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1 similar to those of digoxin, a plant-derived cardiac glycoside.
2 been blocked by endogenous ouabain or other cardiac glycosides.
3 that potently inhibits hERG trafficking are cardiac glycosides.
4 tic uptake transporter for such compounds as cardiac glycosides.
5 alpha-sugar and lactone ring moieties of the cardiac glycosides.
6 the hypothesis for a role of the endogenous cardiac glycosides.
7 steroid derivative closely related to plant cardiac glycosides.
8 ncluding Na/K-ATPase, the putative target of cardiac glycosides.
9 to have homologies to the steroidal core of cardiac glycosides.
10 Na,K-ATPase is responsible for the effect of cardiac glycosides.
11 verse compounds, and has a high affinity for cardiac glycosides.
12 450s differentially affect hepatic uptake of cardiac glycosides.
13 by q(gamma) charge following treatment with cardiac glycosides.
14 d Oatp2 (Slc21a5), mediate hepatic uptake of cardiac glycosides.
15 gs that PB and PCN enhance hepatic uptake of cardiac glycosides.
18 yme activity following inhibition by various cardiac glycosides and their aglycones at different pH v
20 ructurally related to the digitalis class of cardiac glycosides, and its putative target is the Na(+)
21 ,000 known bioactive compounds revealed that cardiac glycosides, antagonists of Na(+),K(+)-ATPase, in
24 ether these hitherto unrecognized effects of cardiac glycosides are obtained in the intact heart and
26 cells) when compared with concentrations of cardiac glycosides (arrhythmogenic index, 4.10; n = 8 ce
27 Additional adjustment for baseline use of cardiac glycosides attenuated the association between AF
29 together these results demonstrate that the cardiac glycoside binding site of the alpha isoforms of
32 at Trp-H100, which is part of the antibody's cardiac glycoside binding site, is a major determinant o
33 Tyr residue (Tyr-H100) which is part of the cardiac glycoside binding site, located approximately 10
37 dynamically by a mechanism that utilizes the cardiac glycoside-binding site and an endogenous ligand(
38 ite and an endogenous ligand(s) and that its cardiac glycoside-binding site can play a physiological
40 f the Na,K-ATPase to investigate whether the cardiac glycoside-binding site plays any physiological r
41 erations perturb the interaction between the cardiac glycoside bufalin and the Na(+)/K(+)-ATPase.
42 oughput screening effort that identified the cardiac glycoside bufalin as a potent small-molecule inh
44 in belongs to a naturally occurring class of cardiac glycosides (CG); digitoxin is clinically approve
47 ly and functionally related compounds of the cardiac glycoside class and known inhibitors of Na(+)K(+
49 ovide evidence that oleandrin, the principal cardiac glycoside component of PBI-05204, can quantitati
50 roids were investigated by comparing various cardiac glycoside compounds like ouabain, digoxin, digit
52 ing a high-content screen, we identified the cardiac glycoside convallatoxin as an effective compound
53 the extent to which high-affinity binding of cardiac glycosides correlates with their potency in inhi
54 rrors of hepatic metabolism and suggest that cardiac glycosides could provide an approach for reducin
58 ell-based reporter system, we identified the cardiac glycoside digoxin as a specific inhibitor of ROR
60 pha3beta1 isoforms showed that the classical cardiac glycoside, digoxin, is partially alpha2-selectiv
61 focuses on the quantitative analysis of the cardiac glycoside drug digitoxin and its three main meta
62 of human cancer cells, is down-regulated by cardiac glycoside drugs digoxin and ouabain, potent inhi
67 .8-48-fold increases in the I50 of different cardiac glycosides for inhibition of the Na,K-ATPase act
68 n derivatives explains beneficial effects of cardiac glycosides for treatment of heart failure and po
71 nd pharmacodynamics of different variants of cardiac glycosides identified the mechanism of inhibitio
72 Because the alpha1 isoform is sensitive to cardiac glycosides in humans, we developed mice in which
73 se findings support further investigation of cardiac glycosides in providing neuroprotection in the c
74 ibian muscle fibres following treatment with cardiac glycosides in the hypertonic gluconate-containin
78 ls and, unpredictably, identified a group of cardiac glycosides, including ouabain and digoxin, as po
79 a divergent mechanistic relationship between cardiac glycoside-induced cytotoxicity and Na+/K+-ATPase
82 this link suggests a possible mechanism for cardiac glycoside inhibition of the Na,K-ATPase, such th
85 to explain the positive inotropic effect of cardiac glycosides invokes altered Na+-Ca2+ exchange act
87 ously that inhibition of hERG trafficking by cardiac glycosides is initiated via direct block of Na(+
91 fer modest increases in the concentration of cardiac glycoside needed to produce 50% inhibition of ac
92 ibition of ATG-dependent phagocytosis by the cardiac glycoside neriifolin, an inhibitor of the Na(+),
93 uroprotective action in ischemic stroke, the cardiac glycoside neriifolin, and demonstrated that its
99 ither indirectly after long-term exposure to cardiac glycosides or directly after exposure to gramici
100 over time and sensitive to inhibition by the cardiac glycoside ouabain, a specific inhibitor of the N
102 uabain (AO), a fluorescent derivative of the cardiac glycoside ouabain, to mAbs 26-10, 45-20, and 40-
104 n of alpha3 using a low concentration of the cardiac glycoside, ouabain, resulted in a modest increas
106 drug-induced trafficking inhibition in which cardiac glycosides produce a [K(+)](i)-mediated conforma
108 These results define the distribution of the cardiac glycoside receptor isoforms in the human heart a
109 ng between anthroylouabain (AO) bound to the cardiac glycoside receptor site on alpha and the carbohy
110 ion is negligible, indicating that the human cardiac glycoside receptors are alpha1beta1, alpha2beta1
113 nfused with Digibind to sequester endogenous cardiac glycoside(s) produced similar effects on both re
116 echanism by which digitoxin and other active cardiac glycosides, such as digoxin, exert system-wide a
117 The Na,K-ATPase contains a binding site for cardiac glycosides, such as ouabain, digoxin, and digito
119 Our results define a novel activity for cardiac glycosides that could prove relevant to the trea
120 e the fact that the molecular target for the cardiac glycosides, the alpha-subunit of sarcolemmal Na+
122 s and inhibitory potencies of a series of 37 cardiac glycosides using radioligand binding and ATPase
124 pha2 isoform, which is normally sensitive to cardiac glycosides, was made resistant to these compound
126 strated that the proapoptotic effects of the cardiac glycosides were linked to their abilities to ind
127 d sample for measurement of electrolytes and cardiac glycosides were taken before treatment and at 12
128 iandrogen therapy, we identify Peruvoside, a cardiac glycoside, which can potently inhibit both andro
129 ansport activity is effectively inhibited by cardiac glycosides, which bind to the extracellular side
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