ライフサイエンスコーパス: tubocurarine

1 nd two antagonists (alpha-bungarotoxin and d-tubocurarine).

2 presence of agonist (5-HT) or antagonist (d-tubocurarine).

3 >(-)nicotine>cytisine>carbamylch oli ne> /=d-tubocurarine).

4 min-sensitive channels are also blocked by d-tubocurarine.

5 tractions evoked by 10 Hz stimulation in (+)-tubocurarine.

6 Cs) in preparations partially blocked with d-tubocurarine.

7 cutting the sympathetic chain or adding (+)-tubocurarine.

8 ed cutaneous responses were abolished by (+)-tubocurarine.

9 ynthesis of the famous arrow poison alkaloid tubocurarine.

10 placeable by the small molecule antagonist d-tubocurarine.

11 agonism by pancuronium, hexamethonium, and d-tubocurarine.

12 e presence of the nACh receptor antagonist d-tubocurarine.

13 ounds including martinelline, scoulerine and tubocurarine.

14 neous addition of the nicotinic antagonist d-tubocurarine.

15 ction group, following muscle paralysis with tubocurarine.

16 ocked by coapplication of mecamylamine and d-tubocurarine.

17 but surprisingly enhanced the affinity for d-tubocurarine.

18 ed in interacting with the 13'-position of d-tubocurarine.

19 ly by alpha-bungarotoxin and completely by D-tubocurarine.

20 tivity to apamin and differential block by d-tubocurarine.

21 Cibacron blue (1-100 microM) and d-tubocurarine (0.1-1 mM) produced rapid (10 sec to 5 min)

22 dihydro-beta-erythroidine (10 microM) and d-tubocurarine (10 microM).

23 c acetylcholine receptor (nAChR) antagonists tubocurarine (100 microM), mecamylamine (100-500 microM)

24 yotube patch responses were antagonized by d-tubocurarine (3 microM).

25 was increased by carbamylcholine (90%) or d-tubocurarine (50%), but it was inhibited by isoflurane (

26 d-Tubocurarine, a conformationally restricted 5-HT3 ligand

27 imes greater than observed previously with d-tubocurarine, a nonselective blocker of nicotinic recept

28 ine with the higher ACh affinity and lower d-tubocurarine affinity of the alpha-delta binding site co

29 Furthermore, d-tubocurarine alone blocked the development of both immat

30 petitive and non-competitive AChR blockers d-tubocurarine and alpha-bungarotoxin, respectively.

31 nce of the acetylcholine receptor blockers d-tubocurarine and alpha-bungarotoxin.

32 bition with the site-selective antagonists d-tubocurarine and alpha-conotoxin MI.

33 arbachol, and the cholinergic antagonists, D-tubocurarine and atropine.

34 can be enhanced by monovalent cations and d-tubocurarine and may be subject to negative allosteric m

35 lcholine and the competitive antagonists (+)-tubocurarine and metocurine for adult mouse receptors is

36 ielding KI values of 58 and 105 microM for d-tubocurarine and nicotine, respectively.

37 in receptor conformation upon binding of (+)-tubocurarine and pancuronium but not cisatracurium.

38 her activation energy for association of (+)-tubocurarine and pancuronium compared with cisatracurium

39 ion (in the absence of acetylcholine) by (+)-tubocurarine and pancuronium on embryonic receptors.

40 116 +/- 10 kJ mol(-1) for cisatracurium, (+)-tubocurarine and pancuronium, respectively.

41 s 2.9- and 1.3-fold greater than that of (+)-tubocurarine and pancuronium, respectively.

42 sociation was 6- and 16-fold higher than (+)-tubocurarine and pancuronium, respectively.

43 The 5-HT3 receptor "antagonists' (+)-tubocurarine and quipazine (both at 3 nM) reduced the in

44 It was also insensitive to apamin, tubocurarine and scyllatoxin (leiurotoxin I), specific b

45 The binding of d-tubocurarine and several of its analogs to the mouse nic

46 The actions of d-tubocurarine and sodium were not additive.

47 eptor antagonist), promethazine, atropine, d-tubocurarine and suramin had no obvious effects on oscil

48 ned synchronous after the application of (+)-tubocurarine and/or gabazine.

49 Mecamylamine, d-tubocurarine, and hexamethonium blocked the function by

50 ists, including dihydro-beta-erythroidine, d-tubocurarine, and methyllycaconitine, also elicited sign

51 ive antagonists of this receptor and, like d-tubocurarine, bind to the alphagamma site with much high

52 subunit correlated with the high-affinity d-tubocurarine binding site, along with a lack of inhibiti

53 a subunit correlated with the low-affinity d-tubocurarine binding site, suggests that the 383C epitop

54 subunit associated with the high-affinity d-tubocurarine binding site.

55 Further, the general nAChR antagonist, d-tubocurarine, blocked all but two of the observed change

56 plied 5-HT was slowed in the presence of (+)-tubocurarine but not in the presence of quipazine.

57 s(benzylisoquinoline) alkaloid family, d-(+)-tubocurarine chloride (DTC), has been evaluated as a chi

58 s in the periphery or cultured cell lines, D-tubocurarine chloride appears to be non-specific in bloc

59 A nicotinic antagonist, d-tubocurarine chloride, completely and reversibly blocked

60 The competitive antagonist d-tubocurarine (curare) has greater potency at mouse than

61 e inhibited by nanomolar concentrations of d-tubocurarine (curare) in a competitive fashion.

62 Here we delineate bound orientations of d-tubocurarine (d-TC) and its methylated derivative metocu

63 studied binding of the curare derivatives d-tubocurarine (d-TC) and metocurine to AChBP using comput

64 ffects were depressed (not obliterated) by D-tubocurarine (D-TC), hexamethonium (C6) and atropine.ACh

65 le ionotropic acetylcholine receptors by (+)-tubocurarine decreased the frequencies of APs and Ca2+ t

66 ing of the site-selective ligands dimethyl-d-tubocurarine (DMT) and alpha-conotoxin M1 (CTX) confirm

67 ies for the curariform antagonist dimethyl d-tubocurarine (DMT).

68 or affinity for the competitive antagonist d-tubocurarine (dTC) 5-35-fold.

69 d-Tubocurarine (dTC) evoked flickering activity of KAp cha

70 ent affinity of the competitive antagonist d-tubocurarine (dTC) for the receptor.

71 ic acetylcholine receptor (nAChR) with [3H]d-tubocurarine (dTC) has identified a residue within the g

72 dies with the competitive antagonist d-[(3)H]tubocurarine (dTC) identified two tryptophans, gammaTrp-

73 d-Tubocurarine (dTC) is a potent competitive antagonist of

74 treated chicken embryos in ovo with either d-tubocurarine (dTC) or muscimol during the naturally occu

75 ns each are run with no ligand, antagonist d-tubocurarine (dTC), agonist acetylcholine (ACh), and ago

76 ine binding of the competitive antagonist, d-tubocurarine (dTC), to the muscle-type nicotinic acetylc

77 n by the reversible competitive antagonist d-tubocurarine (dTC).

78 tely blocked by a nonselective antagonist, d-tubocurarine, for nAChRs, but not by a selective antagon

79 s alpha3/beta4 receptor was mecamylamine > d-tubocurarine > dihydro-beta-erythroidine > hexamethonium

80 th bicuculline or nicotinic receptors with d-tubocurarine had no effect, although exposure to nicotin

81 S), we show that treatment with 100 microm d-tubocurarine has no effect on in-turbulence regulation b

82 nities of three competitive antagonists, (+)-tubocurarine, hexamethonium, and dihydro-beta-erythroidi

83 dro-beta-erythroidine, methyllycaconitine, d-tubocurarine, hexamethonium, decamethonium, and mecamyla

84 50 = 69 nM), cocaine (IC50 = 459 nM) and (+)-tubocurarine (IC50 = 2.8 microM).

85 he concentration of ACh (IC50, ACh) and of d-tubocurarine (IC50,dTC) causing half-maximal retardation

86 aced by the specific nAChRalpha1 inhibitor d-tubocurarine in a dose-dependent manner.

87 etocurine shifted the apparent IC(50) of (+)-tubocurarine in quantitative agreement with complete com

88 affects on the P2X4 purinoceptor and, like d-tubocurarine, increased [35S]ATPgammaS binding.

89 e effects by the general nAChR antagonist, d-tubocurarine, indicated that gene expression changes are

90 agonists and antagonists, we determined that tubocurarine inhibits the spontaneous current whereas Zn

91 nium each shifted the apparent IC(50) of (+)-tubocurarine less than expected for complete competition

92 s only slightly blocked by the antagonists d-tubocurarine, mecamylamine, or dihydro-beta-erythroidine

93 with nicotine or carbamylcholine, but not d-tubocurarine, mecamylamine, or dihydro-beta-erythroidine

94 ed by the blockers dihydrostreptomycin and d-tubocurarine nor by treatment of the apical membrane wit

95 ects, which were blocked by the antagonist d-tubocurarine, on the bacterial replication and cytokine

96 pha7 AChRs was partially blocked by either d-tubocurarine or mecamylamine.

97 uation was similar for cisatracurium and (+)-tubocurarine or metocurine.

98 vated currents in outside-out patches by (+)-tubocurarine, pancuronium and cisatracurium.

99 uced a biphasic competition curve, whereas d-tubocurarine potentiated binding at concentrations in ex

100 ane current that was entirely prevented by d-tubocurarine preincubation or nAChRalpha1 silencing.

101 in control cells to 9.1 (7.2-11.4) microM in tubocurarine-protected cells.

102 in control cells to 0.3 (0.2-0.4) microM in tubocurarine-protected cells.

103 When the pharmacology of residual, tubocurarine-protected receptors was investigated, the E

104 In addition, the IC50 value for tubocurarine's inhibitory effects on release significant

105 The complex effects of cibacron blue and d-tubocurarine seemed to be due to an allosteric interacti

106 Application of curare (d-tubocurarine) selectively blocked the Si3 synapses in bo

107 at non-up-regulating concentrations, only d-tubocurarine significantly inhibited agonist-induced up-

108 ree energy changes for carbamylcholine and d-tubocurarine, suggesting independent contributions of th

109 dition of the K+ channel blockers, apamin, d-tubocurarine, tetraethylammonium (TEA), or intracellular

110 etermined independently in the presence of d-tubocurarine to be -14 mV; the calculated potential at t

111 elease of dye liberated into the medium from tubocurarine-treated nerve-muscle preparations.

112 logenation at various functional groups on d-tubocurarine was measured to both the high affinity (alp

113 When 100 microM tubocurarine was present during alkylation, nicotine-sti

114 Verapamil, tetrahydroaminoacridine, and d-tubocurarine were also sensitive to that chimeric substi

115 antagonists dihydro-beta-erythroidine and d-tubocurarine were more potent at HS receptors.

116 4beta2, chlorisondamine, mecamylamine, and d-tubocurarine were, respectively, 100-, 8-, and 5-fold se

117 extracellular domain was inhibited >90% by d-tubocurarine, whereas addition of either carbamylcholine

118 nversely, chronic in ovo administration of d-tubocurarine, which causes an increase in motoneuron bra