ライフサイエンスコーパス: BAPTA

1 BAPTA applied postsynaptically failed to block the actio

2 BAPTA inhibited RNA synthesis in all mammalian cell type

3 BAPTA inhibited UPR-dependent transcription of the GRP78

4 BAPTA is delivered to the cytoplasm as the acetoxymethyl

5 BAPTA loading of ECs inhibited agonist-induced increases

6 BAPTA, which binds Ca2+ approximately 100-fold faster th

7 BAPTA-AM also reduced DA release from striatal synaptoso

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

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

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

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

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

13 BAPTA-induced vasoconstriction was eliminated by a gener

14 gle APs and AP trains using Oregon Green 488 BAPTA-1 and streaming images at 20-50 Hz.

15 fluorescent Ca2+ indicator, Oregon Green 488 BAPTA-1 dextran or fura-2 dextran in vivo.

16 Fluorescein dextran and Oregon Green 488 BAPTA-5N were used to measure endosomal pH and calcium,

17 henoxy)ethane-N,N,N',N'-tetraacetic acid (5F-BAPTA) by radiofrequency labeling at the Ca(2+)-bound (1

18 to amplify the signal of Ca(2+) onto free 5F-BAPTA and thus indirectly detect low Ca(2+) concentratio

19 could be blocked by treatment with U-73122, BAPTA/AM, Ro-31-8220, or Go6976, indicating requirements

20 clamped to a 129 nm free Ca(2+) level with a BAPTA buffer and this was combined with numerous other m

21 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) reduced amphetamine-induced DA efflux as measured

22 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) significantly suppressed the MeHg-induced increas

23 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) to buffer changes in [Ca2+]i.

24 ophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA) to disrupt tip-links also effectively reduced GTT

25 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) was increased from a concentration of 0.1 to 10 m

26 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), and the changes in gene expression can be partia

27 aminophenoxy)ethane-N'N'N'-tetraacetic acid (BAPTA), application of 4-Aminopyridine (4-AP), expressio

28 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), PKC-overexpressing adenoviruses, and PKC inhibit

29 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), prolonged by the phosphatase inhibitor okadaic a

30 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), thereby reducing the difficulty of catching a sm

31 -aminophenoxy)ethane-N',N'-tetraacetic acid (BAPTA)-acetoxymethyl ester to buffer intracellular calci

32 nophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA)-AM, stretched, and COX-2 mRNA and protein were ev

33 ophenoxyl)ethane-N,N,N',N'-tetraacetic acid (BAPTA)-mediated intracellular Ca(2+) depletion.

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

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

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

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

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

39 Six hours after BAPTA treatment, GTTR uptake remained reduced in compari

40 he hair-cell apical membrane revealed, after BAPTA treatment or during perinatal development, 90-pS s

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

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

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

44 ctivated K(+) channels, including apamin and BAPTA dialysis, increased the duration of plateau potent

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

46 in C or thapsigargin was loaded into ECs and BAPTA into VSMCs, intercellular Ca2+ signaling was compl

47 reover, the differential effects of EGTA and BAPTA (slow and fast Ca(2+) chelators, respectively) sug

48 differential modulation of VDCCs by EGTA and BAPTA offers an alternative or complementary explanation

49 or in the presence of the chelators EGTA and BAPTA without additional adjustments to the model.

50 (2+) oscillations, as determined by EGTA and BAPTA-AM [1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetra

51 greatly reduced by the Ca2+ buffers EGTA and BAPTA.

52 uptake was comparable between untreated and BAPTA-treated hair cells, which again became susceptible

53 Both Cdh23(v2J/v2J) and BAPTA-treated hair cells were protected from degeneratio

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

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

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

57 re, we identified a greater coupling between BAPTA-sensitive, fast Ca(2+) transients and DA transmiss

58 Given evidence that the Ca(2+) buffer BAPTA can significantly reduce inspiratory drive, we hyp

59 by prior incorporation of the Ca(2+) buffer BAPTA, it was probably generated by light-activated Ca(2

60 re loaded with the widely used Ca(2+) buffer BAPTA, which is expected to dampen cytoplasmic [Ca(2+)]

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

62 olished in the presence of the Ca(2+) buffer BAPTA.

63 tion of RNA synthesis by the [Ca(2+)] buffer BAPTA was unanticipated.

64 high concentrations of the fast Ca2+ buffer BAPTA (10 mm).

65 5 mM fast Ca2+ buffer (BAPTA (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacet

66 fected by changing the intracellular buffer (BAPTA instead of EGTA).

67 Third, the intracellular Ca(2+) buffer, BAPTA, and the channel blocker, 2-aminoethoxydiphenyl bo

68 ess-induced JNK2 activation was abolished by BAPTA and isradipine, and partially reduced by extracell

69 Pyk2, c-Src and Raf-1 could be abolished by BAPTA/AM, demonstrating requirement for induction of int

70 ation, which was significantly attenuated by BAPTA, isradipine, or extracellular Ca(2+) depletion.

71 ylation of occludin, which was attenuated by BAPTA, SP600125 (JNK inhibitor), or PP2.

72 ced neonatal GMC apoptosis was attenuated by BAPTA, VIVIT, Fas blocking antibody, and a caspase-3/7 i

73 ry via voltage-gated channels, is blocked by BAPTA chelation, and recruits intracellular calcium rele

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

75 induction in CHO-K1 cells was not blocked by BAPTA.

76 ABA stimulation of small IBDM was blocked by BAPTA/AM and W7.

77 ive to chelation of intracellular calcium by BAPTA.

78 dent mechanisms because [Ca2+]i chelation by BAPTA or inhibition of PKC by bisindolymaleimide (BiM1),

79 Calcium depletion by BAPTA or Ca(2+)-free medium blocked ethanol and acetalde

80 d when Ca(2+) oscillations were inhibited by BAPTA injection.

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

82 TRPC3 that was attenuated by TeNT and not by BAPTA.

83 reviously for PCs in that it is prevented by BAPTA and DAG lipase inhibitors in the recording pipette

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

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

86 GABA-induced changes were prevented by BAPTA/AM, W7, and stable knockdown of the CaMK I gene.

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

88 of HepG2 cells, and this also was reduced by BAPTA.

89 ntracellular Ca(2+) with the Ca(2+) chelator BAPTA (100 micromol/L), indicating that elevated intrace

90 racellular injections of the Ca(2+) chelator BAPTA (20 mm), or bath applications of the L-type Ca(2+)

91 ng cytosolic Ca(2+) with the Ca(2+) chelator BAPTA (by exposure to BAPTA-AM) shifted activation of I(

92 mutations or exposure to the Ca(2+) chelator BAPTA can, however, still respond to mechanical stimuli.

93 ellular concentration of the Ca(2+) chelator BAPTA caused smaller increases in resting open probabili

94 ellular concentration of the Ca(2+) chelator BAPTA from 0.1 mm to 30 mm reduced the amplitude of I(K,

95 the intracellularly applied Ca(2+) chelator BAPTA in CA1 pyramidal cells, fast-spiking interneurons

96 of MDA-MB-231 cells with the Ca(2+) chelator BAPTA or an inhibitor of endoplasmic reticulum Ca(2+)-AT

97 tracellular perfusion of the Ca(2+) chelator BAPTA prevented the increase in intrinsic excitability.

98 by channel blocker NPPB and Ca(2+) chelator BAPTA, but not by cystic fibrosis transmembrane conducta

99 1, CPA and the cell-permeant Ca(2+) chelator BAPTA-AM activated the same 2.6 pS SOC in coronary arter

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

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

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

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

104 Also, dialysis with the fast Ca2+ chelator BAPTA eliminated differences in both I(Ca) amplitude and

105 ialysing cells with either the Ca2+ chelator BAPTA, or with peptide inhibitors of either calcineurin

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

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

108 ant acetoxymethyl ester of the Ca2+ chelator BAPTA.

109 trongly inhibited by the rapid Ca2+ chelator BAPTA.

110 n the failure rate when the calcium chelator BAPTA (10 mm) was introduced into the postsynaptic cell,

111 (PLC) inhibitor U73122 and calcium chelator BAPTA (5,5'-dimethyl-bis(o-aminophenoxy)ethane-N, N, N '

112 Treatment with the calcium chelator BAPTA or the protease subtilisin enabled these links to

113 ng different links with the calcium chelator BAPTA or the protease subtilisin.

114 n C or by the intracellular calcium chelator BAPTA, indicating that SKF83959 stimulates cdk5 and CaMK

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

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

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

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

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

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

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

122 nuated by the intracellular calcium chelator BAPTA.

123 ine (MLA) and intracellular calcium chelator BAPTA.

124 or N-ethylmaleimide and the calcium chelator BAPTA.

125 ressed by the intracellular calcium chelator BAPTA/AM (30 muM).

126 The divalent cation chelator BAPTA inhibited [Ca(2+)](c) responses to mechanical pert

127 lls; effects mitigated by [Ca(2+)]i chelator BAPTA, calcineurin/NFAT inhibitor VIVIT, and TRPC6 chann

128 Inclusion of the Ca2+-specific chelator BAPTA in the pipette-filling solution or preincubation w

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

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

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

132 Furthermore, a specific [Ca2+]int chelator (BAPTA) or Cd2+, a specific blocker of voltage-operated C

133 ional experiments using the Ca(2+) chelator, BAPTA/AM, demonstrated that Ca(2+) influx is sufficient

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

135 exposure to vehicle or the calcium chelator, BAPTA (1-20 microM), primary cortical neurons were label

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

137 re treated with a internal calcium chelator, BAPTA.

138 loading of the cells with the Ca2+ chelators BAPTA and EGTA, and by exposure to the NCX inhibitor KB-

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

140 Although calcium chelators (BAPTA, EGTA) inhibited basal and ionomycin-induced NO pr

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

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

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

144 In contrast, BAPTA had little influence on calcium levels in a brain

145 In contrast, BAPTA loading of the VSMCs blunted the VSMC response but

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

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

148 ns were similar to those caused by cytosolic BAPTA, which promotes release by hampering Ca2+-dependen

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

150 )ethane-N,N,N',N'-tetraacetic acid (dimethyl-BAPTA).

151 the PKC inhibitor Ro-31-8220, PP2, dimethyl-BAPTA, or LY294002, but were abolished by Ro-31-8220 plu

152 e abolished by Ro-31-8220 plus PP2, dimethyl-BAPTA, or LY294002.

153 tte solutions buffered with 1-4 mm of either BAPTA or EGTA gave rise to similar patterns of I(ORCa) o

154 he cytoplasm as the acetoxymethyl (AM) ester BAPTA/AM, but released AM groups, as well as formaldehyd

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

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

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

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

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

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

161 -tetraacetic acid, tetraacetoxymethyl ester (BAPTA/AM) or N-(6-aminohexyl)-5-chloro-1-naphtalenesulfo

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

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

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

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

166 ,N',N'-tetraacetic acid/acetoxymethyl ester, BAPTA/AM) fully inhibits intracellular and luminal Ca(2+

167 Calcium Rubies, a family of functionalizable BAPTA-based red-fluorescent calcium (Ca(2+)) indicators

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

169 Furthermore, BAPTA [bis-(o-aminophenoxy)ethane-N,N',N'-tetraacetic ac

170 ns loaded with either Fluo-4 or Oregon Green BAPTA 5 N, we observed Ca(2+) transients associated with

171 antitative Ca(2+) imaging using Oregon green BAPTA-1 (OGB1), to examine how the balance of exocytic m

172 ced that the calcium indicator (Oregon Green BAPTA-1) blocked the mAHP.

173 e from NP-EGTA and DMn by using Oregon green BAPTA-5N to measure changes in [Ca(2+)] after ultraviole

174 Using HEPES, BAPTA, or carboxyeosin, the effect of XCAR was completel

175 However, BAPTA also blocked cytoplasmic stress-dependent (UPR-ind

176 eas only about 70% of mitochondria did so in BAPTA.

177 NMDA receptor antagonist APV, intracellular BAPTA, the CaM kinase inhibitors KN-62 and autocamtide-2

178 ondition but were abolished by intracellular BAPTA and pretreatment with thapsigargin.

179 +) current that was reduced by intracellular BAPTA at concentrations >or= 1 mM.

180 ond component was inhibited by intracellular BAPTA or by bath application of niflumic acid (100 micro

181 nd that high concentrations of intracellular BAPTA, a high-affinity Ca2+ chelator, and the I(CAN) ant

182 enamic acid, 9-phenanthrol, or intracellular BAPTA.

183 ethacholine was insensitive to intracellular BAPTA, but was attenuated by either acute inhibition of

184 ting Ca(2+) in astrocytes with intracellular BAPTA causes vasoconstriction in adjacent arterioles.

185 -cell patch clamp studies with intracellular BAPTA demonstrated that 98% of the increase in calcium c

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

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

188 le pretreatment of platelets with 100 microM BAPTA/AM (Kd 160 nM) had minimal effects, 100 microM 5,5

189 tracellular Ca(2+) by inclusion of 50 microM BAPTA in the whole-cell pipette reduced the voltage-depe

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

191 cellular Ca(2+) buffering conditions (0.1 mm BAPTA), 1 nm and 10 nm Ang II activated both 2 pS TRPC1/

192 was estimated to be equivalent to about 1 mM BAPTA, suggesting that in physiological conditions the S

193 ather than 5 mm EGTA, and diminished by 1 mm BAPTA.

194 mped with pipette solutions containing 10 mm BAPTA and free Ca2+ concentrations of approximately 17 n

195 Ca(2)(+) buffer is saturated, despite 10 mM BAPTA conditions.

196 intracellular Ca2+ in the presence of 10 mm BAPTA to block I(ORCa) oscillations led to a dose-depend

197 ations of intracellular Ca(2+) buffer (10 mm BAPTA) greatly reduced exocytosis and abolished the tran

198 acellular Ca(2+) buffering conditions (10 mm BAPTA), 10 nm Ang II-induced TRPC6 channel activity was

199 extreme Ca(2)(+) buffering conditions (10 mM BAPTA), our data argue against the Ca(2)(+)-dependent co

200 greatly attenuated in recordings with 20 mm BAPTA containing postsynaptic internal solution, but a d

201 ular Ca(2+) to < 1 nm free Ca(2+) with 20 mm BAPTA in the pipette, but suppression was normal if inte

202 nist-induced increase was abolished in 20 mm BAPTA-filled cells.

203 by WIN, was abolished after dialyzing 40 mm BAPTA into the postsynaptic cell, suggesting that DHPG a

204 EDTA (10 mM), BAPTA (10 microM), and RNAi silencing of IP(3) receptor,

205 ent crowns are removed by subtilisin but not BAPTA.

206 The actions of BAPTA were overcome by exposure to forskolin (10 microm)

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

208 I was blocked by intrapipette application of BAPTA.

209 However, when the concentration of BAPTA was reduced to 0.5 mm, inactivation of Ca2+ curren

210 PMCA activation was prevented by dialysis of BAPTA or the PMCA inhibitor carboxyeosin.

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

212 The effects of BAPTA could be reversed by forskolin (10 mum), a direct

213 The similarities with the effects of BAPTA suggest that the mutation, occurring near the cyto

214 -cell configuration prevented the effects of BAPTA.

215 ither CPA or the acetoxymethyl ester form of BAPTA (BAPTA-AM).

216 r sodium, extracellular Ni(2+), inclusion of BAPTA in the pipette, KB-R7943, and SKF96365.

217 m transients in the ooplasm via injection of BAPTA as a calcium chelator.

218 possibly reflect a fortuitous interaction of BAPTA with the RNA synthesis machinery or a requirement

219 Somatic extracellular ionophoresis of BAPTA during I(sAHP) caused a transient inhibition, but

220 cardiac calcium channels in the presence of BAPTA in intact ventricular myocytes.

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

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

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

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

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

226 BAPTA-AM or BAPTA failed to flatten APD restitution slope to <1 by e

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

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

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

230 imental results in which addition of EGTA or BAPTA produces different effects.

231 Addition of either EGTA or BAPTA to the cis hemi-chamber, representing the cytoplas

232 ring spine depolarization with added EGTA or BAPTA, the model invokes the modulation of CaV2.3 (R-typ

233 currents observed in the presence of EGTA or BAPTA.

234 racellular Ca(2)(+) buffering (EGTA 10 mm or BAPTA 20 mm), and with substitution of Ba(2)(+) for extr

235 In the presence of ryanodine or BAPTA, or when Ba2+ was used as the charge carrier, the

236 ed increase in [Ca2+]i (e.g. thapsigargin or BAPTA (1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacet

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

238 photolytical properties of a photoactivable BAPTA-based Ca(2+) cage containing two photosensitive o-

239 er that could not be blocked by postsynaptic BAPTA, and had no direct effect on transmission.

240 rupted by NBQX, philanthotoxin, postsynaptic BAPTA, or external sequestration of BDNF, consistent wit

241 ally, in brain slices from P7 neonatal rats, BAPTA induced significant loss of calcium in a brain reg

242 addition of the soluble SNARE Vam7p relieves BAPTA inhibition as effectively as Ca2+ or Mg2+, suggest

243 or amplitude of the nonlinear DD (ryanodine, BAPTA, nifedipine or isoproterenol) produced correspondi

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

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

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

247 tetrafluorinated derivative of the BAPTA (TF-BAPTA) chelate as a (19)F chelate analogue of existing o

248 namic exchange between ion-bound and free TF-BAPTA to obtain MRI contrast with multi-ion chemical exc

249 ga) values between the ion-bound and free TF-BAPTA, we exploited the dynamic exchange between ion-bou

250 We demonstrate that TF-BAPTA as a prototype single (19)F probe can be used to s

251 lts led to the unexpected demonstration that BAPTA was a general inhibitor of cellular RNA synthesis

252 We found that BAPTA-based calcium chelators cause immediate depolymeri

253 We found that BAPTA-induced changes in calcium were highly correlated

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

255 using the tetrafluorinated derivative of the BAPTA (TF-BAPTA) chelate as a (19)F chelate analogue of

256 possibility of aromatic substitutions on the BAPTA core for tuning the Ca(2+)-binding affinity.

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

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

259 treatments, tip links are only sensitive to BAPTA, and tectorial membrane attachment crowns are remo

260 he different sensitivities of the spindle to BAPTA and EGTA-suggest that meiotic spindle function in

261 GluK1 receptor agonist was compromised when BAPTA was added in the recording pipette to buffer intra

262 B was significantly greater when BAPTA, which increases release flux, was present in the

263 However, when BAPTA concentration is lowered to 1 mm, I(ORCa) oscillat

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

265 rents by 86%, with a t1/2 = 3.6 min, whereas BAPTA rapidly and completely (100%) eliminated channel a

266 ngle sperm-induced Ca(2+) transient, whereas BAPTA/AM-treated ICSI or fertilized eggs cultured in Ca(

267 th 10 mM EGTA reduced desensitization, while BAPTA completely eliminated it.

268 Chelating intracellular Ca(2+) with BAPTA reproduced the effects of ST.

269 s the chelation of intracellular Ca(2+) with BAPTA, or the absence of external Ca(2+) , suppressed th

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

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

272 by strong buffering of internal Ca(2+) with BAPTA.

273 ocked by buffering intracellular Ca(2+) with BAPTA.

274 when extracellular Ca(2+) was buffered with BAPTA to approximately 30 nM.

275 r, strong postsynaptic Ca(2+) buffering with BAPTA abolished the potentiation and selective antagonis

276 quential treatments of the hair bundles with BAPTA and subtilisin show that the effects are additive.

277 Chelation of intracellular Ca2+ with BAPTA blocked S1P-induced Rac activation, indicating the

278 sts, by chelation of intracellular Ca2+ with BAPTA, and by inhibition of both Ca2+-calmodulin-depende

279 ressing Ca(2+) signaling or calcineurin with BAPTA, cyclosporine A, or FK506 prevented activation of

280 r by buffering the postsynaptic calcium with BAPTA, suggesting that the primary mechanism for hypocre

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

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

283 n inhibition or by preloading the cells with BAPTA (bis-(o-aminophenoxy)-N,N'N'-tetraacetic acid).

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

285 Ca(2+)-chelation with BAPTA + EGTA reduced Shh expression.

286 ing intracellular calcium concentration with BAPTA-AM.

287 r hair cells after tip-link destruction with BAPTA, in transmembrane channel-like protein isoforms 1/

288 2+)), replacement of intracellular EGTA with BAPTA, a fast Ca(2+) chelator, and Gd(3+) and SKF-96365,

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

290 The effect persisted after incubation with BAPTA-AM.

291 ing the stimulated/recorded interneuron with BAPTA did not block barrage firing, suggesting that the

292 hen the astrocytic syncytium was loaded with BAPTA (chelating intracellular Ca(2+)) and enhanced when

293 Na+/Ca2+ exchanger blocker KB-R7943, or with BAPTA in the pipette, consistent with a mechanism based

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

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

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

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

298 and that buffering of these transients with BAPTA slows movement.

299 Treatment with BAPTA, which cleaves tip, kinocilial and ankle links, re

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