ライフサイエンスコーパス: nystatin

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 Experiments with nystatin, a drug known to depolarize cell membranes, pro

8 ced turgor caused by treatment of cells with nystatin, a drug that increases membrane permeability an

9 sembles the clinically important antifungals nystatin A1 and amphotericin B, but it has several disti

10 in vitro activity of nystatin and liposomal nystatin against 103 Candida isolates to determine the e

11 nystatin 2 million units (37 patients) or to nystatin alone (43 patients).

12 nificantly less than that of patients taking nystatin alone; growth of aerobic gram-positive flora, a

13 Treatment of cells with nystatin also inhibited VacA-induced cell vacuolation.

14 BV transcytosis was substantially reduced by nystatin, an inhibitor of caveolin-mediated virus entry.

15 The ergosterol ligands filipin, nystatin and amphotericin B block the in vitro fusion of

16 cytosis via clathrin-coated pits, but not by nystatin and cholera toxin B, which blocks endocytosis v

17 the caveolin-mediated endocytosis inhibitors nystatin and filipin III had no effect.

18 Nystatin and filipin III, two cholesterol-binding agents

19 Also, nystatin and filipin, inhibitors of micropinocytosis fro

20 he lack of effect of the caveolae inhibitors nystatin and filipin.

21 We investigated the in vitro activity of nystatin and liposomal nystatin against 103 Candida isol

22 Nystatin and liposomal nystatin in general showed good a

23 se in parallel with the amphotericin B MICs, nystatin and liposomal nystatin MICs of 1 to 2 and 0.5 t

24 Although the MICs of nystatin and liposomal nystatin tended to rise in parall

25 s at which 90% of isolates were inhibited of nystatin and liposomal nystatin were 2 and 1 microg/ml,

26 cause (1) the sterol-binding agents filipin, nystatin and methyl beta-cyclodextrin specifically block

27 ibited by the cholesterol-sequestering drugs nystatin and methyl-beta-cyclodextrin, the dynamin-speci

28 centrifugation and found to be sensitive to nystatin and oseltamivir.

29 Nystatin and progesterone pretreatment of dCAD cells sig

30 olesterol binding agents such as filipin and nystatin and the tyrosine kinase inhibitor genistein dra

31 ng drugs such as methyl-beta-cyclodextrin or nystatin and then exposed to virus.

32 ynasore, PitStop2, methyl-beta-cyclodextrin, nystatin, and filipin (specific inhibitors of either cla

33 ensitive to the cholesterol-aggregating drug nystatin, and is independent of AP-2 clathrin adaptor an

34 dosomal pathways (amiloride, cytochalasin D, nystatin, and methyl-beta-cyclodextrin) showed that hCTR

35 lesterol-extracting agents, cyclodextrin and nystatin, and polyanion heparin significantly inhibited

36 those previously reported for ketoconazole, nystatin, and propiconazole.

37 elaying systemic treatment, exclusive use of nystatin, and treating for <10 days was associated with

38 permeabilized basolaterally or apically with nystatin, AP activated apical Cl- and basolateral K+ con

39 allel in the presence of the antifungal drug nystatin are frequently incompatible with one another.

40 n and pro-apoptotic effects are inhibited by nystatin but not chlorpromazine, suggesting an involveme

41 le cholesterol-binding agents (digitonin and nystatin), but not the lipid-binding agent xylazine, inh

42 The partition coefficient of nystatin changes dramatically with membrane sterol conte

43 The structure of the nystatin channel is not clear, but it is known that mult

44 ilm, exhibited resistance to amphotericin B, nystatin, chlorhexidine, and fluconazole, with 50% reduc

45 he internalization of rAdpF was inhibited by nystatin, cytochalasin, latrunculin, nocodazole, and wor

46 Treatment with nystatin did not impair SV40 binding but did block the p

47 ." Cholesterol-binding reagents, filipin and nystatin, disrupt the structure and function of caveolae

48 of alcohols on fusion rates, we utilized the nystatin/ergosterol fusion assay to measure fusion of li

49 onstituted into planar lipid bilayers by the nystatin/ergosterol fusion technique.

50 In contrast, nystatin fluorescence intensity responded to changes in

51 n the plane of the membrane as determined by nystatin fluorescence.

52 Nystatin and liposomal nystatin in general showed good activity against all Can

53 Receptor-bound 125I-TGF-beta1 undergoes nystatin-inhibitable rapid degradation in CHO-K1 cells b

54 1Lu cells (which, like CHO-K1 cells, exhibit nystatin-inhibitable rapid degradation of receptor-bound

55 he partition coefficient for partitioning of nystatin into ergosterol/dimyristoyl-L-alpha-phosphatidy

56 Nystatin isolated from Streptomyces is a polyene antibio

57 to I(sc) was unaffected with apical membrane nystatin-mediated permeabilization, whereas the sAC-depe

58 Treatment with the inhibitors nystatin, methyl-beta-cyclodextrin, and genistein, as we

59 provided a slightly wider range of liposomal nystatin MICs (0.06 to >16 microg/ml).

60 -2, they were markedly higher than liposomal nystatin MICs in AM3.

61 similar to or slightly lower than liposomal nystatin MICs in RPMI 1640 and RPMI-2, they were markedl

62 amphotericin B MICs, nystatin and liposomal nystatin MICs of 1 to 2 and 0.5 to 1 microg/ml, respecti

63 etween fluconazole and nystatin or liposomal nystatin MICs was observed.

64 While nystatin MICs were similar to or slightly lower than lip

65 We also compared the nystatin MICs with those of amphotericin B and fluconazo

66 stance, these results suggest that liposomal nystatin might have activity against some amphotericin B

67 is not clear, but it is known that multiple nystatin monomers must aggregate to form channels in a s

68 Nystatin (nys) is an antifungal agent that preferentiall

69 g agents methyl beta cyclodextrin (MBCD) and nystatin (Nys), drugs inhibiting caveolar endocytosis.

70 Here we report that nystatin (NYT), an antifungal drug of the family of poly

71 f clathrin-dependent endocytosis) but not by nystatin or filipin, which inhibit clathrin-independent

72 No correlation between fluconazole and nystatin or liposomal nystatin MICs was observed.

73 ntent of the target cells when administering nystatin or other polyene antibiotics.

74 turgor caused by either hyperosmotic stress, nystatin, or removal of cell wall activate MAPK Hog1 spe

75 eal a new membrane phenomenon, that is, that nystatin partitioning is affected by the extent of stero

76 for example, there is a >3-fold increase in nystatin partitioning with a minute change (approximatel

77 es at 35 degrees C and 1.8 mM Ca2+ using the nystatin patch clamp method.

78 brief microperfusion) as measured using the nystatin patch method of whole cell recording.

79 hout of cytosolic constituents, we next used nystatin perforated patch, but did not find any Epo-indu

80 A nystatin perforated-patch whole-cell method and fluoresc

81 milar activation of 4MalphaG was observed in nystatin-perforated cells, indicating that the entry of

82 ed under an apical to serosal K+ gradient in nystatin-perforated colon is generated at the basolatera

83 ls, when measured with the cell-attached and nystatin-perforated patch clamps, respectively.

84 e freshly isolated and patch-clamped using a nystatin-perforated patch method.

85 Contrary to our expectations, nystatin-perforated patch recordings of whole-cell K+ cu

86 pathological effects of nicotine, we used a nystatin-perforated patch-clamp technique to study Ca(2+

87 Both cell-attached and nystatin-perforated patch-clamping were performed to rec

88 Slow whole-cell recordings, using nystatin-perforated patches from transfected CHO-K1 cell

89 ateral potassium transport was studied using nystatin permeabilization.

90 els of 23 mmHg or 100 mmHg, and subsequently nystatin permeabilized (50 microM), showed that high PO2

91 merase activity: NysKR1 from module 1 of the nystatin PKS, whose stereospecificity can be predicted f

92 nverted to either the candidin polyol or the nystatin polyol.

93 The fluorescent probes used (bis-pyrene, nystatin, prodan, and merocyanine) were chosen because t

94 Colonies were then selected that were nystatin-resistant in the presence of 3-ketoergostadiene

95 GLUT4 is internalized by an AP-2-dependent, nystatin-resistant pathway that requires the FQQI GLUT4

96 lar manner to degrade the receptor through a nystatin-sensitive lipid raft pathway.

97 Insulin inhibits GLUT4 uptake by the nystatin-sensitive pathway and, consequently, GLUT4 is i

98 e selection protocol involving screening for nystatin-sensitive transformants.

99 pendent on sterol esterification for growth, nystatin-sensitive, temperature-sensitive, and anaerobic

100 gents methyl beta-cyclo dextrin (MbetaCD) or nystatin significantly inhibited the expression of viral

101 Although the MICs of nystatin and liposomal nystatin tended to rise in parallel with the amphoterici

102 We next used nystatin to selectively permeabilize the basolateral mem

103 orbitol, galactose, pH 8, minimal medium and nystatin treatment.

104 Following nystatin-treatment, we elevated intracellular levels of

105 Nystatin was employed to selectively permeabilize the ba

106 eral membranes with the monovalent ionophore nystatin was used to isolate basolateral K+ and apical C

107 tes were inhibited of nystatin and liposomal nystatin were 2 and 1 microg/ml, respectively.

108 olished in the presence of either filipin or nystatin, which are cholesterol-binding reagents known t

109 lization pathways, but not by treatment with nystatin, which blocks caveolar uptake.

110 to methyl-beta-cyclodextrin (M beta CD) and nystatin, which disrupt lipid rafts by removing choleste

111 treating cells with the phorbol ester PMA or nystatin, which selectively disrupts caveolae.