ライフサイエンスコーパス: trifluoperazine

1 thiazine-like antipsychotic drugs, including trifluoperazine.

2 ), isradipine, nilotinib, nortriptyline, and trifluoperazine.

3 stoma and glioma cells that was inhibited by trifluoperazine.

4 ith the cell-permeable calmodulin antagonist trifluoperazine.

5 by two calmodulin antagonists, tamoxifen and trifluoperazine.

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

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

8 100 microm), or by the calmodulin antagonist trifluoperazine (50 microm).

9 Trifluoperazine, a calmodulin antagonist, inhibited Fas-

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

11 .2.3, which was inhibited by cytochalasin B, trifluoperazine, a combination of sodium azide and 2-deo

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

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

14 sics, and computer simulations, we show that trifluoperazine acts by thinning the membrane bilayer, m

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

16 Trifluoperazine also inhibited this chimera in the absen

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

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

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

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

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

22 structurally distinct calmodulin antagonists trifluoperazine and CGS9343B attenuated the interaction

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Consistently, trifluoperazine blocked Fas-promoted cell survival.

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

48 Cyclosporin A plus trifluoperazine, blockers of the mitochondrial permeabil

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 nal cord injury model with the licensed drug trifluoperazine inhibited AQP4 localization to the blood

68 We demonstrated that trifluoperazine inhibited CSC tumor spheroid formation a

69 Trifluoperazine inhibited the tumor growth and enhanced

70 Trifluoperazine inhibited Wnt/beta-catenin signaling in

71 Trifluoperazine inhibition is non-competitive for NADH,

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

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

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

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

76 eated with trifluoperazine plus gefitinib or trifluoperazine plus cisplatin.

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

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

79 Trifluoperazine promoted autophagy and bacterial clearan

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

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

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

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

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

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

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

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

88 ating cell phenotype, and we have identified trifluoperazine (TFP) as a compound that interferes with

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

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

91 Importantly, trifluoperazine (TFP), a Nupr1 inhibitor, alleviated UUO

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

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

94 bination with Src (saracatinib), calmodulin [trifluoperazine (TFP)], or proviral integration site of

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

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

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

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

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

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

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

102 The combination of trifluoperazine with either gefitinib or cisplatin overc

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

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