ライフサイエンスコーパス: charybdotoxin

1 r residues than other alpha-K toxins such as charybdotoxin.

2 nnels at much lower concentrations than does charybdotoxin.

3 eriotoxin was significantly more potent than charybdotoxin.

4 KAp channels were insensitive to charybdotoxin.

5 This effect was blocked by TEA and charybdotoxin.

6 block of BK channels with 2 mM TEA or 30 nM charybdotoxin.

7 ex with the high-affinity peptide antagonist charybdotoxin.

8 y the BK channel inhibitors, iberiotoxin and charybdotoxin.

9 yperpolarising factor (EDHF) with apamin and charybdotoxin.

10 yed an enhanced sensitivity to inhibition by charybdotoxin.

11 by glibenclamide and tolbutamide, but not by charybdotoxin.

12 + = 293B >>> azimilide = TEA >>> clofilium = charybdotoxin.

13 itive to tetraethylammonium, kaliotoxin, and charybdotoxin.

14 mentia was not inhibited by either apamin or charybdotoxin.

15 Charybdotoxin 10(-8) mol/L impaired both FID (15+/-3% ve

16 -300 nM; inhibits Kv1.1 and Kv1.2 channels), charybdotoxin (10 nM to 1 microM; inhibits KCa and Kv1.2

17 K+ channel blockers iberiotoxin (10 nM) and charybdotoxin (10 nM).

18 hannels are blocked by low concentrations of charybdotoxin (10 nmol/L) but, unlike BK channels, are i

19 The presence of 40 mmol/L KCl or charybdotoxin (10(-8) mol/L, a blocker of large-conducta

20 odilation is also blocked in the presence of charybdotoxin (100 nM) plus apamin (100 nM), a combinati

21 aethylammonium (4-25 mM), but insensitive to charybdotoxin (100 nM).

22 ctance Ca(2+)-activated K+ channel inhibitor charybdotoxin (100 nM).

23 nhibited by tetraethylammonium (5 mmol/L) or charybdotoxin (100 nmol/L).

24 ve to alpha-dendrotoxin (100 to 500 nmol/L), charybdotoxin (100 to 500 nmol/L), and mast cell degranu

25 a 50-fold increase in the affinity for 125I-charybdotoxin (125I-ChTX) as compared with when the alph

26 h the K(+)-channel blockers TEA (10 mmol/L), charybdotoxin (20 nmol/L)/apamin (100 nmol/L), or elevat

27 We studied the effects of charybdotoxin (20-40 nM) in vitro (perfused/superfused)

28 in human airway myocytes was insensitive to charybdotoxin (200 nM) but blocked by 4-aminopyridine.

29 In contrast, charybdotoxin (a KCa channel inhibitor) and KCl (a depol

30 he KO2 current in PC12 cells is inhibited by charybdotoxin, a blocker of Kv1.2 channels.

31 Charybdotoxin, a peptide neurotoxin of known molecular s

32 The F425G Shaker mutation increases charybdotoxin affinity by 3 orders of magnitude but abol

33 1 and 5 mM 4-aminopyridine (4-AP) and 20 nM charybdotoxin all failed to evoke a significant rise in

34 Apical pretreatment with charybdotoxin also blocked the I(sc) decrease by >90% an

35 the specific KCa channel blockers apamin and charybdotoxin also failed to alter Idelay.

36 Charybdotoxin, an inhibitor of Ca(2+)-sensitive K(+) cha

37 To exploit this difference, three novel charybdotoxin analogs were designed by introducing negat

38 otoxin (ChTX; 100 nM) but not iberiotoxin, a charybdotoxin analogue, which blocks the maxi-KCa channe

39 microM Ba2+ and by the combination of 100 nM charybdotoxin and 100 nM apamin.

40 ective IK(Ca) and SK(Ca) channel inhibitors, charybdotoxin and apamin, inhibit glibenclamide-insensit

41 ervation that two Gardos channel inhibitors, charybdotoxin and clotrimazole, independently blocked th

42 Conversely, inhibitors of K(Ca2+), charybdotoxin and clotrimazole, inhibited HD cell format

43 urrents were Ca2+ dependent and sensitive to charybdotoxin and iberiotoxin but not to apamin, suggest

44 e-cell currents were inhibited by 4-AP, TEA, charybdotoxin and iberiotoxin implicating functional K(v

45 Sensitivity to charybdotoxin and margatoxin indicated that this K+ curr

46 Conversely, with charybdotoxin and niflumic acid present to inhibit K(Ca)

47 s (32 pS at -100 mV) which were sensitive to charybdotoxin and resistant to TEA.

48 TEA, charybdotoxin, and high [K+]0 attenuated the EET relaxat

49 inity of the channel for tetraethylammonium, charybdotoxin, and nifedipine.

50 a show that EDHF is K+ that effluxes through charybdotoxin- and apamin-sensitive K+ channels on endot

51 mensional structure between PiTX-K alpha and charybdotoxin are also observed in both the tight turn a

52 The analogous residues in charybdotoxin are positioned differently on the toxin su

53 ta3 subunit confers a reduced sensitivity to charybdotoxin, as seen with native inactivating BK chann

54 KCh channels were inhibited by charybdotoxin at concentrations > 50 nM, but were insens

55 rohypophysial BK channels are insensitive to charybdotoxin at concentrations as high as 360 nM.

56 The structural data reveal how charybdotoxin binds to the closed form of KcsA and makes

57 ar results were evident with iberiotoxin and charybdotoxin block.

58 A structural model of charybdotoxin bound to a Shaker K+ channel has emerged f

59 voltage oscillations were blocked by 100 nM charybdotoxin, but low-frequency oscillations remained.

60 is inhibited by the BK(Ca) channel inhibitor charybdotoxin, but not by the nitric-oxide synthase inhi

61 IK channel-blockers apamin, dequalinium, and charybdotoxin caused increases in average [Ca(2+)](i) le

62 y blocking NO synthase (L-NMMA) or K(+)(Ca) [charybdotoxin (CbTX)+apamin (AP)].

63 nding modes of two selected scorpion toxins, charybdotoxin (ChTx) and OSK1, to human KCa3.1 are exami

64 Expression has been studied using charybdotoxin (ChTX), a peptidyl inhibitor that binds in

65 Charybdotoxin (ChTX), a venom protein, suppresses Ca2+-a

66 hannel blockers, namely kaliotoxin (KTX) and charybdotoxin (CHTX), on Vm, calcium influx, and cell pr

67 rboxyl termini, with another scorpion toxin, charybdotoxin (ChTX), which blocks both the Ca(2+)-activ

68 inhibited by removal of Ca2+ or addition of charybdotoxin (ChTX).

69 The Ca(2+)-activated K+ channel blocker charybdotoxin (ChTX, 10(-7) M) also inhibited the K+ cur

70 ata are compared with the characteristics of charybdotoxin (ChTx, or its analogs) binding to the Shak

71 ic KCa channel blocker and, surprisingly, by charybdotoxin (ChTX; 100 nM) but not iberiotoxin, a char

72 Consistent with channel blockade, charybdotoxin, clotrimazole, and the highly selective IK

73 potentials, and application of paxilline or charybdotoxin considerably reduced CCK-mediated modulati

74 of internal K+ combined with 100 nM external charybdotoxin (CTX) abolished the outward currents and r

75 Charybdotoxin (CTX) also selectively blocked IKf in a re

76 rhythmicity, intraolivary microinjections of charybdotoxin (CTX) and apamin were used.

77 The pore blockers charybdotoxin (CTx) and iberiotoxin (IbTx), at nanomolar

78 ium (KCa) channels in the silent arteries by charybdotoxin (CTX) and tetraethylammonium ions (TEA) in

79 everal aspects of blockade of BKi current by charybdotoxin (CTX) are consistent with the idea that BK

80 encoded by Kv1.3; a minor K(V) component was charybdotoxin (CTX) resistant.

81 ive Ca2+-activated potassium channel blocker charybdotoxin (CTX) significantly reduced relaxations to

82 paddle chimera, a Kv channel in complex with charybdotoxin (CTX), a pore-blocking toxin.

83 The scorpion toxin, Charybdotoxin (CTX), blocks homotetrameric, voltage-gate

84 As found for other alpha-K toxins such as charybdotoxin (CTX), site-directed mutagenesis at toxin

85 Application of apamin and charybdotoxin (CTX), which selectively block the small a

86 Two strategies that exploit charybdotoxin (CTX)-sensitive subunit variants are appli

87 s, iberiotoxin (5 microm) had no effect, but charybdotoxin (CTX, 5 microm) + apamin (APA, 10 microm)

88 Charybdotoxin (CTX; 10(-8) mol/L), a large-conductance C

89 hibited by 1 mM tetraethylammonium or 100 nM charybdotoxin (CTX; a specific KCa-channel blocker).

90 yridine and partially by tetraethylammonium, charybdotoxin, dendrotoxin, and kaliotoxin.

91 Conversely, blocking SK(Ca)/IK(Ca) (apamin+charybdotoxin) depolarized cells by approximately 10 mV

92 ctivated K+ channel blockers, iberiotoxin or charybdotoxin, did not prevent potentiation by nifedipin

93 s, which are conserved in all members of the charybdotoxin family (alpha-K toxins), anchor one face o

94 oichiometry and competitively inhibited 125I-charybdotoxin from binding to the external vestibule of

95 oM), but inhibited by high concentrations of charybdotoxin ( > 50 nM) or dTC ( > 1 mM).

96 by mutant cycle analyses, establishing that charybdotoxin has a similar docking configuration in the

97 e also show that human KSper is inhibited by charybdotoxin, iberiotoxin, and paxilline, while mouse K

98 )](i) and blocked by external TEA but not by charybdotoxin, iberiotoxin, apamin, or 4-aminopyridine.

99 e conductance Ca(2+)-activated K(+) channel (charybdotoxin, iberiotoxin, quinine, and Ba(2+)) nor inh

100 ed inhibition of rehydration was reversed by charybdotoxin, implying that rehydration was delayed in

101 t and were blocked by tetraethylammonium and charybdotoxin in normal and inflamed cells.

102 calcium-activated potassium channel blocker, charybdotoxin, indicating a mechanism that does not invo

103 rity of the K+ current was blocked by 100 nM charybdotoxin, indicating that it was carried by large-c

104 Although both kappa-PVIIA and charybdotoxin inhibit the Shaker channel, they must inte

105 rs, tetraethylammonium chloride, apamin, and charybdotoxin, inhibit the granulysin-induced increase i

106 Two additional 4-AP- and charybdotoxin-insensitive K+ channels (approximately 90

107 e and mean burst duration of 4-AP-sensitive, charybdotoxin-insensitive K+ channels (KDR1).

108 VIP (1 microM) increased charybdotoxin-insensitive outward currents.

109 s openings of SK channels can be resolved as charybdotoxin-insensitive spontaneous transient outward

110 The charybdotoxin-insensitive STOCs are related to spontaneo

111 II inhibitor KN-93 reduced the occurrence of charybdotoxin-insensitive STOCs.

112 milarly for cat carotid body chemoreceptors, charybdotoxin is expected to stimulate the chemosensory

113 plied tetraethylammonium (Kd = 30 +/- 7 mM), charybdotoxin (Kd = 10 +/- 1 nM), and clotrimazole (Kd =

114 hIK1 currents were reversibly blocked by charybdotoxin (Ki = 2.5 nM) and clotrimazole (Ki = 24.8

115 cing negatively charged residues in place of charybdotoxin Lys(32), which lies in close proximity to

116 JR-FL also was observed with a 32-amino acid charybdotoxin miniprotein construct that contains an epi

117 Cell body BK activity was reduced by 10 nM charybdotoxin (NPo, 37% of control), or 10 nM iberiotoxi

118 tance calcium-dependent potassium channels), charybdotoxin (of less specificity, but probably interme

119 larization was reversibly blocked by 4-DAMP, charybdotoxin or BAPTA-AM, but not by N(omega)-nitro-L-a

120 Na+, and was sensitive to block by external charybdotoxin or tetraethylammonium (TEA) and by interna

121 Inhibition of K+ channels with charybdotoxin or tetraethylammonium chloride produced a

122 ting calcium-activated potassium channels by charybdotoxin or tetraethylammonium slowed the repolariz

123 o significant differences in the response to charybdotoxin or the BK channel opener NS1619 were obser

124 Addition of charybdotoxin or verapamil blocked these K+ channels and

125 50 microM tetraethylammonium chloride, 70 nM charybdotoxin, or 100 nM iberiotoxin).

126 azole, but not by the K(Ca) channel blocker, charybdotoxin, or the cyclooxygenase inhibitor, diclofen

127 In oocytes, iberiotoxin and charybdotoxin, peptidyl scorpion toxins, were both equal

128 2 was reduced by catalase, 40 mmol/L KCl, or charybdotoxin plus apamin, whereas endothelial denudatio

129 uster and are predictably insensitive to the charybdotoxin position 32 analogs, whereas the maxi-K(Ca

130 trum of K+ channels, reducing both Kv1.3 and charybdotoxin-resistant components of KV current and KCa

131 ges of membrane properties and occurrence of charybdotoxin-sensitive (BK) calcium-dependent potassium

132 Transient-rebound cells have a charybdotoxin-sensitive calcium-dependent K(+) current a

133 hich express the beta1 subunit, Tx activated charybdotoxin-sensitive K(+) current.

134 rize neurons by activating high-conductance, charybdotoxin-sensitive K+ channels.

135 The other charybdotoxin-sensitive Kv channels, Kv1.2 and Kv1.6, co

136 ce outward currents due to the activation of charybdotoxin-sensitive large conductance Ca2+-activated

137 A charybdotoxin-sensitive mutant of KcsA exhibits similar

138 SK is a charybdotoxin-sensitive, apamin-insensitive channel that

139 crease in the outward current was blocked by charybdotoxin, suggesting an effect on the calcium-activ

140 e-dimensional scaffold with the well-studied charybdotoxin, the two use different mechanisms in suppr

141 Finally, we used (125)I-labeled charybdotoxin to demonstrate the presence of K+ channels

142 Addition of the SK channel blocker charybdotoxin to growth factor-containing culture medium

143 [KCI] versus 76+/-5% [control] and 47+/-6% [charybdotoxin] versus 91+/-3% [control]; P<0.05 for both

144 Initial docking of charybdotoxin was undertaken with both models, and the a

145 The current was reduced by 80 % by charybdotoxin, was attenuated by 10 mM TEA+ but was unaf

146 in the frequency-response curves, apamin and charybdotoxin were injected into the IO.

147 o)-3-hydroxy-2, 2-dimethyl-chromane (293B) = charybdotoxin, whereas for the colonic epithelium the or

148 strategy to transform the polypeptide toxin charybdotoxin, which blocks several voltage-gated and Ca

149 s stimulated with anti-CD3 were inhibited by charybdotoxin, which can block both KCa3.1 and Kv1.3, wh

150 epithelia which were partially sensitive to charybdotoxin, with the remaining current being inhibite