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1 similar to those of digoxin, a plant-derived cardiac glycoside.
2 450s differentially affect hepatic uptake of cardiac glycosides.
3  by q(gamma) charge following treatment with cardiac glycosides.
4 d Oatp2 (Slc21a5), mediate hepatic uptake of cardiac glycosides.
5 gs that PB and PCN enhance hepatic uptake of cardiac glycosides.
6 mil, also inhibit inflammasome activation by cardiac glycosides.
7 associated with target-site insensitivity to cardiac glycosides.
8  been blocked by endogenous ouabain or other cardiac glycosides.
9  that potently inhibits hERG trafficking are cardiac glycosides.
10 tic uptake transporter for such compounds as cardiac glycosides.
11 alpha-sugar and lactone ring moieties of the cardiac glycosides.
12  the hypothesis for a role of the endogenous cardiac glycosides.
13  steroid derivative closely related to plant cardiac glycosides.
14 ncluding Na/K-ATPase, the putative target of cardiac glycosides.
15  to have homologies to the steroidal core of cardiac glycosides.
16 Na,K-ATPase is responsible for the effect of cardiac glycosides.
17 verse compounds, and has a high affinity for cardiac glycosides.
18 )-ATPase)(7-11), the physiological target of cardiac glycosides(12).
19  resistance and target-site insensitivity to cardiac glycosides(16), culminating in triple mutant 'mo
20 substitutions render the pump insensitive to cardiac glycosides(2)(,)(3), allowing the monarch and ot
21                      Among them were several cardiac glycosides, a class of cardenolides historically
22                              The features of cardiac glycoside action thus parallel those of other ag
23 veal cross talk between ionic modulation via cardiac glycosides and immune checkpoint protein express
24 yme activity following inhibition by various cardiac glycosides and their aglycones at different pH v
25                 One group consists mainly of cardiac glycosides and will be the subject of another st
26 ructurally related to the digitalis class of cardiac glycosides, and its putative target is the Na(+)
27 ,000 known bioactive compounds revealed that cardiac glycosides, antagonists of Na(+),K(+)-ATPase, in
28                                Certain other cardiac glycosides are also active but with much less po
29                          Digitoxin and other cardiac glycosides are important, centuries-old drugs fo
30 ether these hitherto unrecognized effects of cardiac glycosides are obtained in the intact heart and
31                                              Cardiac glycosides are used clinically to increase contr
32  cells) when compared with concentrations of cardiac glycosides (arrhythmogenic index, 4.10; n = 8 ce
33 cal assay for ACE2:Spike binding, and tested cardiac glycosides as inhibitors of binding.
34 resent four major animal clades, implicating cardiac glycosides as keystone molecules(6) and establis
35  'monarch flies' that were as insensitive to cardiac glycosides as monarch butterflies.
36 ate the utility of the screen by identifying cardiac glycosides as potent inducers of miR-132, a key
37 +)-ATPases that are similarly insensitive to cardiac glycosides (as predicted by Whiteman and Mooney)
38    Additional adjustment for baseline use of cardiac glycosides attenuated the association between AF
39                     Thus, a link between the cardiac glycoside binding site and the cation transport
40  together these results demonstrate that the cardiac glycoside binding site of the alpha isoforms of
41               This result indicates that the cardiac glycoside binding site of the alpha1 isoform can
42           This finding demonstrates that the cardiac glycoside binding site of the Na,K-ATPase plays
43 at Trp-H100, which is part of the antibody's cardiac glycoside binding site, is a major determinant o
44  Tyr residue (Tyr-H100) which is part of the cardiac glycoside binding site, located approximately 10
45 y transfer to AO is likely to be part of the cardiac glycoside binding site.
46 r domain that constitutes a core part of the cardiac glycoside binding site.
47  relationship between receptor structure and cardiac glycoside binding.
48 dynamically by a mechanism that utilizes the cardiac glycoside-binding site and an endogenous ligand(
49 ite and an endogenous ligand(s) and that its cardiac glycoside-binding site can play a physiological
50        The physiological significance of the cardiac glycoside-binding site on the Na,K-ATPase remain
51 f the Na,K-ATPase to investigate whether the cardiac glycoside-binding site plays any physiological r
52                        EcCYP87A126 initiates cardiac glycoside biosynthesis via sterol side-chain cle
53      We analyzed gene expression to identify cardiac glycoside biosynthetic enzymes in E. cheiranthoi
54 s begin elucidation of the E. cheiranthoides cardiac glycoside biosynthetic pathway and demonstrate i
55 erations perturb the interaction between the cardiac glycoside bufalin and the Na(+)/K(+)-ATPase.
56 oughput screening effort that identified the cardiac glycoside bufalin as a potent small-molecule inh
57                                       Severe cardiac glycoside cardiotoxicity after ingestion of yell
58                                          The cardiac glycoside (CG) digoxin is a generic drug approve
59 in belongs to a naturally occurring class of cardiac glycosides (CG); digitoxin is clinically approve
60                                          The cardiac glycosides (CGs) digoxin, digitoxin and ouabain,
61                       The therapeutic use of cardiac glycosides (CGs), agents commonly used in treati
62 ly and functionally related compounds of the cardiac glycoside class and known inhibitors of Na(+)K(+
63 ns represent the major binding sites for the cardiac glycoside class of drugs.
64 ovide evidence that oleandrin, the principal cardiac glycoside component of PBI-05204, can quantitati
65 roids were investigated by comparing various cardiac glycoside compounds like ouabain, digoxin, digit
66                                        Other cardiac glycoside compounds tested also showed neuroprot
67 ing a high-content screen, we identified the cardiac glycoside convallatoxin as an effective compound
68 the extent to which high-affinity binding of cardiac glycosides correlates with their potency in inhi
69 rrors of hepatic metabolism and suggest that cardiac glycosides could provide an approach for reducin
70                      Using E. cheiranthoides cardiac glycoside-deficient lines, we conducted insect e
71                                   A purified cardiac glycoside derived from the foxglove plant, digox
72                    Oleandrin, a polyphenolic cardiac glycoside derived from the leaves of Nerium olea
73              The therapeutic efficacy of the cardiac glycoside digitoxin in patients with heart failu
74 igh affinity scFv antibody that binds to the cardiac glycoside digoxigenin.
75                                 Notably, the cardiac glycoside digoxin and other drugs identified in
76 ell-based reporter system, we identified the cardiac glycoside digoxin as a specific inhibitor of ROR
77  patients with chronic LV dysfunction is the cardiac glycoside digoxin.
78 pha3beta1 isoforms showed that the classical cardiac glycoside, digoxin, is partially alpha2-selectiv
79                                Coordinately, cardiac glycosides downregulate known miR-132 targets, i
80  focuses on the quantitative analysis of the cardiac glycoside drug digitoxin and its three main meta
81 ss of CFTR protein, which was rescued by the cardiac glycoside drugs digitoxin and ouabain.
82  of human cancer cells, is down-regulated by cardiac glycoside drugs digoxin and ouabain, potent inhi
83             We had previously shown that the cardiac glycoside drugs digoxin, digitoxin and ouabain b
84                         We hypothesized that cardiac glycoside drugs might block the binding reaction
85           Digitoxin and structurally related cardiac glycoside drugs potently block activation of the
86                This is the first report that cardiac glycoside drugs, by initiating the Src/MAPK sign
87 tly, addition of 30 nM concentrations of the cardiac glycoside drugs, prevented loss of both CFTR pro
88                                              Cardiac glycosides exert a positive inotropic effect by
89 stantially increases adult survivorship upon cardiac glycoside exposure.
90           Here, we report 3 compounds in the cardiac glycoside family, ouabain, gitoxigenin, and digi
91 .8-48-fold increases in the I50 of different cardiac glycosides for inhibition of the Na,K-ATPase act
92 n derivatives explains beneficial effects of cardiac glycosides for treatment of heart failure and po
93 e increased capacity of the liver to extract cardiac glycosides from the plasma.
94                                              Cardiac glycosides had lesser to no effect on two broad
95                                              Cardiac glycosides have played a prominent role in the t
96 ain cleavage, and EcCYP716A418 has a role in cardiac glycoside hydroxylation.
97 nd pharmacodynamics of different variants of cardiac glycosides identified the mechanism of inhibitio
98 ered HDR-suppressing functions of anticancer cardiac glycosides in human glioblastomas and glioma can
99   Because the alpha1 isoform is sensitive to cardiac glycosides in humans, we developed mice in which
100 se findings support further investigation of cardiac glycosides in providing neuroprotection in the c
101 ibian muscle fibres following treatment with cardiac glycosides in the hypertonic gluconate-containin
102                                  The role of cardiac glycosides in treating patients with chronic hea
103         Suppression of autosis by ouabain, a cardiac glycoside, in humanized Na+,K+-ATPase-knockin mi
104                Here, we report that multiple cardiac glycosides, including digitoxin and digoxin, are
105                   Eleven of these drugs were cardiac glycosides, including digoxin, ouabain, and pros
106 ls and, unpredictably, identified a group of cardiac glycosides, including ouabain and digoxin, as po
107 1A1, the a1 subunit of the NKA and target of cardiac glycosides, increased Na(+) levels to a lesser e
108                                              Cardiac glycoside-induced cellular cytotoxicity and IL-1
109 a divergent mechanistic relationship between cardiac glycoside-induced cytotoxicity and Na+/K+-ATPase
110                                              Cardiac glycoside-induced intracellular K(+) depletion c
111                            Digoxin and other cardiac glycosides inhibit hypoxia-inducible factor-1 (H
112  this link suggests a possible mechanism for cardiac glycoside inhibition of the Na,K-ATPase, such th
113                      Furthermore, ouabain, a cardiac glycoside inhibitor of the Na(+)/K(+)-ATPase, po
114               Despite contributing little to cardiac glycoside-insensitivity in vitro, A119S, like su
115                        Our data suggest that cardiac glycosides interact with phosphorylated mediator
116  to explain the positive inotropic effect of cardiac glycosides invokes altered Na+-Ca2+ exchange act
117 ext-preserving OTCD protocol, which improved cardiac glycoside ion yields by at least 1 order of magn
118        Inhibition of Na,K-ATPase activity by cardiac glycosides is believed to be the major mechanism
119 ously that inhibition of hERG trafficking by cardiac glycosides is initiated via direct block of Na(+
120 kers), cocaine, cyanide, digoxin and related cardiac glycosides, local anesthetics, methemoglobinemia
121                     These data indicate that cardiac glycosides may block viral penetration into the
122                                              Cardiac glycoside-mediated effects on NMD are dependent
123                 We report the discovery that cardiac glycosides, natural products in clinical use for
124 he associations among breast cancer, AF, and cardiac glycosides need further investigation.
125 fer modest increases in the concentration of cardiac glycoside needed to produce 50% inhibition of ac
126 ibition of ATG-dependent phagocytosis by the cardiac glycoside neriifolin, an inhibitor of the Na(+),
127 uroprotective action in ischemic stroke, the cardiac glycoside neriifolin, and demonstrated that its
128       We postulated that increased uptake of cardiac glycosides observed after pretreatment of animal
129                     Here, we report that the cardiac glycosides oleandrin, ouabain, and digoxin induc
130 ger is absolutely required for the effect of cardiac glycosides on Ca2+(i).
131 ockdown significantly enhanced the effect of cardiac glycosides on IDO1 expression and kynurenine pro
132                 Effects of topically applied cardiac glycosides on intraocular pressure in rabbits ha
133                            Thus, an existing cardiac glycoside or closely related compound could prov
134 ither indirectly after long-term exposure to cardiac glycosides or directly after exposure to gramici
135 over time and sensitive to inhibition by the cardiac glycoside ouabain, a specific inhibitor of the N
136 appears to be an isomer of the plant-derived cardiac glycoside ouabain, if not ouabain itself.
137 uabain (AO), a fluorescent derivative of the cardiac glycoside ouabain, to mAbs 26-10, 45-20, and 40-
138                       This revealed that the cardiac glycosides ouabain and digoxin inhibited kynuren
139      Blocking Na+, K(+)-ATPase activity with cardiac glycosides (ouabain or strophanthidin, 1 mM) or
140 n of alpha3 using a low concentration of the cardiac glycoside, ouabain, resulted in a modest increas
141 Na,K-ATPase is specifically inhibited by the cardiac glycoside, ouabain.
142 drug-induced trafficking inhibition in which cardiac glycosides produce a [K(+)](i)-mediated conforma
143             We show that resistance to toxic cardiac glycosides produced by plants and bufonid toads
144                         In response to toxic cardiac glycosides produced by these plants, the monarch
145 nthetic pathway and demonstrate in vivo that cardiac glycoside production allows Erysimum to escape f
146               In EcCYP87A126 knockout lines, cardiac glycoside production was eliminated.
147 These results define the distribution of the cardiac glycoside receptor isoforms in the human heart a
148 ng between anthroylouabain (AO) bound to the cardiac glycoside receptor site on alpha and the carbohy
149 ion is negligible, indicating that the human cardiac glycoside receptors are alpha1beta1, alpha2beta1
150                                We found that cardiac glycosides reduce the production of apolipoprote
151 revealed that the treatment of patients with cardiac glycosides reduced serum LDL-C levels.
152  lenta strains, which is attributable to the cardiac glycoside reductase 2 (Cgr2) enzyme.
153 nfused with Digibind to sequester endogenous cardiac glycoside(s) produced similar effects on both re
154  have predators and parasitoids that feed on cardiac-glycoside-sequestering insects also evolved Na(+
155 spectrometry imaging (MALDI MSI) analysis of cardiac-glycoside sequestration in D. plexippus.
156 uces both ancestral glucosinolates and novel cardiac glycosides, served as a model.
157 nd 122) in ATPalpha that are associated with cardiac glycoside specialization(13,14).
158                                              Cardiac glycosides such as ouabain and digoxin specifica
159            Na(+),K(+)-ATPase is inhibited by cardiac glycosides such as ouabain, and palytoxin, which
160 echanism by which digitoxin and other active cardiac glycosides, such as digoxin, exert system-wide a
161  The Na,K-ATPase contains a binding site for cardiac glycosides, such as ouabain, digoxin, and digito
162            Several studies also suggest that cardiac glycosides, such as ouabain, function by mechani
163      Our results define a novel activity for cardiac glycosides that could prove relevant to the trea
164 e the fact that the molecular target for the cardiac glycosides, the alpha-subunit of sarcolemmal Na+
165    'Monarch flies' retained small amounts of cardiac glycosides through metamorphosis, a trait that h
166 ntly evolved to colonize plants that produce cardiac glycoside toxins(6-11).
167 creased Na(+) levels to a lesser extent than cardiac glycoside treatment and did not affect IDO1 expr
168                Mechanistically, we show that cardiac glycoside treatment resulted in curtailing the l
169                                              Cardiac glycoside use was strongly associated with incid
170  toxicity and adverse events associated with cardiac glycosides use in humans and that targeted anti-
171 s and inhibitory potencies of a series of 37 cardiac glycosides using radioligand binding and ATPase
172                             Using a panel of cardiac glycoside variants, we assessed the structural e
173 pha2 isoform, which is normally sensitive to cardiac glycosides, was made resistant to these compound
174 icity > 15% and those containing cardiotoxic cardiac glycosides were eliminated.
175 y experiments with these lines revealed that cardiac glycosides were highly effective defenses agains
176                                 Although the cardiac glycosides were identified in an evaluation of 2
177 strated that the proapoptotic effects of the cardiac glycosides were linked to their abilities to ind
178 d sample for measurement of electrolytes and cardiac glycosides were taken before treatment and at 12
179 iandrogen therapy, we identify Peruvoside, a cardiac glycoside, which can potently inhibit both andro
180 ansport activity is effectively inhibited by cardiac glycosides, which bind to the extracellular side
181          Among these drugs are plant-derived cardiac glycosides, which have been used by various cult
182 alists, from aphids to beetles, to sequester cardiac glycosides, which in turn provide defense agains
183 on of unrelated herbivorous insects to toxic cardiac glycosides, which primarily occurs via a small s

 
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