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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.
16                      Among them were several cardiac glycosides, a class of cardenolides historically
17                              The features of cardiac glycoside action thus parallel those of other ag
18 yme activity following inhibition by various cardiac glycosides and their aglycones at different pH v
19                 One group consists mainly of cardiac glycosides and will be the subject of another st
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
22                                Certain other cardiac glycosides are also active but with much less po
23                          Digitoxin and other cardiac glycosides are important, centuries-old drugs fo
24 ether these hitherto unrecognized effects of cardiac glycosides are obtained in the intact heart and
25                                              Cardiac glycosides are used clinically to increase contr
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
28                     Thus, a link between the cardiac glycoside binding site and the cation transport
29  together these results demonstrate that the cardiac glycoside binding site of the alpha isoforms of
30               This result indicates that the cardiac glycoside binding site of the alpha1 isoform can
31           This finding demonstrates that the cardiac glycoside binding site of the Na,K-ATPase plays
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
34 y transfer to AO is likely to be part of the cardiac glycoside binding site.
35 r domain that constitutes a core part of the cardiac glycoside binding site.
36  relationship between receptor structure and cardiac glycoside binding.
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
39        The physiological significance of the cardiac glycoside-binding site on the Na,K-ATPase remain
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
43                                       Severe cardiac glycoside cardiotoxicity after ingestion of yell
44 in belongs to a naturally occurring class of cardiac glycosides (CG); digitoxin is clinically approve
45                                          The cardiac glycosides (CGs) digoxin, digitoxin and ouabain,
46                       The therapeutic use of cardiac glycosides (CGs), agents commonly used in treati
47 ly and functionally related compounds of the cardiac glycoside class and known inhibitors of Na(+)K(+
48 ns represent the major binding sites for the cardiac glycoside class of drugs.
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
51                                        Other cardiac glycoside compounds tested also showed neuroprot
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
55                                   A purified cardiac glycoside derived from the foxglove plant, digox
56                    Oleandrin, a polyphenolic cardiac glycoside derived from the leaves of Nerium olea
57 igh affinity scFv antibody that binds to the cardiac glycoside digoxigenin.
58 ell-based reporter system, we identified the cardiac glycoside digoxin as a specific inhibitor of ROR
59  patients with chronic LV dysfunction is the cardiac glycoside digoxin.
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
63           Digitoxin and structurally related cardiac glycoside drugs potently block activation of the
64                This is the first report that cardiac glycoside drugs, by initiating the Src/MAPK sign
65                                              Cardiac glycosides exert a positive inotropic effect by
66           Here, we report 3 compounds in the cardiac glycoside family, ouabain, gitoxigenin, and digi
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
69 e increased capacity of the liver to extract cardiac glycosides from the plasma.
70                                              Cardiac glycosides have played a prominent role in the t
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
75                                  The role of cardiac glycosides in treating patients with chronic hea
76                Here, we report that multiple cardiac glycosides, including digitoxin and digoxin, are
77                   Eleven of these drugs were cardiac glycosides, including digoxin, ouabain, and pros
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
80                                              Cardiac glycoside-induced intracellular K(+) depletion c
81                            Digoxin and other cardiac glycosides inhibit hypoxia-inducible factor-1 (H
82  this link suggests a possible mechanism for cardiac glycoside inhibition of the Na,K-ATPase, such th
83                      Furthermore, ouabain, a cardiac glycoside inhibitor of the Na(+)/K(+)-ATPase, po
84                        Our data suggest that cardiac glycosides interact with phosphorylated mediator
85  to explain the positive inotropic effect of cardiac glycosides invokes altered Na+-Ca2+ exchange act
86        Inhibition of Na,K-ATPase activity by cardiac glycosides is believed to be the major mechanism
87 ously that inhibition of hERG trafficking by cardiac glycosides is initiated via direct block of Na(+
88                                              Cardiac glycoside-mediated effects on NMD are dependent
89                 We report the discovery that cardiac glycosides, natural products in clinical use for
90 he associations among breast cancer, AF, and cardiac glycosides need further investigation.
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
94       We postulated that increased uptake of cardiac glycosides observed after pretreatment of animal
95                     Here, we report that the cardiac glycosides oleandrin, ouabain, and digoxin induc
96 ger is absolutely required for the effect of cardiac glycosides on Ca2+(i).
97                 Effects of topically applied cardiac glycosides on intraocular pressure in rabbits ha
98                            Thus, an existing cardiac glycoside or closely related compound could prov
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
101 appears to be an isomer of the plant-derived cardiac glycoside ouabain, if not ouabain itself.
102 uabain (AO), a fluorescent derivative of the cardiac glycoside ouabain, to mAbs 26-10, 45-20, and 40-
103      Blocking Na+, K(+)-ATPase activity with cardiac glycosides (ouabain or strophanthidin, 1 mM) or
104 n of alpha3 using a low concentration of the cardiac glycoside, ouabain, resulted in a modest increas
105 Na,K-ATPase is specifically inhibited by the cardiac glycoside, ouabain.
106 drug-induced trafficking inhibition in which cardiac glycosides produce a [K(+)](i)-mediated conforma
107             We show that resistance to toxic cardiac glycosides produced by plants and bufonid toads
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
111                                We found that cardiac glycosides reduce the production of apolipoprote
112 revealed that the treatment of patients with cardiac glycosides reduced serum LDL-C levels.
113 nfused with Digibind to sequester endogenous cardiac glycoside(s) produced similar effects on both re
114                                              Cardiac glycosides such as ouabain and digoxin specifica
115            Na(+),K(+)-ATPase is inhibited by cardiac glycosides such as ouabain, and palytoxin, which
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
118            Several studies also suggest that cardiac glycosides, such as ouabain, function by mechani
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+
121                                              Cardiac glycoside use was strongly associated with incid
122 s and inhibitory potencies of a series of 37 cardiac glycosides using radioligand binding and ATPase
123                             Using a panel of cardiac glycoside variants, we assessed the structural e
124 pha2 isoform, which is normally sensitive to cardiac glycosides, was made resistant to these compound
125                                 Although the cardiac glycosides were identified in an evaluation of 2
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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