ライフサイエンスコーパス: BAPTA-AM

1 BAPTA-AM also inhibited cell division to the 16-cell sta

2 BAPTA-AM also reduced DA release from striatal synaptoso

3 BAPTA-AM and thapsigargin blocked EGF-induced membrane t

4 BAPTA-AM at 0.5 microM did not significantly alter the b

5 BAPTA-AM did not alter these interactions, suggesting th

6 BAPTA-AM inhibited VEGF- but not insulin-induced eNOS-HS

7 BAPTA-AM or BAPTA failed to flatten APD restitution slop

8 BAPTA-AM reduced Ca(i)T amplitude to 30.5+/-12.9% of con

9 BAPTA-AM was used to chelate intracellular Ca2+.

10 calcium-dependent signals by cyclosporin A, BAPTA-AM [glycine, N,N'-1,2-ethanediylbis(oxy-2,1-phenyl

11 ,N,N',N'-tetraacetic acid-acetomethoxyester (BAPTA-AM).

12 xy) ethane N:, N:, N:, N:-tetra-acetic acid (BAPTA-AM) to buffer changes in [Ca(2+)](i), or the prote

13 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM) both evoked channel currents, which had unitar

14 ophenoxyl)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), an intracellular Ca(2+) chelator known to dep

15 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM).

16 ophenoxy)ethane-N,N,N',N'-tetraacetic acid) (BAPTA-AM) or the PI3K inhibitor LY 294002 prevented Akt

17 y the membrane-permeant Ca2+-chelating agent BAPTA-AM.

18 henoxy)ethane-N,N,N',N'-tetraacetic acid-AM (BAPTA-AM), 8-amino-2-[(2-amino-5-methylphenoxy)methyl]-6

19 treated with the membrane-permeant analogue BAPTA AM.

20 r's solution, Ca-free Ringer's solution, and BAPTA AM-pretreated preparations; imaging of nerve termi

21 ilitation, but in contrast to low Ca(2+) and BAPTA-AM, EGTA-AM increased long-lasting paired-pulse de

22 vesicle transport inhibitor brefeldin A and BAPTA-AM significantly blocked Alternaria-stimulated inc

23 comparable to the effects of brefeldin A and BAPTA-AM.

24 pletion of internal Ca(2+) stores by CPA and BAPTA-AM.

25 SOCs evoked by cyclopiazonic acid (CPA) and BAPTA-AM.

26 Dantrolene and BAPTA-AM prevented the increase in intracellular calcium

27 (2+) oscillations, as determined by EGTA and BAPTA-AM [1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetra

28 s modulated by the addition of both EGTA and BAPTA-AM, agents chelating either external or internal C

29 hostin C (a protein kinase C inhibitor), and BAPTA-AM (an intracellular Ca2+ chelator) reduced phagoc

30 ent of growth plate chondrocytes with RA and BAPTA-AM, a cell permeable Ca2+ chelator, inhibited the

31 rkA to the membrane was Ca(2+) dependent, as BAPTA-AM Ca(2+) chelation abrogated the response.

32 with the acetoxymethyl ester form of BAPTA (BAPTA AM).

33 A and the acetoxymethyl ester form of BAPTA (BAPTA-AM) was markedly inhibited by the PKC inhibitors c

34 PA or the acetoxymethyl ester form of BAPTA (BAPTA-AM).

35 intracellular calcium mobilization, because BAPTA-AM blocked DRAK2 kinase activity, whereas the SERC

36 The cell-permeable Ca(2+) buffer BAPTA-AM, the IP(3) receptor antagonist Xestospongin C a

37 is was significantly inhibited or blocked by BAPTA-AM or by low or no extracellular Ca(2+); and P2X(7

38 Moreover, calcium chelation by BAPTA-AM raised the threshold for alternans and inhibite

39 0(RSK) was not inhibited but was enhanced by BAPTA-AM.

40 osphorylation and activity were inhibited by BAPTA-AM (an intracellular free calcium chelator), rottl

41 and caspase 3 activation) were inhibited by BAPTA-AM in both the wild-type and the PARS-deficient th

42 ction was calcium-dependent and inhibited by BAPTA-AM.

43 Blocking intracellular Ca2+ mobilization by BAPTA-AM or thapsigargin did not inhibit glutamate relea

44 the presence of Ca2+, which was prevented by BAPTA-AM loading (to preserve the workload), or in Ca2+-

45 ced dye uptake by astrocytes is prevented by BAPTA-AM or a phospholipase C (PLC) inhibitor.

46 When intracellular Ca(2+) was reduced by BAPTA-AM in wild-type sperm, they exhibited flagellar be

47 Blockade of intracellular calcium release by BAPTA-AM (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraa

48 embrane-permeant intracellular Ca2+ chelator BAPTA AM eliminates this odor adaptation.

49 The calcium chelator BAPTA AM and agents that block calcium release from ER a

50 with the membrane-permeant calcium chelator BAPTA AM significantly decreased the accumulation of NAD

51 ells pre-incubated with the calcium chelator BAPTA AM.

52 ncrease with the cytoplasmic Ca(2+) chelator BAPTA-AM [1,2-bis(2-aminophenoxy)ethane-N,N,N1,N-tetraac

53 1, CPA and the cell-permeant Ca(2+) chelator BAPTA-AM activated the same 2.6 pS SOC in coronary arter

54 Furthermore, both the fast Ca(2+) chelator BAPTA-AM and the slow chelator EGTA-AM reduced the mIPSC

55 The cell-permeable Ca(2+) chelator BAPTA-AM blocked activation of Jak2, complex formation b

56 The Ca(2+) chelator BAPTA-AM blocked Ser-54 phosphorylation during dark adap

57 Since the fast Ca(2+) chelator BAPTA-AM inhibits LFD but the slow chelator EGTA-AM does

58 jection of the intracellular Ca(2+) chelator BAPTA-AM, or the cPLA(2) blockers AACOCF(3) and MAFP.

59 y loading the cells with the Ca(2+) chelator BAPTA-AM, showing that it was the consequence of the act

60 n effect is prevented by the Ca(2+) chelator BAPTA-AM.

61 of pIgR, while the intracellular Ca chelator BAPTA-AM inhibits transcytosis.

62 1 mmol/L) or the intracellular Ca2+ chelator BAPTA-AM (20 mumol/L).

63 Cd2+, or a membrane permeable Ca2+ chelator BAPTA-AM (when BAPTA was loaded in the recording electro

64 sin D and to the intracellular Ca2+ chelator BAPTA-AM but not the Ca2+ channel blocker verapamil.

65 addition of the intracellular Ca2+ chelator BAPTA-AM or the Ca2+/calmodulin-dependent (CaM) kinase i

66 nfiguration the cell-permeable Ca2+ chelator BAPTA-AM stimulated SOC activity and after excision of a

67 t is completely blocked by the Ca2+ chelator BAPTA-AM.

68 atelets with the intracellular Ca2+ chelator BAPTA-AM.

69 of cells with the intracellular Ca2+chelator BAPTA-AM rescued both FRDA fibroblasts and controls from

70 ment with the intracellular calcium chelator BAPTA-AM (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraa

71 lls were incubated with the calcium chelator BAPTA-AM (1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraa

72 0 microM), or the cytosolic calcium chelator BAPTA-AM (50 microM) each strongly impaired PACAP-induce

73 nterestingly, the cytosolic calcium chelator BAPTA-AM and K-201 protected RA-treated chondrocytes fro

74 undergoing PA-LTx with the calcium chelator BAPTA-AM and the anti-oxidant MCI-186 significantly reve

75 pathways, an intracellular calcium chelator BAPTA-AM and the Ca(2+)(mito) uniporter blocker rutheniu

76 ore, the membrane-permeable calcium chelator BAPTA-AM had no effect on BK-induced COX-2 expression an

77 reatment with intracellular calcium chelator BAPTA-AM or disruption of lipid rafts using methyl beta-

78 73122, by the intracellular calcium chelator BAPTA-AM, and by the specific calmodulin antagonist W-7.

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

80 which was inhibited by the calcium chelator BAPTA-AM, the calcium channel blocker SK&F 96365, and ca

81 The calcium chelator BAPTA-AM, which reduces cytosolic calcium, rescues the d

82 agonists, tetrodotoxin, and calcium chelator BAPTA-AM.

83 since the intracellular calcium ion chelator BAPTA-AM, but not the extracellular chelator EGTA abolis

84 ar Ca2+ with the membrane-permeable chelator BAPTA-AM (10 microM) significantly reduced (and in some

85 rrolidine dithiocarbamate), Ca(2+) chelator (BAPTA-AM), and calpain inhibitor (N-acetyl-Leu-Leu-Met-H

86 ubation with an intracellular Ca2+ chelator (BAPTA-AM and its derivatives) partially blocked the late

87 We used a calcium chelator (BAPTA-AM) to abolish Ca(i)T and test its involvement in

88 e 2 inhibitor (STO-609) or calcium chelator (BAPTA-AM).

89 aq or phospholipase C and the Ca2+ chelator, BAPTA-AM, abrogated thrombin-induced RhoA activation.

90 lication of the cell-permeant Ca2+ chelator, BAPTA-AM, also activated similar currents, indicating th

91 n addition, the intracellular Ca2+ chelator, BAPTA-AM, blocked the differentiation response and atten

92 ntrast, the cell-permeable calcium chelator, BAPTA-AM (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraa

93 I, or by the intracellular calcium chelator, BAPTA-AM.

94 evident in presence of the calcium chelator, BAPTA-AM.

95 ways: (1) applying cell permeable chelators BAPTA-AM or EGTA-AM; (2) decreasing Ca(2+) concentration

96 olidine dithiocarbamate) and Ca2+ chelators (BAPTA-AM and TMB-8).

97 n of calcium increases by calcium chelators, BAPTA-AM and EGTA-AM, abrogated NF-kappaB activation by

98 of two membrane-permeant calcium chelators, BAPTA-AM and EGTA-AM.

99 r Ca2+ using the membrane-permeable compound BAPTA-AM, abolished the effects of purinoceptor activati

100 th a cell-permeable Ca2+-chelating compound (BAPTA-AM) significantly inhibited ATP release, indicatin

101 an important role in SOC activation by CPA, BAPTA-AM and PDBu.

102 SOCs stimulated by CPA, BAPTA-AM and the phorbol ester phorbol 12,13-dibutyrate

103 Strikingly, deciliation, BAPTA-AM, and apyrase also blocked the flow-dependent in

104 ,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA-AM) and completely eliminated by the calmodulin an

105 ,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA-AM) and decreased by 1.7-fold (P < 0.05) by nifedi

106 N', N'-tetraacetic acid-acetoxymethyl ester (BAPTA-AM) reduced cytosolic Ca(2+) by approximately 31%

107 ,N',N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM), a Ca2+ chelator.

108 N,N',N'-tetraacetate-AM acetoxymethyl ester (BAPTA-AM), cyclosporine, and inhibitor of nuclear factor

109 ,N',N'-tetraacetic acid acetoxymethyl ester (BAPTA-AM); and (4) after pretreatment with the protein k

110 tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM) or inhibiting NO synthase activity with N(G)-n

111 raacetic acid tetrakis(acetoxymethyl) ester (BAPTA-AM) or the CaM antagonist W7, whereas the transien

112 etraacetic acid tetra (acetoxymethyl) ester (BAPTA-AM) reduced 5-HT release.

113 tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM) was added in some studies.

114 tetraacetic acid-tetra(acetoxymethyl) ester (BAPTA-AM), and PI3-K inhibitor (LY294002).

115 ',N'-tetraacetic acid-(acetoxymethyl) ester (BAPTA-AM), indicating that Ca(2+) triggers the fatal sig

116 N',N'-tetraacetic acid (acetoxymethyl)ester (BAPTA-AM) abolished aggregation induced by convulxin und

117 -tetraacetic acid tetra(acetoxymethyl)ester (BAPTA-AM).

118 t of oocytes with BAPTA-acetoxymethyl-ester (BAPTA-AM) nearly completely prevented dephosphorylation

119 '-tetraacetic acid tetraacetoxymethyl ester (BAPTA-AM).

120 ',N'-tetraacetic acid (acetoxymethyl ester) (BAPTA AM) did the opposite.

121 aacetic acid tetrakis (acetoxymethyl ester) (BAPTA-AM) blocked both ERK and Ras activation, suggestin

122 -acetic acid tetrakis (acetoxymethyl ester) (BAPTA-AM) or blockade of extracellular signal-regulated

123 ',N'-tetraacetic acid (acetoxymethyl ester) (BAPTA-AM) or the three specific calcineurin inhibitors F

124 aacetic acid tetrakis (acetoxymethyl ester) (BAPTA-AM), an intracellular Ca(2+) chelator, indicating

125 raacetic acid tetrakis(acetoxymethyl ester) (BAPTA-AM), leads to a dramatic redistribution of the ves

126 aacetic acid-tetrakis (acetoxymethyl ester) (BAPTA-AM).

127 Further, BAPTA-AM chelation of intracellular calcium also inhibit

128 ipine or when myocytes were pre-incubated in BAPTA-AM.

129 Either intracellular (BAPTA-AM) or intra-endosomal (Rhod-dextran) calcium chel

130 Ca(2+) increases were abolished by 20 microM BAPTA AM, a result suggesting that ATP hydrolysis was mi

131 elation of intracellular Ca(2+) by 10 microm BAPTA-AM.

132 However, exposure of cells to 5 microM BAPTA-AM, in order to reduce [Ca(2+)](i) transients, als

133 Treatment of monolayers with 50 microm BAPTA-AM completely blocked the effects of UTP on K(+) c

134 ess, neither GF109203X, a PKC inhibitor, nor BAPTA-AM, a calcium chelator, blocked phosphorylation of

135 In sup- cells in low serum, addition of BAPTA-AM also resulted in a significant ( approximately

136 educed I(CaL), but subsequent application of BAPTA-AM further reduced I(CaL).

137 This effect of BAPTA-AM, in the presence of CaMKII inhibition, demonstr

138 tion, a process inhibited in the presence of BAPTA-AM, suggesting that the Ca(2+) binding motifs in A

139 In the presence of BAPTA-AM, the actions of IBMX were reduced.

140 ternucleosomal DNA cleavage was increased on BAPTA-AM pretreatment in the wild-type cells but decreas

141 arteriolar ECs were loaded with Fluo-4 AM or BAPTA AM by intraluminal perfusion, after which blood fl

142 h the acetoxymethyl ester forms (benz2 AM or BAPTA AM).

143 e of 2'5'-dideoxyadenosine 0.64 +/- 0.03, or BAPTA-AM 0.45 +/- 0.23) but independent of inhibition of

144 Low Ca(2+)-high Mg(2+) or BAPTA-AM dramatically reduced the amplitude of corticost

145 peak Ca(2+) (i.e. low Ca(2+)-high Mg(2+) or BAPTA-AM).

146 brane region was decreased by brefeldin-A or BAPTA-AM.

147 fering intracellular calcium with EGTA-AM or BAPTA-AM reduced asynchronous EPSC rates earlier and to

148 versibly blocked by 4-DAMP, charybdotoxin or BAPTA-AM, but not by N(omega)-nitro-L-arginine methyl es

149 jections with cytochalasin D, colchicine, or BAPTA-AM had no affect on firm adhesion.

150 ment of A23187-stimulated cells with EGTA or BAPTA-AM demonstrated that a substantial pool of cPLA2-a

151 g the wild-type VSMC [Ca2+]i by Verapamil or BAPTA-AM significantly increased cellular cAMP concentra

152 olutions containing thapsigargin, ryanodine, BAPTA-AM, 18-alpha-glycyrrhetinic acid (18alpha-GA), apy

153 Similarly, BAPTA-AM prevented the activation of p70(S6K) by Ang II,

154 and actin cytoskeleton reorganization since BAPTA AM, cytochalasin D, and inhibitors of Rho and myos

155 )ethane-N,N,N',N'-tetraacetic acid tetrakis (BAPTA-AM).

156 y, thapsigargin and ionomycin attenuated the BAPTA-AM effects and promoted NF-kappaB activation by th

157 lic acid (1 mM; an I(Cl)(Ca) blocker) and to BAPTA AM, but was abolished by 1 microM nifedipine.

158 Embryos exposed to BAPTA-AM, a chelator of intracellular Ca2+, exhibited a

159 Exposure to BAPTA-AM (1,2bis-(-aminophenoxy)ethans-N,N,N', N'-tetraa

160 th the Ca(2+) chelator BAPTA (by exposure to BAPTA-AM) shifted activation of I(f) in the hyperpolariz

161 cytosolic Ca(2+) by exposure of myocytes to BAPTA-AM (5 mum) reduced I(CaL) amplitude, as did inhibi

162 timulated by 1 nM ryanodine was sensitive to BAPTA-AM preincubation but independent of thapsigargin-s

163 or chelation of intracellular calcium using BAPTA AM prevented the induction of the depolarizing aft

164 Chelation of intracellular Ca(2+) using BAPTA-AM, or inhibition of the Ca(2+)-dependent proteins

165 modulating calcium in the murine brain using BAPTA-AM augments AAV gene expression in vivo Taking the

166 ); (b) buffering intracellular calcium using BAPTA-AM loading; (c) blockade of SR calcium release wit

167 elevation of intracellular Ca2+ levels using BAPTA-AM results in a block of PN1 induction by NGF.

168 obulin-binding protein (BiP) levels, whereas BAPTA-AM increased XBP1 splicing and BiP expression, sug

169 65 mV, 44 +/- 2% with Li+ and 20 +/- 2% with BAPTA AM).

170 ith Li+ or buffering intracellular Ca2+ with BAPTA AM resulted in the loss of a transient inward curr

171 Pretreatment of the cells with BAPTA AM, thapsigargin or the phospholipase C (PLC) inhi

172 n intracellular free Ca2+ concentration with BAPTA AM significantly increases neurite sprouting and e

173 itor) or chelating intracellular Ca(2+) with BAPTA-AM failed to attenuate any of the oxLDL effects as

174 e, or buffering of intracellular Ca(2+) with BAPTA-AM.

175 ed by chelation of intracellular Ca(2+) with BAPTA-AM.

176 Chelation of cytosolic free Ca2+ with BAPTA-AM, but not inhibition of protein kinase A activit

177 -dextran or chelating cytosolic calcium with BAPTA-AM attenuated Tat endolysosome escape and LTR tran

178 lar calcium, since chelation of calcium with BAPTA-AM significantly reduced Act-induced IL-8 producti

179 alpha(q)-mediated intracellular calcium with BAPTA-AM, pertussis toxin inhibition of Galpha(i/o), or

180 Pretreatment of cells with BAPTA-AM (a cytosolic Ca2+ chelator) or catalase (enzyma

181 slowing was blocked by incubating cells with BAPTA-AM (a membrane-permeant analogue of BAPTA) or by t

182 Preincubation of cells with BAPTA-AM prevented activation of SOK-1.

183 for 24 h) but not by calcium chelation with BAPTA-AM (acetoxymethyl ester of BAPTA) (75 microM for 3

184 ing intracellular calcium concentration with BAPTA-AM.

185 r Ca(2+), or chelation of [Ca(2+)](cyt) with BAPTA-AM, failed to inhibit TG toxicity, although they p

186 ring DAMGO-induced changes in [Ca(2+)]i with BAPTA-AM completely blocked the inhibition of both I(Ca)

187 solution, or (iv) buffering [Ca(2+)](i) with BAPTA-AM.

188 EGTA) and was ablated after incubation with BAPTA-AM (5 microm) or caffeine (10 mm), indicating that

189 The effect persisted after incubation with BAPTA-AM.

190 Inhibition of Ca(2+) oscillations with BAPTA-AM prevented alpha IIb beta 3 activation but not t

191 utes) when the fibers were preincubated with BAPTA-AM or when they were exposed to 1 mM [Ca2+]o in Na

192 ct was prevented by conditioning slices with BAPTA-AM (200 muM), and by blockers of the BK calcium-de

193 bility was prevented by treating slices with BAPTA-AM or bumetanide, suggesting that gp120 activates

194 or buffering the global Ca2+i transient with BAPTA-AM or BAPTA.

195 HL-60 cells or sensitive cells treated with BAPTA-AM.

196 ved in deciliated cells, upon treatment with BAPTA-AM, or upon inclusion of apyrase in the perfusion

197 Pre-treatment with BAPTA-AM, so as to buffer internal Ca2+, partly protecte

198 ped cardiac myocytes treated with or without BAPTA-AM (1,2-bis[2-aminophenoxy]ethane-N,N,N',N'-tetraa