ライフサイエンスコーパス: calcium chelator

1 -N,N,N',N'-tetraacetic acid tetrakis (BAPTA; calcium chelator).

2 llergenicity using diets supplemented with a calcium chelator.

3 in cells loaded with EGTA, a slower-binding calcium chelator.

4 d is not very sensitive to the intracellular calcium chelator.

5 '-tetraacetic acid (BAPTA), an extracellular calcium chelator.

6 nd failed to bind in the presence of EGTA, a calcium chelator.

7 cell pairs to BAPTA/AM, a membrane-permeant calcium chelator.

8 s in the ooplasm via injection of BAPTA as a calcium chelator.

9 tide 3-kinase inhibitors or an intracellular calcium chelator.

10 acid acetoxymethyl ester), an intracellular calcium chelator.

11 nd points were abrogated by treatment with a calcium chelator.

12 ormation can be inhibited by the addition of calcium chelators.

13 tosolic calcium were completely prevented by calcium chelators.

14 which was inhibited by U0126, GF109203, and calcium chelators.

15 s transduction recovers after the removal of calcium chelators.

16 (GFX203290), Src (PP2), Jak2 (AG490), or the calcium chelator 1, 2-bis(2-aminophenoxy)ethane-N,N,N',N

17 by buffering cytosolic calcium rise with the calcium chelator 1, 2-bis-(o-aminophenoxy)ethane-N,N,N',

18 location are unaffected by the intracellular calcium chelator 1, 2-bis-o-aminophenoxyethane-N,N,N',N'

19 InsP3-induced LTD was prevented by calcium chelator 1,2-bis(2-amino phenoxy)ethane-N,N,N',

20 tment are sensitive to the membrane-permeant calcium chelator 1,2-bis(2-amino phenoxy)ethane-N,N,N',N

21 presence of the PLC inhibitor U73122 or the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N, N',N

22 abrogated by pretreatment of cells with the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'

23 blocked by the addition of the intracellular calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'

24 t of the cells with either the intracellular calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'

25 The cell-permeable calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'

26 of AEA ACh currents were not altered by the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'

27 ts, achieved by loading guard cells with the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'

28 In contrast, the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'

29 Pre-treatment of wildtype cochleae with the calcium chelator 1,2-bis(o-aminophenoxy) ethane-N,N,N',N

30 We broke tip links with the calcium chelator 1,2-bis(O-aminophenoxy) ethane-N,N,N',N

31 d cell death is blocked by the intracellular calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'

32 ed by an inhibitor of phospholipase C or the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'

33 by Ca(2+)-channel blocking agents and by the calcium chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'

34 ptor (KDR/Flk-1) inhibitor, SU-1498, and the calcium chelator 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'

35 II protein in HL-60/S cells treated with the calcium chelator 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N

36 n binding was inhibited by the intracellular calcium chelators 1,2-bis(2-aminophenoxy)ethane-N,N,N',

37 n inhibitor (cyclosporin A, 0.5 micromol/l), calcium chelator (1,2-Bis(2-amino-5-fluorophenoxy)ethane

38 t treating cells with the membrane-permeable calcium chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N

39 se C, but is blocked by loading cells with a calcium chelator, 1,2-bis-(2-aminophenoxy)ethane-N,N,N',

40 The intracellular calcium chelator, 1,2-bis-(o-aminophenoxy)ethane-N,N,N',

41 noethyl)-N,N,N',N'-tetraacetoxymethyl ester (calcium chelator), 2-aminoethoxydiphenyl borate (inhibit

42 hibitor 2',5'-dideoxyadenosine (ddA), or the calcium chelators 3,4,5-trimethoxybenzoic acid 8-(diethy

43 fibroblasts, we found that the intracellular calcium chelator, 3,4,5-trimethoxybenzoic acid, and the

44 Protein kinase C inhibitor, Ro 31-8220, or a calcium chelator 5,5'-dimethyl-BAPTA shifted the concent

45 ced SFK phosphorylation was inhibited by the calcium chelator 5,5'-dimethyl-bis-(o-aminophenoxy)ethan

46 ialysis, of an NMDA receptor antagonist or a calcium chelator abolished DAMGO-induced LTP.

47 Calcium chelators act similarly and mitochondrially targ

48 ial experiments showed that treatment with a calcium chelator after spinal cord injury reduced apopto

49 Incubation with an intracellular calcium chelator also reduced the appearance of antiport

50 A calcium chelator and several antioxidants antagonized Do

51 s reduced by presynaptic injection of a slow calcium chelator and was accompanied by an increase in t

52 ce and modest sensitivities to intracellular calcium chelators and external barium ions suggest that

53 alpain even in the presence of intracellular calcium chelators and in calcium-free media.

54 he inducible pathway and can be inhibited by calcium chelators and some calpain inhibitors.

55 ed by specific inhibitors, including mannan, calcium chelators, and Abs to the lectin domain of the S

56 pp140, the inhibition of R-ring formation by calcium chelators, and the concentration of Nopp140 and

57 Addition of calcium chelators, antibodies to E-cadherin (but not to

58 Calcium influx is blocked by extracellular calcium chelators, as well as by divalent heavy metals s

59 alcium, since tyrosine kinase inhibitors and calcium chelators attenuated VEGF-induced NO release.

60 ked by pertussis toxin, by the intracellular calcium chelator BAPTA (1,2-bis(aminophenoxy) ethane-N,N

61 hibitor wortmannin, and by the intracellular calcium chelator BAPTA (1,2-bis(aminophenoxy)ethane-N,N,

62 nificant effect on the failure rate when the calcium chelator BAPTA (10 mm) was introduced into the p

63 as blocked in recordings made with the rapid calcium chelator BAPTA (11 mM) in the pipette solution.

64 a phospholipase C (PLC) inhibitor U73122 and calcium chelator BAPTA (5,5'-dimethyl-bis(o-aminophenoxy

65 Staurosporine, but not the calcium chelator BAPTA [1,2-bis(o-aminophenoxy)ethane-N,

66 The calcium chelator BAPTA AM and agents that block calcium

67 alcium stores, or with the membrane-permeant calcium chelator BAPTA AM significantly decreased the ac

68 ntly reduced in cells pre-incubated with the calcium chelator BAPTA AM.

69 s however unaffected by incorporation of the calcium chelator BAPTA and seemed therefore not to refle

70 are reversibly blocked after docking by the calcium chelator BAPTA have passed the point of sensitiv

71 lding potentials of +60 and -60 mV; with the calcium chelator BAPTA in the recording pipette and with

72 agonists increased [Ca2+]i in PDEC, and the calcium chelator BAPTA inhibited the secretory effects o

73 ion of astrocytic calcium signaling with the calcium chelator BAPTA or by antagonists of the ionotrop

74 Treatment with the calcium chelator BAPTA or the protease subtilisin enable

75 caused by removing different links with the calcium chelator BAPTA or the protease subtilisin.

76 Prior injection into the motor neuron of the calcium chelator BAPTA, GDP-beta-S or GTP-gamma-S blocke

77 hibitor calphostin C or by the intracellular calcium chelator BAPTA, indicating that SKF83959 stimula

78 eliminated by intracellular injection of the calcium chelator BAPTA, suggesting that the inactivation

79 In cells loaded with the calcium chelator BAPTA, the transient Ca2+ release was b

80 duced after treatment with the intracellular calcium chelator BAPTA-AM (1,2-bis(2-aminophenoxy)ethane

81 calcium entry, cells were incubated with the calcium chelator BAPTA-AM (1,2-bis(o-aminophenoxy)ethane

82 ruthenium red (10 microM), or the cytosolic calcium chelator BAPTA-AM (50 microM) each strongly impa

83 Interestingly, the cytosolic calcium chelator BAPTA-AM and K-201 protected RA-treated

84 tment of cultures undergoing PA-LTx with the calcium chelator BAPTA-AM and the anti-oxidant MCI-186 s

85 calcium signaling pathways, an intracellular calcium chelator BAPTA-AM and the Ca(2+)(mito) uniporter

86 Furthermore, the membrane-permeable calcium chelator BAPTA-AM had no effect on BK-induced CO

87 However, pretreatment with intracellular calcium chelator BAPTA-AM or disruption of lipid rafts u

88 amma inhibitor U-73122, by the intracellular calcium chelator BAPTA-AM, and by the specific calmoduli

89 , the purinergic receptor agonist PPADS, the calcium chelator BAPTA-AM, and calpain inhibitors.

90 ed cell adhesion, which was inhibited by the calcium chelator BAPTA-AM, the calcium channel blocker S

91 The calcium chelator BAPTA-AM, which reduces cytosolic calci

92 NMDA receptor antagonists, tetrodotoxin, and calcium chelator BAPTA-AM.

93 blocked by intracellular application of the calcium chelator BAPTA.

94 t methyllycaconitine (MLA) and intracellular calcium chelator BAPTA.

95 pool but decreased sensitivity for the fast calcium chelator BAPTA.

96 E protein inhibitor N-ethylmaleimide and the calcium chelator BAPTA.

97 ation can be attenuated by the intracellular calcium chelator BAPTA.

98 ipettes contained high concentrations of the calcium chelator BAPTA.

99 lination was suppressed by the intracellular calcium chelator BAPTA/AM (30 muM).

100 We used a calcium chelator (BAPTA-AM) to abolish Ca(i)T and test i

101 otein kinase kinase 2 inhibitor (STO-609) or calcium chelator (BAPTA-AM).

102 Although calcium chelators (BAPTA, EGTA) inhibited basal and iono

103 Thus, following exposure to vehicle or the calcium chelator, BAPTA (1-20 microM), primary cortical

104 In addition, intracellular application of a calcium chelator, BAPTA through a patch pipette was foun

105 -free media; calcium ionophore, A23187; and calcium chelator, BAPTA, on the globulization of fiber c

106 We have demonstrated that an intracellular calcium chelator, BAPTA, was able to delay by 5- to 20-f

107 In contrast, the cell-permeable calcium chelator, BAPTA-AM (1,2-bis(2-aminophenoxy)ethan

108 calpain inhibitor I, or by the intracellular calcium chelator, BAPTA-AM.

109 , as it was still evident in presence of the calcium chelator, BAPTA-AM.

110 rved when cells were treated with a internal calcium chelator, BAPTA.

111 Inhibition of calcium increases by calcium chelators, BAPTA-AM and EGTA-AM, abrogated NF-ka

112 ifferential effects of two membrane-permeant calcium chelators, BAPTA-AM and EGTA-AM.

113 By contrast, calcium chelator BAPTM/AM and MEK inhibitor (U0126) can

114 In the presence of calcium chelators, binding between HCN1 and protocadheri

115 levels, as shown by their sensitivity to the calcium chelator bis(2-aminophenoxy)ethane-N,N,N',N'-tet

116 ostsynaptic intradendritic injections of the calcium chelator bis(2-aminophenoxy)ethane-N,N,N',N'-tet

117 ane-N,N,N',N'-tetraacetic acid (Bapta-AM), a calcium chelator, blocked MI-219-induced apoptosis.

118 GF109203X, a PKC inhibitor, nor BAPTA-AM, a calcium chelator, blocked phosphorylation of CREB induce

119 ophenoxy)ethane-N,N',N'-tetraacetic acid], a calcium chelator, blocked the VEGF secretion induced by

120 A calcium chelator, but not a protein kinase C inhibitor,

121 sence of low concentrations of intracellular calcium chelators, calcium influx through P/Q-type chann

122 ow that citrate, an environmentally relevant calcium chelator, can impact LapG activity and thus biof

123 We found that BAPTA-based calcium chelators cause immediate depolymerization of sp

124 or PP2, the PKC inhibitor Ro-31-8220, or the calcium chelator demethyl-1,2-bis(2-aminophenoxy)ethane-

125 87 also induced NOD-dependent signaling, and calcium chelators demonstrated a role for both intracell

126 Flash photolysis of the caged calcium chelator diazo-2 inside neurones diminished the

127 Noninvasive photoactivation of a calcium chelator (Diazo-2) was used to specifically disr

128 Light-driven uncaging of the photolabile calcium chelator DMNP-EDTA stimulates rapid localized se

129 , as competitive mannosylated inhibitors and calcium chelators each interfered with T cell stimulatio

130 ing activation as quickly as addition of the calcium chelator EDTA in vitro.

131 was blocked by pretreating parasites with a calcium chelator, EGR2 expression was significantly redu

132 ive conditions, while co-infiltration of the calcium chelator EGTA attenuated this effect.

133 by increasing the concentration of the slow calcium chelator EGTA from 1.5 to 5 mM.

134 Extracellular treatment with the calcium chelator EGTA had no effect on the pattern or ma

135 not blocked by caspase inhibitors or by the calcium chelator EGTA, but was reduced by Bcl-2 overexpr

136 el-blockers gadolinium and verapamil and the calcium chelator EGTA, further suggesting the involvemen

137 the NDMA receptor antagonist memantine, the calcium chelator EGTA, or a specific inhibitor for calci

138 ule dendrites have been loaded with the slow calcium chelator EGTA, suggesting a tight coupling betwe

139 when Ca(2+) is depleted by the high-affinity calcium chelator EGTA, suggesting that the calcium prese

140 by concomitant incubation of cells with the calcium chelator EGTA.

141 Similar results were also observed with the calcium chelator EGTA.

142 locker lanthanum and to a lesser extent, the calcium-chelator EGTA.

143 The intracellular calcium chelator (EGTA/AM) further increased ERK activat

144 Calcium chelators, EGTA or EDTA, blocked motility, even

145 e nanoparticle-mediated sustained release of calcium chelator (EI-NP) strongly enhances the intracell

146 transmission with high K(+), zero Ca(2+) and calcium chelator ethylene glycol-bis (beta-aminoethyl et

147 Application of the calcium chelator, ethylene-glycol-bis-(beta-aminoethylet

148 was inhibited by pretreating leaves with the calcium chelator ethyleneglycol-bis(aminoethyl ether)-N,

149 The calcium chelator, ethyleneglycol-bis(beta-amino-ethyl et

150 Because the effects of calcium chelators have been studied predominantly in cel

151 B3GALT5-KO rendered hESCs more resistant to calcium chelator in blocking entry into naive state.

152 ls and inclusion of high concentrations of a calcium chelator in recording pipettes decreased the dep

153 With high levels of calcium chelators in the pipette solution, or bath appli

154 ,N,-trimethylammonium salt, an intracellular calcium chelator, indicating that P2Y2R-stimulated intra

155 i) occurred in the presence of intracellular calcium chelators, indicating that calcium is not requir

156 Applications of calcium chelators inhibit the light response.

157 An intracellular calcium chelator inhibited both the rapid and sustained

158 a(acetoxymethyl)-ester, a membrane-permeable calcium chelator, inhibits MMS-induced activation of RAF

159 activity with intracellular injections of a calcium chelator into individual astrocytes inhibits spo

160 (2+) with Ba(2+) or Sr(2+) or microinjecting calcium chelators into the cytoplasm relieves the block

161 g ethylene glycol tetraacetic acid (EGTA), a calcium chelator, into a calcium-crosslinked alginate hy

162 ts that extra buffering by a fast and a slow calcium chelator may have on the calcium transient.

163 this regard, we have studied the effects of calcium chelators on both anterograde and retrograde pro

164 Addition of an intracellular calcium chelator or an AMPK inhibitor to either mouse ma

165 erformed in the presence of an intracellular calcium chelator or an inhibitor of cyclic AMP-activated

166 eveloped when the cells were dialyzed with a calcium chelator or kept hyperpolarized during induction

167 m binding by PilY1 using either an exogenous calcium chelator or mutation of a single residue disrupt

168 inally, cell pretreatment with intracellular calcium chelator or PKC inhibitors significantly diminis

169 reduced by postsynaptic injection of a rapid calcium chelator or postsynaptic hyperpolarization.

170 ation can also be mediated experimentally by calcium chelators or by mutations that destabilize the N

171 Either calcium chelators or inhibitors of voltage-gated L-type

172 line tetra-(acetoxymethyl)ester (Quin/AM), a calcium chelator, or with the combined presence of [8-(d

173 r antagonist, intracellular or extracellular calcium chelators, or hypertonic sucrose.

174 anes were removed by disaggregation with the calcium-chelator phosphate buffer.

175 The addition of antioxidants and iron or calcium chelators prevented cell death but did not preve

176 titrations performed in the presence of the calcium chelator Quin 2.

177 y thrombin by loading with the cell permeant calcium chelator Quin-2 AM inhibited GPIb-IX centralizat

178 Use of the fluorescent calcium chelator Quin-2 and consideration of the ATP con

179 inhibited by BAPTA-AM (an intracellular free calcium chelator), rottlerin (a protein kinase Cdelta in

180 apidly dismantling E-cadherin junctions with calcium chelators, significantly improved controllabilit

181 In combination with a light-sensitive calcium chelator, spin-labeled calmodulin can be used to

182 bitor) and ethylene glycol tetraacetic acid (calcium chelator) suggested existence of intermediate mo

183 as restored by the addition of intracellular calcium chelators, suggesting a role for the C2 region i

184 rg-chloromethylketone (Dec-RVKR-cmk), and by calcium chelators, suggesting that the parasite expresse

185 sensory neuron with EGTA, a relatively slow calcium chelator that does not alter rapid release but e

186 d membranes are incubated in the presence of calcium chelators, the membranes "uncoat," indicating th

187 d nuclear microinjection of a non-diffusible calcium chelator to block increases in nuclear, but not

188 The use of an intracellular calcium chelator to delay calcium signaling should have

189 FIV vector formulated with a calcium chelator transduced fully differentiated, nondiv

190 The intracellular calcium chelator was used to examine whether the intrace

191 etoxymethyl ester (MAPT/AM), a cell-permeant calcium chelator which reduced resting cytoplasmic [Ca2+

192 n of TRPN1 upon treatment of hair cells with calcium chelators, which disrupts the transduction appar

193 Interestingly, BAPTA, a calcium chelator with fast binding kinetics, is more pot