ライフサイエンスコーパス: EGTA

1 EGTA (a buffer with slow 'on-rate') speeded Ca2+ signals

2 EGTA reduced PC2hst channel currents by 86%, with a t1/2

3 EGTA sensitivity and divalent cation stress phenotypes i

4 EGTA was also found to increase T3SS1 gene expression an

5 EGTA-AM had the opposite effects.

6 EGTA-AM produced a smaller reduction in EPSC amplitude a

7 nally Ca(2+)-free medium (no added Ca(2+); 0 EGTA) a smaller, slow response occurred.

8 cytes dialysed with 250 nM Ca2+ (50 mmol l-1 EGTA).

9 hanging cations from Ca(2+)/Mg(2+) to Mg(2+)/EGTA and to Mn(2+) caused longer lifetime in the same 10

10 nal antibody KIM185-activated but not Mg(2+)/EGTA-activated leukocyte function-associated antigen-1 (

11 removal of Ca(2+) ions and addition of 1.2mM EGTA did not alter the action of harmane on [(3)H]5-HT r

12 e PKC inhibitors calphostin C or Ro-31-8220, EGTA to chelate Ca(2+), or the c-Src inhibitor PP1 befor

13 Accordingly, EGTA blocked almost all of the complement activation.

14 d (EDTA) and ethyleneglycoltetraacetic acid (EGTA), are used extensively during protein purification.

15 minoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) + 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraace

16 minoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) in the CA1 region of hippocampus in vivo.

17 igargin or ethylene glycol tetraacetic acid (EGTA) inhibited the proliferation.

18 ) chelator ethylene glycol tetraacetic acid (EGTA) significantly reduced wound induction of RSRE::LUC

19 aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA) to regulate the free calcium concentration ([Ca(2+

20 s, such as ethylene glycol tetraacetic acid (EGTA), or inhibitors, such as sodium azide, to compare t

21 ontrol CaMKII activation observed with added EGTA during depolarization.

22 amics during spine depolarization with added EGTA or BAPTA, the model invokes the modulation of CaV2.

23 tivation seen in dendritic spines with added EGTA, and suggests that differential modulation of VDCCs

24 confirmed by internalization with ZO-1 after EGTA-induced disruption of cell junctions.

25 t, bacteria penetrated blotted corneas after EGTA treatment and in SP-D knockouts.

26 temperatures, but no effects were seen after EGTA treatment.

27 oval of Ca(2+) from GyrA by dialysis against EGTA leads to a modest loss in relaxation activity that

28 by denaturation of GyrA and dialysis against EGTA results in an enzyme with greatly reduced enzyme ac

29 Chelating agents EGTA and EDTA also inhibited nuclease activity.

30 but in contrast to low Ca(2+) and BAPTA-AM, EGTA-AM increased long-lasting paired-pulse depression.

31 by staurosporine, PP2, wortmannin, BAPTA/AM, EGTA, and L-655238, implicating src-tyrosine kinases, PI

32 Blockade of calcium accumulation with AM-EGTA also prevents the conversion of exocytic mode.

33 reaction medium containing ATP, Mg(2+), and EGTA.

34 increases by calcium chelators, BAPTA-AM and EGTA-AM, abrogated NF-kappaB activation by these agents

35 the cells with the Ca2+ chelators BAPTA and EGTA, and by exposure to the NCX inhibitor KB-R7943 (5 m

36 nt sensitivities of the spindle to BAPTA and EGTA-suggest that meiotic spindle function in frog oocyt

37 ed and progressed only in aged, blotted, and EGTA-treated, SP-D knockout mice.

38 rify its coincident induction by calcium and EGTA.

39 that were blocked by cyclosporin A (CsA) and EGTA.

40 tants suffered from inefficient, delayed and EGTA-supersensitive release.

41 oteosome inhibitor MG132 and also by E64 and EGTA, suggesting that proteolysis is initiated by cystei

42 rb surprisingly large quantities of EDTA and EGTA that elute from the resin at NaCl concentrations of

43 Upon addition of EDTA and EGTA, the divalent cations were sequestered from the sta

44 mag-fura-2, nitrilotriacetic acid, EDTA, and EGTA estimate K(D) Ni(II) for the tightest site of InrS

45 ted by antipain, N-ethylmaleimide, EDTA, and EGTA.

46 pathway in normal human serum with Mg2+ and EGTA resulted in the survival of this uspA2 mutant.

47 reased the decay of IPSCs in LF neurons, and EGTA-AM reduced the decay of IPSCs in MF/HF neurons.

48 tion of mechanotransduction with quinine and EGTA protected against cisplatin-induced hair cell death

49 mA, which suppresses sensitivity to salt and EGTA.

50 In the presence of skeletal troponin and EGTA, the decrease in fluorescence was followed by the r

51 of sensitivity to salt and chelators such as EGTA and greatly diminished endotoxic activity.

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

53 Although calcium chelators (BAPTA, EGTA) inhibited basal and ionomycin-induced NO productio

54 s necessary to work at [Ca(2+)](free) beyond EGTA's buffering capabilities.

55 In the blotting-EGTA model, exsA mutants were defective in capacity for

56 Both EGTA and clodronate also prevented the bisphosphonate-in

57 elease was modulated by the addition of both EGTA and BAPTA-AM, agents chelating either external or i

58 lock of exocytosis by the slow Ca(2+) buffer EGTA (10 mM) in basal hair cells tuned to high frequenci

59 release sensitive to the slow Ca(2+) buffer EGTA.

60 release sensitive to the slow Ca(2+)-buffer EGTA, suggesting that synaptic ribbons mediate nano-doma

61 In cells loaded with the Ca2+ buffer EGTA (5 mmol/L) and the fluorescent Ca2+-indicator fluo-

62 racellular concentrations of the slow buffer EGTA (0.5 mm), but not with high concentrations of the f

63 sely mimicked the actions of the slow buffer EGTA, whereas CR showed important differences from the f

64 xcess of a high-affinity but slow Ca buffer (EGTA).

65 In the presence of 0.5 mM slow Ca2+ buffer (EGTA (ethylene glycolbis(2-aminoethylether)-N,N,N',N'-te

66 with high intracellular Ca(2)(+) buffering (EGTA 10 mm or BAPTA 20 mm), and with substitution of Ba(

67 e it was greatly reduced by the Ca2+ buffers EGTA and BAPTA.

68 Here we used dialysis of Ca(2+) buffers (EGTA) into voltage-clamped rat atrial myocytes to isolat

69 tilled H2O released surface-bound BAD-1, but EGTA washes were an order of magnitude more efficient, s

70 ations of the slow Ca(2+)-chelator EGTA, but EGTA had no effect in synaptotagmin-7 knock-out neurons

71 Chelation of Ca(2+) by EGTA significantly inhibits the induction of PR genes by

72 It was abolished by EGTA, which preferentially blocked endocytosis of retrie

73 gion of TRPC3-MDCK cells that was blocked by EGTA addition to the apical medium.

74 of SC signaling by glutamate was blocked by EGTA and dizocilpine and by silencing expression of the

75 ulation during activity; both are blocked by EGTA-AM, and LTF is also prevented by stimulation in a l

76 .023), despite constant [Ca(2+)] buffered by EGTA (4 mm).

77 With intracellular Ca2+ buffered by EGTA in the recording pipette, vitronectin-activated K+

78 d mucin secretion in SPOC1 cells buffered by EGTA, suggesting that IP3 generates a local Ca2+ gradien

79 s sensitive to cytosolic Ca(2+) buffering by EGTA, suggesting that the QCR component is attributable

80 The removal of calcium by EGTA perturbed the Sertoli cell tight junction barrier,

81 but was restored to a normal time course by EGTA-AM treatment.

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

83 ited voltage-gated Ca(2+) influx followed by EGTA-sensitive CICR from the mitochondria.

84 Disruption of cadherin ligation by EGTA or prevention of cadherin ligation by maintenance o

85 ven when subsarcolemmal Ca(2+) is lowered by EGTA.

86 could be blocked by thapsigargin but not by EGTA.

87 Suppressing asynchronous release by EGTA-AM abolished reverberation, whereas elevating async

88 These effects were reduced substantially by EGTA and ruthenium red.

89 sts that differential modulation of VDCCs by EGTA and BAPTA offers an alternative or complementary ex

90 d these increases were inhibited in vitro by EGTA, a calcium chelating agent.

91 inhibitors of Ca(2+) influx and calcineurin, EGTA and FK506, eliminate the hyperresponsiveness.

92 persisted even in perfusions of zero calcium-EGTA Krebs solution suggesting that the calcium oscillat

93 hannel blocker La(3+) or the Ca(2+) chelator EGTA is accompanied by an increase in the rate of cell e

94 translocation induced by the Ca(2+) chelator EGTA, the broad-spectrum Ca(2+) channel inhibitor ruthen

95 Similarly, perfusion of the Ca(2+) chelator EGTA-AM into the slice progressively eliminated ectopic

96 calmodulin antagonist or the Ca(2+) chelator EGTA.

97 h concentrations of the slow Ca(2+)-chelator EGTA, but EGTA had no effect in synaptotagmin-7 knock-ou

98 polarity upon treatment with Ca(2+)-chelator EGTA.

99 tracellular application of the Ca2+-chelator EGTA or of a calmodulin inhibitor.

100 hile co-infiltration of the calcium chelator EGTA attenuated this effect.

101 e concentration of the slow calcium chelator EGTA from 1.5 to 5 mM.

102 aspase inhibitors or by the calcium chelator EGTA, but was reduced by Bcl-2 overexpression.

103 r antagonist memantine, the calcium chelator EGTA, or a specific inhibitor for calcium/calmodulin-dep

104 pleted by the high-affinity calcium chelator EGTA, suggesting that the calcium present in the gut is

105 were also observed with the calcium chelator EGTA.

106 BAPTA-AM inhibits LFD but the slow chelator EGTA-AM does not, the Ca(2+) sensor for LFD may be close

107 (2+) chelator BAPTA-AM and the slow chelator EGTA-AM reduced the mIPSC frequency, suggesting that Ca(

108 trieval is blocked by the Ca(2)(+) chelator, EGTA, as well as FK506, a specific inhibitor of Ca(2)(+)

109 counted for in the presence of the chelators EGTA and BAPTA without additional adjustments to the mod

110 why Slc11a2, but not Slc11a1, can complement EGTA sensitivity in smf1Delta/smf2Delta/smf3Delta yeast.

111 thanolamine addition is sufficient to confer EGTA and polymyxin resistance on Salmonella msbB strains

112 In addition to conferring EGTA resistance correlated with somA, the deletion confe

113 triacetic acid (NTA) to solutions containing EGTA.

114 Thus, we correlate EGTA resistance and polymyxin resistance with phosphoeth

115 Isolated rods are stable in dithiothreitol, EGTA, Ca(2+), and ATP.

116 etalloproteinase inhibitors, including EDTA, EGTA, and TAPI-1, inhibit the shedding of KL, whereas in

117 ected by Mg(2+), Mn(2+), Ca(2+), K(+), EDTA, EGTA, or 1.0 M NaCl.

118 rapGAP3(-) cells exhibit some increased EDTA/EGTA sensitive cell-cell adhesion at the late mound stag

119 The EDTA/EGTA elution and saturation parameters were determined f

120 ed (Mn2+, Ca2+, not Mg2+), blocked with EDTA/EGTA, RGD-based peptides, and select integrin subunit an

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

122 Pretreatment with either EGTA acetoxymethyl ester or vitamin E resulted in a sign

123 is, followed by Ca(2+) chelation with excess EGTA.

124 al-evoked transients in the presence of high EGTA concentrations suggest that the reduction in the ev

125 w affinity indicator in the presence of high EGTA concentrations under voltage clamp conditions.

126 e Z-line transient under conditions of high [EGTA], it predicted a significantly narrower Ca(2+) doma

127 as isolated by infusing the cells with high [EGTA].

128 ls in normal human sera as well as SC5b-9 in EGTA-chelated/Mg2+ supplemented serum), since methylatio

129 aradoxical finding that dFull moved actin in EGTA suggests that binding of the molecule to the substr

130 Only dFull has low ATPase activity in EGTA, and significantly higher activity in calcium.

131 ch adopts a folded inhibited conformation in EGTA, becomes extended and active in the presence of cal

132 ease rate from acto-M5aFull was decreased in EGTA by >1,000-fold, which makes this step the rate-limi

133 [Ca(2+)](i) transient and that incubation in EGTA-buffered saline is able rapidly to deplete this sto

134 ull showed unexpected processive movement in EGTA, suggesting that a small population of extended, ac

135 PMA-induced secretion in EGTA was insensitive to heparin.

136 Confocal imaging revealed that in EGTA, almost all mitochondria picked up Ca2+ released fr

137 iting traversal by adherent bacteria include EGTA-sensitive factors and SP-D.

138 ions with minimal concentrations of internal EGTA, Ishear showed an outwardly rectifying current-volt

139 gh sensitivity to nifedipine and to internal EGTA, are essentially involved in recruiting SRP vesicle

140 Moreover, we show using internal EGTA and photo-release of caged Ca2+ and caged Ca2+ chel

141 were immobilized using either intracellular EGTA or N-benzyl-p-toluene sulphonamide, an inhibitor of

142 In the presence of 20 mM intracellular EGTA, I(SkCRAC) activation occurred over tens of seconds

143 is was poorly affected by 5 mm intracellular EGTA, suggesting that the Cav1.3 short isoforms are clos

144 lcium (Ca(2+)), replacement of intracellular EGTA with BAPTA, a fast Ca(2+) chelator, and Gd(3+) and

145 ics and were abolished by 1 mM intraterminal EGTA, suggesting that Ca(2+) acted through a high-affini

146 ained with EGTA pretreatment (83%) than just EGTA + L,D-MDP (47%).

147 peated APs with pipettes containing 2 mmol/L EGTA and single LCC activity in cell-attached patches de

148 Memantine, EGTA, or autocamtide-2-related inhibitory peptide (AIP)

149 the binding of C3b that was inhibited by Mg-EGTA.

150 membrane-localized receptors) and 100 microm EGTA.

151 reduced greatly in cells subjected to 5 min EGTA pre-treatment.

152 fer capacity by internal perfusion with 1 mM EGTA limited SR Ca(2+) release to the SS region, indicat

153 2+)-free Tyrode buffer (no added Ca2+ + 1 mM EGTA) followed by superfusion with control (Ca2+-contain

154 plemented 0.1 M Pipes buffer (1 mM GTP, 1 mM EGTA, 1 mM MgSO4, pH 6.4).

155 is blocked when Ca(2+) is chelated by 10 mM EGTA in the patch pipette.

156 Buffering with 10 mM EGTA reduced desensitization, while BAPTA completely eli

157 centrations of a slow Ca(2)(+) buffer (10 mM EGTA), we found that the number of synaptic vesicles at

158 ies, with filling solutions containing 10 mm EGTA, revealed that calyculin A (100 nm) increased I(Ca)

159 60% of its activity in the presence of 10 mm EGTA.

160 both preparations differed in that in 10-mM EGTA Ca(2+) microdomains had smaller amplitudes and were

161 with 5 mM EGTA (slow Ca(2+) buffer) or 15 mM EGTA plus 5 mM BAPTA (fast Ca(2+) buffer).

162 by 4 min incubation in 0 Ca(2+) medium (2 mM EGTA) but in nominally Ca(2+)-free medium (no added Ca(2

163 ll patch clamp pipette, in addition to 20 mM EGTA and other constituents included for the charge move

164 with the internal solution containing 20 mM EGTA plus added calcium and antipyrylazo III.

165 g was confirmed by experiments showing 20 mm EGTA preferentially blocked distally coupled SVs.

166 ocytes were loaded with 1 mM fluo-3 and 3 mM EGTA via the patch pipette to buffer diadic cleft Ca2+,

167 eres of FDB fibers loaded with 10- and 30-mM EGTA.

168 Ca(2+) transients, were eliminated in 30-mM EGTA.

169 30 mM citrate and 10 mM ATP along with 5 mM EGTA (slow Ca(2+) buffer) or 15 mM EGTA plus 5 mM BAPTA

170 ing an intracellular Ca(2+) buffer of 0.5 mm EGTA rather than 5 mm EGTA, and diminished by 1 mm BAPTA

171 resent only with mild Ca2+ buffering (0.5 mM EGTA) characteristic of many neurons.

172 a(2+) buffer of 0.5 mm EGTA rather than 5 mm EGTA, and diminished by 1 mm BAPTA.

173 f the bad-1 null yeast was inhibited by 5 mm EGTA, and re-expression of BAD-1 in trans or the additio

174 was minimized by dialysing cells with 0.5 mM EGTA, the steady-state response was reduced to approxima

175 ion of the two pools were unaffected by 5 mm EGTA.

176 s of approximately 240 mM (EDTA) and 140 mM (EGTA).

177 in the Ringer was replaced with equal molar EGTA.

178 Separate experiments used 350 mum EGTA (600 nm Ca(2)(+)) to limit Ca(2)(+) diffusion but a

179 Perfusing with 600 nm Ca(2)(+) (50 mum EGTA) caused regular spontaneous Ca(2)(+) waves that wer

180 n photorelease from nitrodibenzofuran (NDBF)-EGTA just outside the permeabilized plasma membrane.

181 NDBF-EGTA has a two-photon cross-section of approximately 0.6

182 Use of NDBF-EGTA allowed for the separate modification of resting [C

183 Ultraviolet (UV)-laser photolysis of NDBF-EGTA:Ca(2+) rapidly released Ca(2+) (rate of 20,000 s(-1

184 The caged calcium probe o-nitrophenyl EGTA and UV uncaging were used to increase calcium in en

185 Caged-Ca(2+) compounds such as nitrophenyl-EGTA (NP-EGTA) and DM-nitrophen (DMn) are extremely usef

186 olytic uncaging of Ca(2+) from o-nitrophenyl-EGTA in somatic ER caused an abrupt Ca(2+) increase in s

187 t, photolysis of caged Ca(2+) (o-nitrophenyl-EGTA) in astrocytes led to neuronal depolarization and i

188 s, induced by uncaging Ca(2+), o-nitrophenyl-EGTA, increased action potential-driven spontaneous inhi

189 Flash photolysis of caged Ca(2+) (NP-EGTA) produced both transient and prolonged increases in

190 Mg(2+) binding/unbinding rates of DMn and NP-EGTA, we built a mathematical model to assess the utilit

191 mouse beta cells loaded with caged Ca2+ (NP-EGTA), a GLP-1 receptor agonist (exendin-4) is demonstra

192 aded with the photolabile Ca(2+) chelator NP-EGTA, the UV flash photolysis-catalysed uncaging of Ca(2

193 photolysis of the caged calcium compound NP-EGTA also altered extracellular H(+) flux.

194 a(2+) compounds such as nitrophenyl-EGTA (NP-EGTA) and DM-nitrophen (DMn) are extremely useful in bio

195 ned the properties of Ca(2+) release from NP-EGTA and DMn by using Oregon green BAPTA-5N to measure c

196 [Ca(2+)] with photorelease of Ca(2+) from NP-EGTA to maximal k(tr), where Ca(2+) binding to thin fila

197 thematical model to assess the utility of NP-EGTA and DMn in rapid Ca(2+)-uncaging experiments in the

198 Low intensity photolysis of NP-EGTA produced a slow [Ca2+] ramp and revealed that trans

199 tic release [Ca2+] by laser photolysis of NP-EGTA was Ca2+ sensitive and biphasic: a rapid component

200 Using photolysis of NP-EGTA, the maximal kinetics of translocation was determin

201 A large fraction (65%) of NP-EGTA, which has a negligible Mg(2+) affinity, uncages wi

202 lae was studied using laser photolysis of NP-EGTA.

203 eculae, while maintaining constant total [NP-EGTA] and [Ca(2+)].

204 ollowing procedures changed [Ca2+]i:0[Ca2+]o+EGTA reduced [Ca2+]i by about 50%, suggesting that the r

205 O4, was reduced (not eliminated) in 0[Ca2+]o+EGTA, suggesting that some calcium was intracellularly r

206 m inflow since it was eliminated in 0[Ca2+]o+EGTA.

207 s recorded from mdx fibres in the absence of EGTA also displayed a marked prolongation of the slow de

208 In addition, the action of EGTA-AM suggests that basal Ca(2+) regulates the recover

209 sion of extracellular Ca(2+) and addition of EGTA (2 mM) inhibited ischemia-induced efflux only durin

210 13 was completely blocked by the addition of EGTA and mannan.

211 er experimental results in which addition of EGTA or BAPTA produces different effects.

212 d Sr2+ and could be inhibited by addition of EGTA or clodronate, both of which chelate calcium ions.

213 , but they could be abolished by addition of EGTA or La(3+).

214 ndergo reverse dissociation upon addition of EGTA, but can be distinguished by isotopic exchange indi

215 f NADH and was not reversed upon addition of EGTA.

216 ccurs very slowly even following addition of EGTA.

217 However, a high concentration of EGTA led to a reduction in EPSCs that was significantly

218 ter than with an equivalent concentration of EGTA, indicating the importance of buffer kinetics in mo

219 Different concentrations of EGTA (0-40 mm) added to Dulbecco's modified essential me

220 uent experiments using low concentrations of EGTA (1 mm) produced the same result, suggesting that so

221 tion was sensitive to high concentrations of EGTA, suggesting that intracellular Ca(2+) buffers play

222 orter blocker, and by high concentrations of EGTA.

223 Photolysis of a NDBF derivative of EGTA (caged calcium) is about 16-160 times more efficien

224 ment model of Ca(2+) indicated the effect of EGTA on CICR was due to buffering of released mitochondr

225 Moreover, the differential effects of EGTA and BAPTA (slow and fast Ca(2+) chelators, respecti

226 g is demonstrated by studying the effects of EGTA, reserpine, and prolonged stimulation by K(+).

227 ut inhibition of a Ca2+ rise by injection of EGTA into follicle-enclosed mouse oocytes does not inhib

228 g the intracellular buffer (BAPTA instead of EGTA).

229 d cell model by the slow binding kinetics of EGTA.

230 High concentrations (5-40 mm) of EGTA dose-dependently inhibited free L,D-MDP binding to

231 2+)] imaging, and patch pipette perfusion of EGTA at the calyx of Held.

232 ve phosphoenzyme (E1P), and a rapid phase of EGTA-induced phosphoenzyme (E2P) hydrolysis.

233 (VDCC) currents observed in the presence of EGTA or BAPTA.

234 bridge detachment at low Ca(2+) (presence of EGTA), allowing for a direct comparison between the two

235 In the presence of EGTA-AM to prevent global increases in free Ca(2+), the

236 ed a small transient even in the presence of EGTA.

237 pmrA(Con)] suppresses msbB growth defects on EGTA-containing media.

238 pplying cell permeable chelators BAPTA-AM or EGTA-AM; (2) decreasing Ca(2+) concentration in the extr

239 levations that were blocked by antagonist or EGTA.

240 ions buffered with 1-4 mm of either BAPTA or EGTA gave rise to similar patterns of I(ORCa) oscillatio

241 presence of a competitive chelator (EDTA or EGTA).

242 nt strains in the presence of either EDTA or EGTA.

243 In comparison, in nominally Ca(2+)-free or EGTA-containing solution, the DRP was completely blocked

244 Inclusion of RGDS peptides or EGTA, during activation, led to a biphasic response; Arf

245 cetyl-sn-glycerol but not by pyrrophenone or EGTA.

246 that mucin secretion from SLO-permeabilized, EGTA-buffered SPOC1 cells was stimulated by PMA at low C

247 e aminoarabinose biosynthetic genes restored EGTA and polymyxin sensitivity to Salmonella msbB pmrA(C

248 Surprisingly, EGTA at similar or higher intracellular concentrations h

249 results from NTA having a lower K'(dCa) than EGTA.

250 inds Ca2+ approximately 100-fold faster than EGTA, diminished IP3-induced mucin release over a range

251 least 2-fold greater when Ca(2+) rather than EGTA was present.

252 leting ER Ca(2+) with prolonged thapsigargin/EGTA treatment.

253 These findings demonstrate that EGTA, when used in conjunction with NTA, improves and ex

254 e hind paws of the reporter mice showed that EGTA and MDL28170 diminished capsaicin-induced ablation.

255 Compatible with its transport function, the EGTA- and ouabain-insensitive ATPase activity of purifie

256 Lipid A structural analysis of the EGTA- and polymyxin-resistant triple mutant msbB pmrA(Co

257 permeabilized cells to PMA, relative to the EGTA-buffered control: at PMA below 30 nm, BAPTA abolish

258 it was reduced significantly relative to the EGTA-buffered controls.

259 When cells were exposed to EGTA-containing saline (5 min) and then returned to nomi

260 MsbB- salmonellae mutate extragenically to EGTA-tolerant derivatives at a frequency of 10(-4) per d

261 d vesicular release became less sensitive to EGTA, whereas fixed Ca(2+) buffer properties remained co

262 bled in comparison to cells not subjected to EGTA pre-treatment.

263 Using EGTA-Ca buffers, the dependence of PDP1 or PDP1c on the

264 Competitive experiments using EGTA confirmed that metal-citrate complex formation prom

265 yo1c (1IQ) was >10-fold higher in Ca (2+) vs EGTA +/- exogenous calmodulin, showing that regulation i

266 When EGTA was omitted from the pipette solution, the number o

267 epileptiform activity could be induced when EGTA was replaced by the excitatory postsynaptic amino a

268 aM-Sepharose in the presence of Ca2+ whereas EGTA, a Ca2+ chelator, abolished binding, confirming tha

269 s under pressure, the authors tested whether EGTA chelation of Ca(2+) improves survival and whether,

270 Lowering extracellular Ca(2+) with EGTA or blocking store operated Ca(2+) entry with SKF963

271 upled by buffering intracellular Ca(2+) with EGTA-AM.

272 pithelial injury (tissue paper blotting with EGTA treatment) and immunocompromise (MyD88 deficiency)

273 reasing intraterminal calcium buffering with EGTA-AM or decreasing calcium influx with omega-agatoxin

274 Thus, reducing subsarcolemmal Ca2+ with EGTA in NCX KO mice reveals the dependence of Ca2+ relea

275 d by removal of extracellular free Ca2+ with EGTA.

276 Removal of calcium with EGTA or exposure to pHs as low as 5.0 had little effect

277 or buffering the intracellular calcium with EGTA significantly inhibited rapid endocytosis, suggesti

278 Buffering intracellular calcium with EGTA-AM or BAPTA-AM reduced asynchronous EPSC rates earl

279 s and by lowering extracellular calcium with EGTA.

280 ired by chelating intracellular calcium with EGTA.

281 Treating cells with EGTA lowered Ca(2+) and blocked both loss of mitochondri

282 Treatment of A23187-stimulated cells with EGTA or BAPTA-AM demonstrated that a substantial pool of

283 for this process since Ca(2+) chelation with EGTA, or pharmacological inhibition with diazoxide and n

284 native conformation by Ca(2+) chelation with EGTA.

285 th anti-annexin I or removing annexin I with EGTA was inhibitory.

286 ses in Ca2+ levels following incubation with EGTA or A23187.

287 of the respiratory epithelium integrity with EGTA or N-acetylcysteine.

288 ting homotypic VE-cadherin interactions with EGTA, antibodies to the extracellular domain of VE-cadhe

289 lar calcium signaling in T cells loaded with EGTA revealed significantly higher Ca2+ concentration ne

290 nts reported by other authors were made with EGTA Mg(2)(+) buffer, permitting autoactivation of C3.

291 pressed by further lowering [Ca(2+)](o) with EGTA.

292 3 activity in RK(13) cells was obtained with EGTA pretreatment (83%) than just EGTA + L,D-MDP (47%).

293 the mitochondrial Ca(2+) uniporter, or with EGTA acetoxymethyl ester, but not with vitamin E, preven

294 Preincubation with EGTA suppressed p38 activation, while calcium ionophore

295 e tear fluid or corneas were pretreated with EGTA to disrupt Ca(2+)-dependent factors.

296 e of extracellular Ca(2+) or pretreated with EGTA-AM or wortmannin, suggesting that the entry of Ca(2

297 n small interfering RNA or pretreatment with EGTA (0.1 mm) prior to LPA (1 microm) treatment attenuat

298 a(2+) diffusion was markedly restricted with EGTA, however, only alpha2(f)GCaMP2 detected the local,

299 ion of the tight junctions by treatment with EGTA overcame the restriction on basolateral infection b

300 is Ca(2+)-dependent, because treatment with EGTA reduces levels of Ser(P)473-Akt.