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1 g rats exposed to fungicide (fluconazole and nystatin).
2 cidification but was not sensitive to PMA or nystatin.
3 re also resistant to the polyene antibiotic, nystatin.
4 ther cholesterol-binding agents, filipin and nystatin.
5 sting of gentamicin 80 mg+polymyxin E 100 mg+nystatin 2 million units (37 patients) or to nystatin al
6 ith filipin (0.16-0.3 micrograms/ml) or with nystatin (25 micrograms/ml) for 30 min showed depletion
7  the C10 hydroxylation of 10-deoxynystain to nystatin A(1), a clinically important antifungal.
8 esolution crystal structure of NysL bound to nystatin A(1).
9                             Experiments with nystatin, a drug known to depolarize cell membranes, pro
10 ced turgor caused by treatment of cells with nystatin, a drug that increases membrane permeability an
11  TKP 4-decorating liposomes were loaded with nystatin, a renal-protective compound with systemic side
12 sembles the clinically important antifungals nystatin A1 and amphotericin B, but it has several disti
13                  Results showed that AmB and nystatin actually increased SARS-CoV-2 replication in Ve
14  in vitro activity of nystatin and liposomal nystatin against 103 Candida isolates to determine the e
15 nystatin 2 million units (37 patients) or to nystatin alone (43 patients).
16 nificantly less than that of patients taking nystatin alone; growth of aerobic gram-positive flora, a
17                      Treatment of cells with nystatin also inhibited VacA-induced cell vacuolation.
18 BV transcytosis was substantially reduced by nystatin, an inhibitor of caveolin-mediated virus entry.
19              The ergosterol ligands filipin, nystatin and amphotericin B block the in vitro fusion of
20 cytosis via clathrin-coated pits, but not by nystatin and cholera toxin B, which blocks endocytosis v
21 the caveolin-mediated endocytosis inhibitors nystatin and filipin III had no effect.
22                                              Nystatin and filipin III, two cholesterol-binding agents
23                                        Also, nystatin and filipin, inhibitors of micropinocytosis fro
24 he lack of effect of the caveolae inhibitors nystatin and filipin.
25     We investigated the in vitro activity of nystatin and liposomal nystatin against 103 Candida isol
26                                              Nystatin and liposomal nystatin in general showed good a
27 se in parallel with the amphotericin B MICs, nystatin and liposomal nystatin MICs of 1 to 2 and 0.5 t
28                         Although the MICs of nystatin and liposomal nystatin tended to rise in parall
29 s at which 90% of isolates were inhibited of nystatin and liposomal nystatin were 2 and 1 microg/ml,
30 cause (1) the sterol-binding agents filipin, nystatin and methyl beta-cyclodextrin specifically block
31 ibited by the cholesterol-sequestering drugs nystatin and methyl-beta-cyclodextrin, the dynamin-speci
32  centrifugation and found to be sensitive to nystatin and oseltamivir.
33                                              Nystatin and progesterone pretreatment of dCAD cells sig
34                        Raft perturbation via nystatin and resveratrol significantly altered DR4/raft
35 olesterol binding agents such as filipin and nystatin and the tyrosine kinase inhibitor genistein dra
36 ng drugs such as methyl-beta-cyclodextrin or nystatin and then exposed to virus.
37 sruptors (methyl-beta-cyclodextrin (MCD) and Nystatin) and Ang II stimulation variably increased O(2)
38 ynasore, PitStop2, methyl-beta-cyclodextrin, nystatin, and filipin (specific inhibitors of either cla
39 ensitive to the cholesterol-aggregating drug nystatin, and is independent of AP-2 clathrin adaptor an
40 dosomal pathways (amiloride, cytochalasin D, nystatin, and methyl-beta-cyclodextrin) showed that hCTR
41 lesterol-extracting agents, cyclodextrin and nystatin, and polyanion heparin significantly inhibited
42  those previously reported for ketoconazole, nystatin, and propiconazole.
43 elaying systemic treatment, exclusive use of nystatin, and treating for <10 days was associated with
44 permeabilized basolaterally or apically with nystatin, AP activated apical Cl- and basolateral K+ con
45 ry mucormycosis, using AmB.IMPORTANCEAmB and nystatin are common treatments for fungal infections but
46 allel in the presence of the antifungal drug nystatin are frequently incompatible with one another.
47 n and pro-apoptotic effects are inhibited by nystatin but not chlorpromazine, suggesting an involveme
48 le cholesterol-binding agents (digitonin and nystatin), but not the lipid-binding agent xylazine, inh
49                 The partition coefficient of nystatin changes dramatically with membrane sterol conte
50                         The structure of the nystatin channel is not clear, but it is known that mult
51 ilm, exhibited resistance to amphotericin B, nystatin, chlorhexidine, and fluconazole, with 50% reduc
52 he internalization of rAdpF was inhibited by nystatin, cytochalasin, latrunculin, nocodazole, and wor
53                         The antifungal agent nystatin decreased C. albicans-specific Th17 cells in th
54                               Treatment with nystatin did not impair SV40 binding but did block the p
55 ." Cholesterol-binding reagents, filipin and nystatin, disrupt the structure and function of caveolae
56 of alcohols on fusion rates, we utilized the nystatin/ergosterol fusion assay to measure fusion of li
57 onstituted into planar lipid bilayers by the nystatin/ergosterol fusion technique.
58 ibiotic treatment, local antifungal therapy (nystatin eye ointment and propamidine isethionate eye dr
59                                 In contrast, nystatin fluorescence intensity responded to changes in
60 n the plane of the membrane as determined by nystatin fluorescence.
61 pension containing colistin, tobramycin, and nystatin for the duration of mechanical ventilation, plu
62  this study, we first predicted that AmB and nystatin had strong interactions with severe acute respi
63         These findings indicate that AmB and nystatin have the potential to enhance disease when give
64                       Nystatin and liposomal nystatin in general showed good activity against all Can
65           At optimal concentrations, AmB and nystatin increase SARS-CoV-2 replication by up to 100- a
66      Receptor-bound 125I-TGF-beta1 undergoes nystatin-inhibitable rapid degradation in CHO-K1 cells b
67 1Lu cells (which, like CHO-K1 cells, exhibit nystatin-inhibitable rapid degradation of receptor-bound
68 he partition coefficient for partitioning of nystatin into ergosterol/dimyristoyl-L-alpha-phosphatidy
69                                              Nystatin isolated from Streptomyces is a polyene antibio
70 rmacological inhibition of endocytosis using nystatin, leads to reduced entry into the intestinal muc
71 to I(sc) was unaffected with apical membrane nystatin-mediated permeabilization, whereas the sAC-depe
72                Treatment with the inhibitors nystatin, methyl-beta-cyclodextrin, and genistein, as we
73 provided a slightly wider range of liposomal nystatin MICs (0.06 to >16 microg/ml).
74 -2, they were markedly higher than liposomal nystatin MICs in AM3.
75  similar to or slightly lower than liposomal nystatin MICs in RPMI 1640 and RPMI-2, they were markedl
76  amphotericin B MICs, nystatin and liposomal nystatin MICs of 1 to 2 and 0.5 to 1 microg/ml, respecti
77 etween fluconazole and nystatin or liposomal nystatin MICs was observed.
78                                        While nystatin MICs were similar to or slightly lower than lip
79                         We also compared the nystatin MICs with those of amphotericin B and fluconazo
80 stance, these results suggest that liposomal nystatin might have activity against some amphotericin B
81  is not clear, but it is known that multiple nystatin monomers must aggregate to form channels in a s
82 equently, we investigated the impact of AmB, nystatin, natamycin, fluconazole, and caspofungin on SAR
83                                              Nystatin (nys) is an antifungal agent that preferentiall
84 g agents methyl beta cyclodextrin (MBCD) and nystatin (Nys), drugs inhibiting caveolar endocytosis.
85                          Here we report that nystatin (NYT), an antifungal drug of the family of poly
86 f clathrin-dependent endocytosis) but not by nystatin or filipin, which inhibit clathrin-independent
87       No correlation between fluconazole and nystatin or liposomal nystatin MICs was observed.
88 ntent of the target cells when administering nystatin or other polyene antibiotics.
89 turgor caused by either hyperosmotic stress, nystatin, or removal of cell wall activate MAPK Hog1 spe
90 eal a new membrane phenomenon, that is, that nystatin partitioning is affected by the extent of stero
91  for example, there is a >3-fold increase in nystatin partitioning with a minute change (approximatel
92 es at 35 degrees C and 1.8 mM Ca2+ using the nystatin patch clamp method.
93  brief microperfusion) as measured using the nystatin patch method of whole cell recording.
94 hout of cytosolic constituents, we next used nystatin perforated patch, but did not find any Epo-indu
95                                            A nystatin perforated-patch whole-cell method and fluoresc
96 milar activation of 4MalphaG was observed in nystatin-perforated cells, indicating that the entry of
97 ed under an apical to serosal K+ gradient in nystatin-perforated colon is generated at the basolatera
98 ls, when measured with the cell-attached and nystatin-perforated patch clamps, respectively.
99 e freshly isolated and patch-clamped using a nystatin-perforated patch method.
100                Contrary to our expectations, nystatin-perforated patch recordings of whole-cell K+ cu
101  pathological effects of nicotine, we used a nystatin-perforated patch-clamp technique to study Ca(2+
102                       Both cell-attached and nystatin-perforated patch-clamping were performed to rec
103            Slow whole-cell recordings, using nystatin-perforated patches from transfected CHO-K1 cell
104 ateral potassium transport was studied using nystatin permeabilization.
105 els of 23 mmHg or 100 mmHg, and subsequently nystatin permeabilized (50 microM), showed that high PO2
106 merase activity: NysKR1 from module 1 of the nystatin PKS, whose stereospecificity can be predicted f
107 nverted to either the candidin polyol or the nystatin polyol.
108     The fluorescent probes used (bis-pyrene, nystatin, prodan, and merocyanine) were chosen because t
109        Colonies were then selected that were nystatin-resistant in the presence of 3-ketoergostadiene
110  GLUT4 is internalized by an AP-2-dependent, nystatin-resistant pathway that requires the FQQI GLUT4
111 lar manner to degrade the receptor through a nystatin-sensitive lipid raft pathway.
112         Insulin inhibits GLUT4 uptake by the nystatin-sensitive pathway and, consequently, GLUT4 is i
113 e selection protocol involving screening for nystatin-sensitive transformants.
114 pendent on sterol esterification for growth, nystatin-sensitive, temperature-sensitive, and anaerobic
115 -vesicular sterol exchange and alleviate the nystatin-sensitivity of lam2Delta yeast cells.
116 gents methyl beta-cyclo dextrin (MbetaCD) or nystatin significantly inhibited the expression of viral
117  Although the MICs of nystatin and liposomal nystatin tended to rise in parallel with the amphoterici
118                                 We next used nystatin to selectively permeabilize the basolateral mem
119 orbitol, galactose, pH 8, minimal medium and nystatin treatment.
120                                    Following nystatin-treatment, we elevated intracellular levels of
121                                              Nystatin was employed to selectively permeabilize the ba
122 eral membranes with the monovalent ionophore nystatin was used to isolate basolateral K+ and apical C
123 tes were inhibited of nystatin and liposomal nystatin were 2 and 1 microg/ml, respectively.
124 olished in the presence of either filipin or nystatin, which are cholesterol-binding reagents known t
125 lization pathways, but not by treatment with nystatin, which blocks caveolar uptake.
126  to methyl-beta-cyclodextrin (M beta CD) and nystatin, which disrupt lipid rafts by removing choleste
127 treating cells with the phorbol ester PMA or nystatin, which selectively disrupts caveolae.

 
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