ouabain in Stx2-exposed tubular cells.
125 related to the presence of plants containing ouabain in the geographic locations where both inversion
126 ated the involvement of maternal circulating ouabain in the regulation of fetal growth and organ deve
127  tubular cells, cardiotonic steroids such as ouabain in vitro signal through Na/K-ATPase, which resul
128 ut was evoked using dorsal-root stimulation, ouabain increased burst frequency and extended locomotor
129                   The sodium pump inhibitor, ouabain, increased the frequency and decreased the ampli
130                                              Ouabain increases the endocytosis and degradation of Na/
131                         The O2 dependence of ouabain-independent K+ transport mechanisms has been stu
132 aft model of retinoblastoma, the cardenolide ouabain induced complete tumor regression in the treated
133                              In this system, ouabain induced Na/K-ATPase/c-Src signaling and redistri
134 cal inhibition of the Na(+)/K(+)-ATPase with ouabain induced neurite degeneration, which was attenuat
135                                      Second, ouabain induced phosphorylation of PLC-gamma1 at Tyr(783
136 -K(+) ATPase antagonists (ouabain or dihydro-ouabain) induced either a membrane depolarization in cur
137 ly, both Src and caveolin-1 are required for ouabain-induced activation of Akt and up-regulation of N
138              Concomitantly it also abolished ouabain-induced activation of Src and ERK1/2.
139                      Consequently, it blocks ouabain-induced activation of Src, ERK, and hypertrophic
140 d Ca2+ transients were augmented, and 100 nM ouabain-induced amplification was abolished.
141                            Here we show that ouabain-induced cell growth regulation is intrinsically
142 fish alpha1a.1 or rat alpha1 mRNA, while the ouabain-induced defect was rescued by expression of ouab
143  kinase kinase (MEK) inhibitor U0126 blocked ouabain-induced ERK activation and cell proliferation, s
144 /mTOR pathway by rapamycin completely blocks ouabain-induced expression of Na/K-ATPase and converts o
145 duced expression of Na/K-ATPase and converts ouabain-induced growth stimulation to growth inhibition
146 Na(+)] was increased to 20 mm or more (using ouabain-induced inhibition of the Na(+),K(+)-ATPase or t
147 damage and regeneration of photoreceptors or ouabain-induced inner retinal damage.
148 nlike previous studies in other systems, the ouabain-induced internalization was insensitive to Src o
149 digoxin, it did potentiate both digoxin- and ouabain-induced p53 reduction in sensitive lines.
150 -ATPase/Src receptor complex and antagonizes ouabain-induced protein kinase cascades.
151 he Na/K-ATPase affect basal Src activity and ouabain-induced signal transduction.
152   In alpha1-resistant/alpha2-resistant mice, ouabain infusion had no effect on TGF responses.
153                                    Prolonged ouabain infusion induces hypertension in rodents, and ou
154                                     However, ouabain-inhibitable respiration did not decrease during
155 pproximately 85% in both cell types, whereas ouabain inhibited K(+)-hyperpolarization differently in
156                                              Ouabain inhibited the FF from either side of the prepara
157                                              Ouabain inhibited the fluid flow across both species, in
158 ility of digoxin-like CTSs to reactivate the ouabain-inhibited complex can be explained by de-oligome
159 st to NHK cells, the dose-response curve for ouabain inhibition of Na,K-ATPase activity indicated tha
160            The implication is that nanomolar ouabain inhibits alpha3 Na(+) pumps, increases (local) i
161                                              Ouabain-initiated phosphorylation of Ser(16) alpha1 was
162 ine and ganglion cells were lost by 7 d post-ouabain injection (dpi).
163                                By 24 h after ouabain injection, maximal numbers of terminal deoxynucl
164                                        After ouabain injection, receptor and postreceptor uptake of m
165 wildtype zebrafish at 0, 3 and 18 days after Ouabain injection.
166 rgeted mouse (alpha2(R/R)) which expresses a ouabain-insensitive alpha2 isoform of the Na,K-ATPase to
167                            Overexpression of ouabain-insensitive rat alpha1 failed to inhibit interna
168  specific reduction in NCX1 protein and were ouabain-insensitive.
169        These results support the notion that ouabain is a growth factor and suggest that a reduction
170                                   Endogenous ouabain is an adrenal stress hormone associated with adv
171 e effects is heightened by the evidence that ouabain is endogenous in mammals.
172                   The final model shows that ouabain is trapped within the external ion permeation pa
173 nd Ser(16), respectively, the latter because ouabain itself increased Ser(16) phosphorylation; thus,
174 nt-derived cardiac glycoside ouabain, if not ouabain itself.
175  After the reduction in maternal circulating ouabain, kidney expression of cyclin D1 was reduced and
176 /K(+)-ATPase, NO, and prostaglandins (BaCl2, ouabain, L-NMMA [N(G)-monomethyl-L-arginine] and ketorol
177 ng human pregnancy, the circulating maternal ouabain level increased and the highest concentration of
178 esulted in a >80% decline in the circulating ouabain level.
179               Preoperative plasma endogenous ouabain levels are powerful biomarkers of acute kidney i
180                     Furthermore, circulating ouabain levels in women with small-for-gestational age n
181              Most CTSs could be divided into ouabain-like (ouabagenin, dihydroouabain (DHO), strophan
182 n each group, the CTSs were synergistic, but ouabain-like and digoxin-like CTSs antagonized one anoth
183 hronic salt retention elevates an endogenous ouabain-like compound (EOLC) and induces salt-dependent
184 train has a 10-fold increase in hypothalamic ouabain-like compound that is linked to the pathogenesis
185 n of the latter gene decreased production of ouabain-like factor from neural tissue.
186 hat preoperative plasma levels of endogenous ouabain may function as this type of biomarker.
187                              Thus, nanomolar ouabain may strongly influence synaptic transmission in
188                                          The ouabain-mediated downregulation of GlyT2 also occurs in
189 in a feed-forward mechanism of regulation of ouabain-mediated renal proximal tubule Na/K-ATPase signa
190 Bcl-xL, an inhibitor of Bax, suggesting that ouabain might protect renal cells from Stx2-triggered ap
191 w and high levels of the specific NKA ligand ouabain modulate the endocytosis and total expression of
192      Using a systematic approach, we applied ouabain (Na(+)/K(+)-ATPase inhibitor), bumetanide (Na(+)
193 red due to the very slow dissociation of the ouabain.Na(+)/K(+)-ATPase complex.
194                            Signaling via the ouabain/Na,K-ATPase/IP3R/NF-kappaB pathway increases exp
195                          We tested nanomolar ouabain on Ca(2+) signalling (fura-2) in rat hippocampal
196 ase dictate the growth regulatory effects of ouabain on cells.
197 enal parameters in rats and the influence of ouabain on podocyte proteins both "in vivo" and "in vitr
198 rolonged elevations of circulating exogenous ouabain on renal parameters in rats and the influence of
199 tion of cholesterol abolished the effects of ouabain on this interaction.
200 G and a similar Na(+)/K(+)-ATPase inhibitor, ouabain, on the phosphorylation status of Jnk, p38, and
201  perfusion of Na(+)-K(+) ATPase antagonists (ouabain or dihydro-ouabain) induced either a membrane de
202          Preincubation of lenses with either ouabain or low-[Na(+)] solutions resulted in reduced rat
203 e pumps that have been blocked by endogenous ouabain or other cardiac glycosides.
204 lace-cell-train-induced AHPs were blocked by ouabain or removal of extracellular potassium, but not b
205 a1 and alpha3 isoforms of Na(+)/K(+)-ATPase, ouabain or strophanthidin, inhibited this Na(+) current.
206                  This delay was abolished by ouabain or zero K(+) saline, which eliminate the usAHP.
207 hate-buffered saline (PBS, vehicle) or PBS + ouabain, or after intraperitoneal injection of sodium io
208 r calcium, but were blocked by tetrodotoxin, ouabain, or the removal of extracellular potassium.
209                Here we tested the ability of ouabain (OUA, 3 microm), digoxin (DIG, 20 microm) or ace
210 ot different than that observed for combined ouabain plus BaCl(2) administration.
211 verage 56 +/- 5% (n = 16) following combined ouabain plus BaCl(2) infusion.
212 lated by cardiac glycoside drugs digoxin and ouabain, potent inhibitors of Na(+)/K(+)-ATPase.
213               A Na(+)/K(+)-ATPase inhibitor (ouabain) potentiated EA-induced cytotoxicity and direct
214 e survival factor Bcl-xL; co-incubation with ouabain prevented all of these effects.
215                                        Bound ouabain protects the site with the strongest influence o
216                             Group 2 received ouabain rather than BaCl2 in the second trial.
217                    The Na,K-ATPase inhibitor ouabain reduced and enhanced the carbachol-promoted phos
218 ally, in the rat model, elevated circulating ouabain reduced creatinine clearance (-18%, p < 0.05), i
219 rat model of pregnancy-induced hypertension, ouabain reduced mean arterial pressure and enhanced plac
220 arities in the Atpalpha variants, conferring ouabain resistance in both arrangements, may be the resu
221                                              Ouabain-resistance test detecting mutations in the Na(+)
222 lpha1 isoform of mice and rats is relatively ouabain resistant, gene-targeting strategies were used t
223 e alpha1 isoform mice were equivalent to the ouabain-resistant alpha1 isoform mice.
224 eloped mice in which the naturally occurring ouabain-resistant alpha1 isoform was made ouabain-sensit
225 espectively); both also express pumps with a ouabain-resistant alpha1 subunit.
226 ertension in WT mice but not in mice with an ouabain-resistant alpha2 isoform of Na,K-ATPase.
227 opus alpha1beta3 Na/K pumps, which were made ouabain-resistant by point mutation, after expressing th
228 nfusion induces hypertension in rodents, and ouabain-resistant mutation of the alpha2 ouabain binding
229  Na/K pumps from ventricular myocytes and in ouabain-resistant pumps expressed in Xenopus oocytes.
230 -induced defect was rescued by expression of ouabain-resistant zebrafish alpha1a.1 or rat alpha1 mRNA
231 lpha1 is ouabain-sensitive and NKA-alpha2 is ouabain-resistant, we assessed the effects of PLM phosph
232 IR channels and Na(+)/K(+)-ATPase (BaCl2 and ouabain, respectively), and combined inhibition of KIR c
233  low concentration of the cardiac glycoside, ouabain, resulted in a modest increase in intracellular
234      Furthermore, in vivo, administration of ouabain reversed the imbalance between Bax and Bcl-xL in
235 nduces hypertension, and digoxin antagonizes ouabain's hypertensinogenic effect.
236 mitochondrial depolarization observed before ouabain-SD was abolished by L-type channel block, and Zn
237 ) and Zn(2+) removal was required to prevent ouabain-SD when A(1) receptors were blocked.
238 ncreases were observed in CA1 neurons before ouabain-SD, and L-type channel block prevented the intra
239 oval of extracellular Ca(2+) did not prevent ouabain-SD.
240 an play a critical role in the generation of ouabain-SD.
241 e into susceptible eucaryotic cells under an ouabain selection regime.
242 diotonic steroids (CTSs) such as digoxin and ouabain selectively inhibit Na+, K+ -ATPase (the Na+ pum
243                            In all cases, the ouabain sensitive component of the influx contributed ap
244 es Na(+),K(+)-ATPase activity as assessed by ouabain-sensitive (86)Rb(+) uptake.
245  fragment, the sodium excretion rates in the ouabain-sensitive alpha1 isoform mice were equivalent to
246                     Circulating EO modulates ouabain-sensitive alpha2 Na(+) pump activity and Ca(2+)
247        Elevated hydrostatic pressure induced ouabain-sensitive alveolar fluid secretion that coincide
248  wild-type mice and mice where NKA-alpha1 is ouabain-sensitive and NKA-alpha2 is ouabain-resistant, w
249                               Measurement of ouabain-sensitive ATPase activity and radiolabeled catio
250 sgenic mice also exhibited a 36% decrease in ouabain-sensitive sodium reabsorption and a significantl
251  pNBTEA concentration and V(M) dependence of ouabain-sensitive transient charge movements in whole-ce
252 ep changes in V(M) elicited pNBTEA-activated ouabain-sensitive transient currents that had similariti
253 ximately 60 s), activity-dependent, TTX- and ouabain-sensitive, hyperpolarization ( approximately 5 m
254                                  Endogenous, ouabain-sensitive, Xenopus alpha1beta3 Na/K pumps were s
255 ng ouabain-resistant alpha1 isoform was made ouabain-sensitive.
256 nsistent with the established differences in ouabain sensitivity between pig and rat alpha1.
257  Currently, the basis for the differences in ouabain sensitivity of NHK and ADPKD cells is unknown.
258 by micropuncture in mutant mice with altered ouabain sensitivity of the alpha1 and alpha2 Na,K-ATPase
259 of the alpha2 isoform to ouabain, conferring ouabain sensitivity to alpha1 augmented the natriuretic
260                Cardiotonic steroids (such as ouabain) signaling through Na/K-ATPase regulate sodium r
261 hown that the caveolar Na/K-ATPase transmits ouabain signals via multiple signalplexes.
262           Values for preoperative endogenous ouabain significantly improved (area under curve: 0.85)
263 t was found that nanomolar concentrations of ouabain, similar to those circulating in blood, induced
264                                 Furthermore, ouabain stimulated direct carbonylation of two amino aci
265                                              Ouabain-stimulated Na(+),K(+)-ATPase signaling has recen
266 he antioxidant N-acetyl-L-cysteine prevented ouabain-stimulated Na/K-ATPase.c-Src signaling, protein
267 tive oxygen species are required to initiate ouabain-stimulated Na/K-ATPase.c-Src signaling.
268                                              Ouabain-stimulated protein carbonylation is reversed aft
269 /K-ATPase.c-Src signaling complex attenuated ouabain-stimulated protein carbonylation.
270                         It is concluded that ouabain stimulates proliferation in ADPKD cells by bindi
271                                     However, ouabain stimulates the PI3K/Akt/mTOR pathway and consequ
272 mparison with the low-affinity [K2]E2-MgF(x)-ouabain structure shows that the CTS binding pocket of [
273  reveal that SSA78 binding is antagonized by ouabain, supporting the interaction of SSA78 at one of t
274 ) increased with the preoperative endogenous ouabain tertile.
275 ith each incremental preoperative endogenous ouabain tertile.
276 by bath application of low concentrations of ouabain that selectively inhibit NKAalpha3 while alpha-m
277                           In the presence of ouabain, the action potential collapses.
278                     In constructs exposed to ouabain, the increased percentage of collagen per constr
279                            At 1 mumol l(-1), ouabain, the secreted saliva was hyperosmotic.
280 Src kinase and inhibit its activity, whereas ouabain, the specific Na,K-ATPase inhibitor, binds and s
281 c activity but also serves as a receptor for ouabain to activate protein kinases.
282 nses of the alpha1 and/or alpha2 isoforms to ouabain to assess for altered natriuretic responses to a
283 wn converts the growth stimulatory effect of ouabain to growth inhibition in LLC-PK1 cells.
284 t-shock protein 27 (HSP27) was necessary for ouabain to inhibit HIF-1alpha translation.
285                         Combined infusion of ouabain (to inhibit Na(+)/K(+)-ATPase) and barium chlori
286 a receptor for cardiotonic steroids, such as ouabain, to regulate cellular protein kinase cascades.
287 400 and KB-R7943) normalize myogenic tone in ouabain-treated arteries.
288 ) current was fully inhibited by basolateral ouabain treatment, suggesting that the Na(+),K(+)-ATPase
289 ression analysis, the circulating endogenous ouabain value before surgery was the strongest predictor
290 ffected differently by Na(+) modulation with ouabain versus Ca(2+) modulation with ionomycin.
291                                Surprisingly, ouabain virtually abolished NKA-PLM FRET but only partia
292                                 In addition, ouabain was able to stimulate Src and ERK1/2 in the resc
293                      Preoperative endogenous ouabain was measured in 407 patients admitted for electi
294 TP hydrolysis in the presence and absence of ouabain was used to measure Na,K-ATPase activity.
295 nergy transfer distances measured with bound ouabain, we carried out molecular dynamics simulations w
296                        Low concentrations of ouabain were also found to disrupt cortical network osci
297                                     Dopamine/ouabain were not involved in activation of protein secre
298 ternalization of alpha1 induced by >/=100 nm ouabain which occurs in a time scale of hours.
299 were subjected to intravitreal injections of ouabain, which destroys the inner retina.
300 diac glycosides (CGs) digoxin, digitoxin and ouabain, which directly inhibit ATP1A1 function, exhibit

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