ライフサイエンスコーパス: trifluoperazine

1 thiazine-like antipsychotic drugs, including trifluoperazine.

2 stoma and glioma cells that was inhibited by trifluoperazine.

3 ith the cell-permeable calmodulin antagonist trifluoperazine.

4 by two calmodulin antagonists, tamoxifen and trifluoperazine.

5 Tamoxifen, 10 microm, and trifluoperazine, 10 microm, induce 7.3 +/- 1.8-fold and

6 Incubation with trifluoperazine (30 microM) and W-7 (150 microM) shifted

7 100 microm), or by the calmodulin antagonist trifluoperazine (50 microm).

8 Trifluoperazine, a calmodulin antagonist, inhibited Fas-

9 In contrast, trifluoperazine, a cell-permeable calmodulin antagonist,

10 .2.3, which was inhibited by cytochalasin B, trifluoperazine, a combination of sodium azide and 2-deo

11 Interestingly, trifluoperazine, a compound that protects cells from isc

12 ion assays; this interaction is inhibited by trifluoperazine, a drug known to hamper binding of wild-

13 Finally, chlorpromazine, dibucaine, and trifluoperazine, agents that induce pores in an arrested

14 Trifluoperazine also inhibited this chimera in the absen

15 In contrast, trifluoperazine, an antagonist of calcium/calmodulin kin

16 d by 84 and 91% in the presence of 25 microM trifluoperazine and 100 microM W-7, two calmodulin inhib

17 at tau-1 site is approximately 20 microM for trifluoperazine and approximately 120 microM for chlorpr

18 l markers to identify drug binding sites for trifluoperazine and bepridil on cTnC.

19 was inhibited by the calmodulin antagonists, trifluoperazine and calmidazolium.

20 structurally distinct calmodulin antagonists trifluoperazine and CGS9343B attenuated the interaction

21 e commonly used neuroleptics chlorpromazine, trifluoperazine and clozapine inhibit PP-2B but not PP-1

22 n be inhibited by the calmodulin antagonists trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthal

23 The calmodulin antagonists trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthal

24 re, we have examined the previously reported trifluoperazine and other pharmaceuticals that have simi

25 with pFN, and 3) the calmodulin antagonists trifluoperazine and tamoxifen completely inhibit the pFN

26 xytamoxifen, and the calmodulin antagonists, trifluoperazine and the calmidazolium, with IC50 values

27 d on the known phenothiazine Ndh inhibitors, trifluoperazine and thioridazine.

28 ely eliminated by the calmodulin antagonists trifluoperazine and W-7 and the Ca2+/calmodulin-dependen

29 promoter of protein phosphorylation, whereas trifluoperazine and W-7, antagonists of calmodulin, caus

30 was compared to the effects of okadaic acid, trifluoperazine and W-7, which are commonly used in stud

31 izing responses were abolished by apamin and trifluoperazine and were accentuated by the SK channel a

32 inobutyl)-5-chloro-1-naphthalenesulfonamide; trifluoperazine), and CaM-activated protein kinases (N-[

33 (inorganic phosphate, butanedione monoxime, trifluoperazine, and blebbistatin) are modified by twitc

34 rally disparate calmodulin antagonists (W-7, trifluoperazine, and calmidazolium) resulted in the robu

35 napthalenesulfonamide derivatives W-7/W-13, trifluoperazine, and calmidazolium, are used widely to i

36 ral antipsychotic drugs, such as sertraline, trifluoperazine, and fluphenazine, were found to be dire

37 ationic amphiphiles, such as chlorpromazine, trifluoperazine, and imipramine, which mimic the effect

38 bongkrekic acid, Nortriptyline, Desipramine, Trifluoperazine, and Maprotiline.

39 wn PT inhibitors, namely cyclosporin A, ADP, trifluoperazine, and Mg(2+).

40 h was inhibited by the calmodulin antagonist trifluoperazine, and reaction with anti-bovine brain cal

41 sting phenothiazine-like antipsychotic drug, trifluoperazine, as a potential anti-CSC agent that coul

42 ]Met-labeled cTnC indicate that bepridil and trifluoperazine bind to similar sites but only in the pr

43 s with vanadate did not induce Cap43 nor did trifluoperazine block its induction by nickel; however,

44 Consistently, trifluoperazine blocked Fas-promoted cell survival.

45 Calmodulin inhibitors (W7 and trifluoperazine) blocked the P(f) response to vasopressi

46 Cyclosporin A plus trifluoperazine, blockers of the mitochondrial permeabil

47 Here we demonstrate that tamoxifen and trifluoperazine, both potent calmodulin antagonists, ind

48 inohexyl)-5-chloro-1-naphthalenesulfonamide; trifluoperazine), but not their less-active analogues (N

49 nd were blocked by one calmodulin inhibitor, trifluoperazine, but not by another, calmidazolium.

50 ated phosphorylation was markedly reduced by trifluoperazine, chlorpromazine, and naphthalene sulfona

51 Phenothiazine analogues, trifluoperazine, Compound 1, and Compound 2 inhibit the

52 At high trifluoperazine concentrations, shedding of WT L-selecti

53 After anti-Fas antibody, cyclosporin A and trifluoperazine decreased cytochrome c release but did n

54 compound EGTA and by calmodulin antagonists trifluoperazine dimaleate and W-7.

55 n inhibitors, monodansylcadaverine, W-7, and trifluoperazine, followed by measurement of cAMP.

56 ro-1-naphthalene sulfonamide, tamoxifen, and trifluoperazine) greatly inhibit Fas-CaM interactions by

57 a substrate, PP-2B activity is inhibited by trifluoperazine > chlorpromazine > clozapine.

58 urthermore, the use of the FDA-approved drug trifluoperazine hydrochloride (TFP), which has been show

59 did not respond to class 2 amphiphiles (e.g. trifluoperazine, imipramine, and U18666A); these agents

60 Fas antibody, tamoxifen, and trifluoperazine induced dose-dependent apoptosis only in

61 Calmodulin inhibition by trifluoperazine induced shedding in both WT and chimera

62 Both tamoxifen- and trifluoperazine-induced apoptosis are increased 1.6 +/-

63 of the calmodulin antagonists, tamoxifen or trifluoperazine, induces osteoclast apoptosis dose-depen

64 The calmodulin antagonists W-7 and trifluoperazine inhibited Abeta formation and enhanced t

65 We demonstrated that trifluoperazine inhibited CSC tumor spheroid formation a

66 Trifluoperazine inhibited the tumor growth and enhanced

67 Trifluoperazine inhibited Wnt/beta-catenin signaling in

68 Trifluoperazine inhibition is non-competitive for NADH,

69 genetic inhibition of alpha-CaMKII by using trifluoperazine, KN93, and alpha-CaMKII small interferin

70 ition of CaMKII by the calmodulin antagonist trifluoperazine or the CaMKII antagonist KN93 reduces al

71 (thioridazine, chlorpromazine, haloperidol, trifluoperazine, or risperidone) for 12 months or to swi

72 ctrometry showed that the antipsychotic drug trifluoperazine penetrates well into the SR microsome as

73 eated with trifluoperazine plus gefitinib or trifluoperazine plus cisplatin.

74 ase inhibitor or cisplatin were treated with trifluoperazine plus gefitinib or trifluoperazine plus c

75 hemically different inhibitors (e.g. W-7 and trifluoperazine) produce similar effects, investigators

76 Trifluoperazine promoted autophagy and bacterial clearan

77 on of the MPT inhibitors, cyclosporin A, and trifluoperazine, protected Ad5IkappaB-infected hepatocyt

78 The calmodulin antagonist, trifluoperazine, rescues bone loss in ovariectomized mic

79 ed with other apoptosis-accelerating agents (trifluoperazine, staurosporine, dexamethasone, ionomycin

80 n the pro-apoptotic effects of tamoxifen and trifluoperazine support an underlying molecular mechanis

81 king phospholipase A(2) (PLA(2)) activity by trifluoperazine suppressed AA incorporation into phospho

82 efflux from choroid plexus was stimulated by trifluoperazine, taurine, and hypo-osmotic stress.

83 was to determine if allopurinol (AL) and/or trifluoperazine (TFP) added to the Belzer machine preser

84 h those of two well-studied CaM antagonists: trifluoperazine (TFP) and W-13.

85 Using a unique biosensor-based assay, trifluoperazine (TFP) was identified as an inhibitor tha

86 c CSQ1 induced by depleted Ca(2+) stores, or trifluoperazine (TFP), a blocker of CSQ folding and aggr

87 um ion and small molecule inhibitors such as trifluoperazine (TFP).

88 in permeabilized smooth muscle treated with trifluoperazine (TFP).

89 miconazole, clotrimazole, nitrendipine, and trifluoperazine) that in the absence of loperamide effec

90 When osteoclasts are treated with 10 microm trifluoperazine, the binding between Fas and calmodulin

91 SCs with different EGFR mutation status with trifluoperazine to examine its anti-CSC properties.

92 aracteristics when added to perfusate: PGE1, trifluoperazine, verapamil, and papaverine.

93 )), interfere with calmodulin function (e.g. trifluoperazine, W13, and W7), or block Ca2+/calmodulin-

94 AM19; however, three calmodulin antagonists, trifluoperazine, W7, and calmidazolium, impaired this cl

95 Trifluoperazine, W7, or ethylene glycol-bis-(beta-aminoe

96 The combination of trifluoperazine with either gefitinib or cisplatin overc

97 he anti-CSC effect and synergistic effect of trifluoperazine with gefitinib.

98 ibited by tamoxifen, 4-hydroxytamoxifen, and trifluoperazine with IC50 values of approximately 1 micr