ライフサイエンスコーパス: A23187

1 on-gamma (IFN-gamma), and calcium ionophore (A23187).

2 nly ethanol but also by a calcium ionophore (A23187).

3 stimulation with PMA and calcium ionophore (A23187).

4 e, was activated in response to IL-1beta and A23187.

5 easing intraoocyte Ca(2+) with the ionophore A23187.

6 he absence and presence of a potent agonist, A23187.

7 % of the levels induced by calcium ionophore A23187.

8 onRI cross-linking and the calcium ionophore A23187.

9 e anion in response to the calcium ionophore A23187.

10 intracellular Ca2+ levels with the ionophore A23187.

11 ion and NO increase induced by bradykinin or A23187.

12 re relaxation responses to calcium ionophore A23187.

13 anced by treatment with the Ca(2+) ionophore A23187.

14 ignificantly improved relaxations to ACh and A23187.

15 FAT activity induced by either UV or UV plus A23187.

16 n of NHE3 activity by calcium ionophore 4-Br-A23187.

17 by zymosan, PMA and, okadaic acid but not by A23187.

18 n evoked by Ang II and the calcium ionophore A23187.

19 se under basal conditions and in response to A23187.

20 ular Ca2+ overload induced by Ca2+ ionophore A23187.

21 et-activating factor or the Ca(2+) ionophore A23187.

22 F-alpha in response to the calcium ionophore A23187.

23 s to acetylcholine and the calcium ionophore A23187.

24 nduced by phorbol 12-myristate 13-acetate or A23187.

25 inutes by phorbol ester or calcium ionophore A23187.

26 ment of SW1353 with 0.5 muM Ca(2+) ionophore A23187.

27 protein levels were coordinately reduced by A23187.

28 lls from apoptosis induced by agents such as A23187.

29 is upon activation by the calcium ionophore, A23187.

30 um-dependent relaxation to calcium ionophore A23187.

31 trongly responsive to the calcium ionophore, A23187.

32 KKgamma in the presence of calcium ionophore A23187.

33 ion of the CESS cells with calcium ionophore A23187.

34 ) when stimulated with the calcium ionophore A23187.

35 sis are induced by PMA and calcium ionophore A23187.

36 ibroblasts treated with the Ca(2+) ionophore A23187.

37 ut not that induced by the calcium ionophore A23187.

38 ion produced by the ionophores ionomycin and A23187.

39 ved after stimulation with calcium ionophore A23187.

40 which explains its decreased sensitivity to A23187.

41 alcium concentration by use of the ionophore A23187.

42 which was reversed by the calcium ionophore A23187.

43 a2+ levels following incubation with EGTA or A23187.

44 ycin, thapsigargin, and the Ca(2+) ionophore A23187.

45 se of AA release in response to IL-1beta and A23187.

46 a2+]i produced by the Ca2+ ionophore 4-bromo-A23187 (0.25 microM) is four to five times greater in ph

47 rine (20-100 ng/mL) or the calcium ionophore A23187 (0.5 microM).

48 Within 1 min of A23187 (0.5 mum) exposure, the NHERF2-NHE3 FRET signal w

49 E3 cells, with the Ca(2+) ionophore, 4-bromo-A23187 (0.5 mum): 1) inhibited NHE3 V(max) activity; 2)

50 tly regulated, neither the calcium ionophore A23187 (1 microM) nor depolarization by potassium-rich s

51 Application of the Ca(2+) ionophore A23187 (1 microM), to activate Ca(2+)-activated non-sele

52 agen, 4 microg/ml; and the calcium ionophore A23187, 1 microM) results in shedding of microparticles.

53 In ionophore-stimulated (A23187; 1-2.5 muM) human blood neutrophils or differenti

54 (CCCP, 10 microM) and the calcium ionophore A23187 (10 microM), abolished TPP+ accumulation and caus

55 after stimulation with the calcium ionophore A23187 (10(-6) M).

56 ndent endothelial agonist, calcium ionophore A23187 (10(-7) mol/L and 3 x 10(-7) mol/L), was obtained

57 icroM) caused 45% and the calcium ionophore, A23187, 11% of maximal tyrosine phosphorylation of p125(

58 eled endothelial cells to the Ca2+ ionophore A23187 (2 mumol/L) resulted in a 4-fold increased releas

59 s altered by incubating sheep red cells with A23187 (20 microM) and different values of extracellular

60 A23187, 4-BrA23187, and ionomycin transport several lant

61 on of bradykinin (-59%) or calcium ionophore A23187 (-49%) and by systemic hypercapnia (-58%) (P<0.05

62 (1 micromol/L) or the Ca2+ ionophore 4-bromo-A23187 (5 micromol/L).

63 25 microL/min) and to the calcium ionophore A23187 (5 x 10(-8) to 10(-6) mol/L), norepinephrine (NE;

64 aglandin E2, theophylline, calcium-ionophore A23187, 8-bromoadenosine 3':5'-cyclic monophosphate, and

65 s 75+/-2%, P<0.05) and the calcium ionophore A23187 (92+/-2% versus 72+/-3%, P<0.05) were also impair

66 ere also noted after treatment with cAMP and A23187 (a calcium ionophore).

67 the exchange rate by a factor of 1.4+/-0.1; A23187 (a modulator of calcium-activated chloride channe

68 This effect is mimicked by A23187, a Ca ionophore that promotes Ca(2+) entry at the

69 ther Bay K8644, a Ca2+ channel activator, or A23187, a Ca2+ ionophore, caused sustained increases in

70 A23187, a calcium ionophore known to block furin maturat

71 a mixture of polychlorinated biphenyls, and A23187, a calcium ionophore.

72 tion of these vessels with calcium ionophore A23187, a known secretagogue of Weibel-Palade bodies, in

73 s by phorbol myristate acetate and ionophore A23187, a perinuclear ring pattern was observed for 5LO.

74 These data suggest that Aroclor 1242 and A23187 activate distinct isoforms of PLA2 that are linke

75 Strikingly, coexpression of FLAP in A23187-activated HEK293 cells effectively restored forma

76 had more FV activity than either thrombin or A23187-activated platelets, and that COAT-FV platelets w

77 d-based protein kinase C inhibitors, blocked A23187-activated pro-BTC shedding.

78 t releases AA for the generation of O2-, and A23187 activates a calcium-dependent PLA2 that mobilizes

79 r C1CCP, or of the divalent cation ionophore A23187 (all agents known to release mitochondrial calciu

80 compared with that in cells treated with PMA/A23187 alone.

81 butyrate together with the calcium ionophore A23187 also promoted ubiquitination and proteasomal degr

82 Ionophore A23187, although it caused germinal vesicles to disappea

83 0.3 mM), and with a combination of 10 microM A23187 and 2 mM EDTA (to reduce intracellular Mg2+ conce

84 xed complexes of the type (ionophore)2La-OH (A23187 and 4-BrA23187) or (ionophore)La-OH (ionomycin),

85 rs through complexes of type (ionophore)3La (A23187 and 4-BrA23187) or (ionophore)La-OH (ionomycin).

86 ic acid, and the calcium-mobilizing agonists A23187 and CryIC toxin induce arachidonic acid release a

87 The calcium agonists A23187 and cyclopiazonic acid increased [Ca(2+)](c) leve

88 rected against cPLA2 decreased the effect of A23187 and EGF on IL-8 and COX-2 protein expression.

89 tered in its responses to the Ca2+ ionophore A23187 and found the affected gene encodes a homologue o

90 ure of human polymorphonuclear leukocytes to A23187 and granulocyte macrophage-colony-stimulating fac

91 tion and arachidonic acid release induced by A23187 and H2O2.

92 A23187 and ionomycin induced weak MAPK activation, and a

93 ia an electrogenic mechanism, in contrast to A23187 and ionomycin, which function in a charge neutral

94 A23187 and LPS increased intracellular PGE2 in a dose-de

95 e responses to phenylephrine, acetylcholine, A23187 and nitroglycerin were studied in organ baths.

96 , a cPLA2 inhibitor, inhibited the effect of A23187 and of EGF on both IL-8 and COX-2 reporter gene a

97 PAR-gamma1 and -gamma2 blunted the effect of A23187 and of EGF on IL-8 and COX-2 protein expression.

98 examined the effects of the Ca(2+) ionophore A23187 and phorbol myristate acetate (PMA).

99 that increase intracellular calcium [Ca++]i (A23187 and thapsigargin) in human monocytic cells also i

100 cellular calcium (i.e. the calcium ionophore A23187 and thapsigargin) or protein kinase C activity (t

101 al muscle cells using the calcium ionophore, A23187 and the mitochondrial uncoupler, 2,4-dinitropheno

102 Calcium ionophore A23187 and the muscarinic cholinergic agonist carbachol

103 , convulxin, collagen, PMA, thapsigargin, or A23187) and all led to a time-dependent decrease in Arf6

104 shedding was activated by calcium ionophore (A23187) and by the metalloprotease activator p-aminophen

105 ial lipopolysaccharide and calcium ionophore A23187, and biosynthesis was blocked by inhibitors of 5-

106 ogesterone, but not by the calcium ionophore A23187, and elicited a concomitant reduction of in vitro

107 The CBF increase produced by bradykinin, A23187, and hypercapnia, but not acetylcholine or vibris

108 ions to acetylcholine, the calcium ionophore A23187, and nitroglycerin, as well as superoxide product

109 hat induce ER stress, including tunicamycin, A23187, and thapsigargin, promotes leukocyte binding.

110 ingly, treatment with the calcium ionophore, A23187, and the PKC activator, PMA, rescues the inhibite

111 r Ca2+ in the presence of the Ca2+-ionophore A23187, and when treated with mastoparan, an inducer of

112 several cell lines to the calcium ionophore A23187, bacterial lipopolysaccharide (LPS), nonsteroidal

113 e pharmacological Ca(2+) carrier calcimycin (A23187) because contraction induces marked increases in

114 bryonic fibroblasts exposed to thapsigargin, A23187, brefeldin A, DTT, geldanamycin, or bortezomib ma

115 nduction of ER stress with calcium ionophore A23187, brefeldin A, or tunicamycin is associated with t

116 gregation by collagen (COLL), TRAP, PAF, and A23187 but did not block platelet aggregation by ristoce

117 ependent NO-mediated agonists bradykinin and A23187 but not to endothelium-independent NO donor sodiu

118 igargin, okadaic acid, and calcium ionophore A23187, but not by phenobarbital or the steroid PP dehyd

119 ated vasodilator responses to bradykinin and A23187 (by 40% and 60%, respectively).

120 k2 was also induced by the calcium ionophore A23187, by phorbol myristate acetate, or by stimulation

121 creased in C cells, by the calcium ionophore A23187, by physiologic concentrations of the P2 purinerg

122 NF alpha supernatants from calcium ionophore A23187 (CaI)-stimulated mast cells or appropriate contro

123 Incubation of DCs with A23187 calcium ionophore for 48 h induced an expression

124 ntrations did not increase during culture in A23187, calcium uptake in the lens may be responsible fo

125 The Ca2+ ionophore A23187 can induce chloroplast rotation within a single n

126 the light response, and a calcium ionophore, A23187, can substitute for light.

127 Treatment of eggs with the Ca(2+) ionophore A23187 caused MAP kinase inactivation and triggered DNA

128 Both Aroclor 1242 and A23187 caused release of [3H]AA; however, O2- production

129 of storage granules by the calcium ionophore A23187 caused release of ET into the culture supernatant

130 fected host cells with the calcium ionophore A23187 causes the parasites to undergo rapid egress in a

131 (661W) was treated with the Ca(2+) ionophore A23187, cGMP-gated channel agonist 8-bromo-cGMP, or phos

132 cells following stimulation with calcium and A23187 contained CARd6 similar to that present in vesicl

133 histamine, thrombin or the calcium ionophore A23187, cPLA2-alpha relocated to intracellular membranes

134 endothelial cells with a calcium ionophore, A23187, decreased alpha-actinin-4-eNOS interaction, lead

135 n beta3 is reversed by the calcium ionophore A23187, demonstrating that these effects of calyculin A

136 ivate p70(S6K) was confirmed by blocking the A23187-dependent activation through chelation of extrace

137 The calcium ionophore A23187 destabilized YY1 in cultured myoblasts, and the d

138 marker, was reduced with PMA treatment, but A23187 did not affect keratin 14 expression.

139 AMP or treatment with the calcium ionophore A23187 do not cause SPR phosphorylation, treatment with

140 ion of cPLA(2)alpha by the calcium ionophore A23187 enhanced PPARdelta binding to PPARdelta response

141 -1,2-dithiane, tunicamycin, thapsigargin, or A23187 expressed ER stress proteins and were resistant t

142 The divalent cation ionophore A23187 facilitates the manipulation of intracellular Mg2

143 Treatment of cells with 10 microM A23187 for 30 min resulted in the release of 47.9 % of C

144 trophils required a greater concentration of A23187 for activation than did blood neutrophils (half-m

145 A23187 had a synergistic effect with UV for NFAT inducti

146 with thapsigargin or the calcium ionophore, A23187, had no effect on SOK-1 activity, but preincubati

147 in ligand affinity was not caused by ADP or A23187; (ii) did not require cytosolic components, e.g.,

148 roduce COAT-FV platelets, although ionophore A23187 in conjunction with either thrombin or convulxin

149 reverses the androgen-induced resistance to A23187 in LNCaP cells.

150 nism did not affect responses to thrombin or A23187 in more mature arteries.

151 lux in oxygenated cells exposed to ionophore A23187 in the presence of external Ca(++), but this effe

152 utase attenuated responses to bradykinin and A23187 in wild-type mice but not in COX-1(-/-) mice, sug

153 , neither phorbol myristate acetate (PMA) or A23187 increased receptor levels on the PMN surface.

154 Although the calcium ionophore A23187 increased the expression of CD14 and TLR4, they d

155 exposure of cells to the calcium ionophore, A23187, increased CCTalpha degradation, whereas overexpr

156 Ca(2+) ionophore A23187 increases nuclear localization of PTEN and decrea

157 d convulxin was less than that observed with A23187, indicating that microparticles were not responsi

158 1beta (IL-1beta), and the calcium ionophore, A23187, induce an increase in C-1-P levels within the re

159 Interestingly, the calcium ionophore A23187 induced accumulation of a polyubiquitinated TRE17

160 Staurosporine, ExM, and A23187 induced DNA fragmentation in HCE and RCE cells.

161 gen, ADP, epinephrine, and calcium ionophore A23187 induced RAFTK phosphorylation.

162 uced SAPK activity and the calcium ionophore A23187 induced SAPK activity 3-fold.

163 The calcium ionophore A23187 induced SFK phosphorylation in both wild-type and

164 tivation of cPLA2 by ceramide-1-phosphate or A23187 induced spinal neuronal death, which was substant

165 le EL4 T-lineage cells, stimulation with PMA/A23187 induced strong acetylation of histone H3 and H4,

166 the majority of thapsigargin and ionophore (A23187)-induced arachidonic acid release from SMCs.

167 delta-EGFP at the PM after Ca(2+) ionophore (A23187)-induced PI(4,5)P2 hydrolysis, followed by Ca(2+)

168 Omission or chelation of calcium abolished A23187-induced AA release, but did not alter AA release

169 d significantly increases the sensitivity to A23187-induced apoptosis in both LNCaP and PC-3 cells.

170 ever, although ERK inhibition did not affect A23187-induced arachidonic acid release, it suppressed z

171 cPLA(2)zeta expressed in Sf9 cells mediated A23187-induced arachidonic acid release, which was inhib

172 -01 cells showed that DREAM is important for A23187-induced Ca(2+) mobilization and its regulatory fu

173 t enhanced NO bioactivity by 70% measured as A23187-induced cGMP accumulation.

174 cant protection against both DNP-induced and A23187-induced damage to the myotubes.

175 channels, caused a strong inhibition of the A23187-induced increase in [K(+)]o.

176 Ca(2+) + A23187-induced K(+)-permeabilization of SS R1 fractions

177 e MAPK kinase inhibitor, PD 98059 suppressed A23187-induced MAPK activation and cPLA2 gel shift but h

178 xposed to SK 7111 or SB 203347 did not alter A23187-induced PGE2 or LTC4 generation, respectively, in

179 Addition of quercetin subsequent to A23187-induced PI(4,5)P2 hydrolysis reduces PI(4,5)P2 re

180 Moreover, A23187-induced thromboxane A(2) synthesis, platelet aggr

181 We confirm that ionophore A23187 induces substantial [(3)H]arachidonate release fr

182 ular Ca(2+) concentration with the ionophore A23187 inhibited the activation of Akt-1 by IGF-I, Ca(2+

183 ver, both spontaneous and calcium ionophore (A23187)-initiated AR were unaffected.

184 12-myristate 13-acetate (PMA) plus ionophore A23187 (Io), which induces NFAT activation, increased RE

185 ent of thymocytes with the calcium ionophore A23187, ionomycin, or forskolin.

186 ythrocytes deprived of glucose or exposed to A23187 ionophore alone, whereas IMP accumulates when Ca(

187 han secretion triggered by depolarization or A23187; it does not, however, depend on the cation entry

188 increasing Ca(2+) using the Ca(2+) ionophore A23187 leads to immediate cessation of elongation and th

189 endothelial cells with the calcium ionophore A23187 leads to the rapid disruption of the eNOS-caveoli

190 of unfertilized eggs in the Ca(2+) ionophore A23187 led to inactivation of MEK and MAP kinase with th

191 Eggs activated by ionophore A23187 may show multiple initiation sites.

192 rbol-13-acetate; TPA) and calcium ionophore (A23187)-mediated induction of PGE2 synthesis.

193 cts synthesized during thrombin or ionophore A23187-mediated activation of endothelial cells.

194 on by the phorbol ester TPA and by ionophore A23187-mediated calcium influx (which experimentally cor

195 A23187-mediated inhibition of collagenase 1 protein was

196 ctivation of secretion by the Ca2+ ionophore A23187, MIC2 initially occupied the apical surface of th

197 e single application of a calcium ionophore, A23187, mimicked effects of glucose, sorbitol, and VEGF

198 ages to the calcium ionophores, ionomycin or A23187, mimicked receptor ligation and inhibited IL-12(p

199 the range of relative rates are as follows: A23187, Nd3+ > La3+ > Eu3+ > Gd3+ > Er3+ > Yb3+ > Lu3+ (

200 by five stimuli; PMA, the calcium ionophore A23187, nigericin, Candida albicans and Group B Streptoc

201 influx, we examined the effects of H2O2 and A23187 on PC12 cells.

202 l growth factor (EGF) and calcium ionophore (A23187) on IL-8 and COX-2 reporter gene activity, mRNA l

203 ased in both groups after the Ca2+ ionophore A23187 or 14,15-epoxyeicosatrienoic acid, independent of

204 in the presence of either the Ca2+ ionophore A23187 or a combination of dibutyryl cAMP and 3-isobutyl

205 ated mice aortas to either calcium ionophore A23187 or bradykinin significantly increased AMPK Thr-17

206 )alpha(-/-) lung fibroblasts stimulated with A23187 or serum.

207 Treatment with calcium ionophores A23187 or thapsigargin markedly inhibited the basal and

208 re treated with either the calcium ionophore A23187 or thapsigargin, z-VAD failed to prevent cell shr

209 reatment of LNCaP with the calcium ionophore A23187 or the phorbol ester phorbol 12-myristate 13-acet

210 Endothelial stimulation with A23187 or thrombin caused constriction in P1 arteries, n

211 trifluoromethyl ketone (AACOCF3), prevented A23187 or zymosan-stimulated monocyte prostanoid formati

212 Activation with Ca(2+) ionophore (A23187) or IgE-anti-IgE induced eNOS phosphorylation and

213 mulated by bradykinin, the calcium ionophore A23187, or arachidonic acid.

214 inase and phospholipase C, calcium ionophore A23187, or heat resulted in the dramatic increase in the

215 activation with thrombin, calcium ionophore A23187, or phorbol 12-myristate 13-acetate, alpha and ga

216 cyclic nucleotide analogs, calcium ionophore A23187, or phorbol 12-myristate 13-acetate.

217 icamycin, brefeldin A, the calcium ionophore A23187, or thapsigargin increased the expression of VEGF

218 timuli that bypass these receptors (PMA plus A23187, or TNF-alpha) activated NF-kappaB normally.

219 Finally, A23187- or bradykinin-enhanced AMPK activation was signi

220 at therapeutic concentrations inhibited Ab-, A23187-, or PMA-induced platelet particle formation by i

221 HrHRF, followed by stimulation with PMA and A23187 overnight.

222 ponse to acetylcholine and calcium ionophore A23187 (P < .0001).

223 ed Rap1 activation, as did calcium ionophore A23187, phorbol ester, forskolin, 8-bromo-cyclic AMP, an

224 A23187 potentiated the effect of TPA.

225 ne glycol bis N,N,N',N' tetraacetic acid and A23187 prevented light-induced changes in protein phosph

226 Only treatment with EDTA and A23187 prevented stimulation by the combination of 1 mM

227 Addition of calcium ionophore A23187 produced a rapid release of 20-[(3)H]HETE from th

228 Treatment with the calcium ionophore A23187 recapitulated the force-induced perinuclear actin

229 ed question markCa(2+)(c) with the ionophore A23187 reduced intracellular viability by 50%.

230 Norepinephrine contracted aorta treated with A23187 relaxes in an endothelium-dependent fashion despi

231 endothelial cells stimulated with 10 microM A23187 released a stable flux of .NO, as detected by .NO

232 dramatically inhibited, but the response to A23187 remains robust.

233 tor activating peptide (TRAP), collagen, and A23187, respectively.

234 n activation induced by overexpression or Ca/A23187 resulted in PTP1B cleavage, which can be blocked

235 Exposure to Ca2+ ionophore A23187 resulted in rapid PS exposure in those cell lines

236 owed by treatment with the calcium ionophore A23187 resulted in the formation of PGE2, 5-HETE, and LT

237 ion of platelets with the calcium ionophore, A23187, resulted in complete proteolysis of 4-phosphatas

238 al pH, treatment with the calcium ionophore, A23187, resulted in increased GFAP-IR which could be blo

239 sal and stimulated (by the calcium ionophore A23187) secretion of NO and intracellular cGMP were incr

240 d SERCA cDNAs released 33.0 +/- 0.04% of the A23187-sensitive pool within 30 s of 1 micrometer adenop

241 Human and macaque lenses cultured in A23187 showed elevated lenticular calcium and superficia

242 adaptation to H2O2 and the calcium ionophore A23187, stable DSCR1 (Adapt78) transfection and overexpr

243 e production of IFN-gamma was similar in PMA/A23187 stimulated cells with or without HrHRF.

244 ncreases in [Ca2+]i by the calcium ionophore A23187 stimulated p130(Cas) phosphorylation.

245 The Ca2+ ionophore A23187 stimulated pheromone biosynthesis alone, whereas

246 Both thapsigargin and A23187 stimulated robust [(3)H]arachidonate (AA) release

247 Neither fMLP, PMA, or A23187 stimulated the release of soluble CD14 from PMNs.

248 endent inhibition in intracellular PGE2 with A23187-stimulated 3T3 cells.

249 The PMA/A23187-stimulated activity of a proximal promoter IL-13,

250 glandin E2, and thromboxane B2 released from A23187-stimulated alveolar macrophages were significantl

251 adioactivity recovered in the supernatant of A23187-stimulated cells but <20% of the radioactivity re

252 membrane binding to membranes isolated from A23187-stimulated cells but not those isolated from nons

253 Treatment of A23187-stimulated cells with EGTA or BAPTA-AM demonstrat

254 and diminished 5-LOX membrane association in A23187-stimulated cells.

255 t of ascorbic acid was also specific because A23187-stimulated cGMP accumulation in PAECs was insensi

256 referentially released arachidonic acid, but A23187-stimulated cPLA(2)alpha(-/-) fibroblasts nonspeci

257 Inhibition of CSE activity reversed A23187-stimulated mitochondrial ATP production.

258 Kinetic experiments with A23187-stimulated mouse 3T3 fibroblast cells revealed a

259 n basal PGI2 production, and bradykinin- and A23187-stimulated PGI2 were diminished 96% and 94%, resp

260 PD 098059 only partially inhibited A23187-stimulated PLA(2) activity primed by SCF, suggest

261 TPA- and A23187-stimulated release of arachidonic acid from membr

262 re incubated with LDL+/-L-4F, and changes in A23187-stimulated.NO and O2*- generation were determined

263 Upon A23187 stimulation, RSK2 induced nuclear localization of

264 (+) cells with stem cell factor (SCF) before A23187-stimulation resulted in primed PLA(2) activity, w

265 myristate acetate, or the calcium ionophore, A23187; such mast cells can rapidly release VPF/VEGF, ap

266 lin-1 was also mimicked by calcium ionophore A23187, suggesting the importance of Ca2+ in the mechani

267 We report that IL-22 induction by TPA/A23187 (T/A) or alphaCD3 is inhibited by CsA or related

268 ts of caldesmon are blocked by the ionophore A23187, thapsigargin, and membrane depolarization, presu

269 element mediated by treatment of cells with A23187, thapsigargin, and tunicamycin.

270 After SMCs were exposed to A23187, thapsigargin, or tunicamycin, intracellular calc

271 (2) In mesangial cells stimulated with A23187, the secretion of endogenously produced PAF was i

272 n-related peptide, adenosine 5'-diphosphate, A23187, thrombin, or U46619).

273 4 is stimulated by phorbol myristate acetate/A23187 to a greater level when compared to normals.

274 otherapy drug VP-16 or the calcium ionophore A23187 to induce apoptosis in Burkitt's lymphoma cell li

275 Adding calcium ionophore A23187 to Mphi inoculated with Mtb further increased cal

276 aling, and with PMA and a calcium ionophore (A23187) to bypass membrane-mediated signaling events.

277 ed from the plastic substrate in response to A23187 treatment was blocked by N-ethylmaleimide.

278 However, following A23187 treatment, LPS promoted physical proximity betwee

279 howed that the venules were not denuded with A23187 treatment, suggesting that platelets adhered to v

280 -tetraacetic acid (EGTA) + calcium ionophore A23187 treatments resulted in reduced levels of in vivo

281 In mouse lung fibroblasts A23187 triggered mitochondrial permeability transition p

282 in the mammalian cells by chemicals, such as A23187, tunicamycin, thapsigargin, and brefeldin A, that

283 The effect of A23187 was attenuated in CaM binding-deficient mutants o

284 In P1 arteries, constriction to thrombin or A23187 was inhibited by endothelial-denudation, by ET-1

285 The divalent cation ionophore A23187 was used to induce equilibrium distribution of Ca

286 sorelaxation induced by a calcium ionophore (A23187) was increased in both groups but was only statis

287 concentration of cAMP (forskolin) or Ca(2+) (A23187) was not different in WT and Clcn5 KO mice.

288 (+) cells stimulated with calcium ionophore (A23187) was of similar magnitude to that of mature neutr

289 onists, using the caged-calcium ionophore Br-A23187, was capable of inducing the formation of a new g

290 anoylphorbol-13-acetate and Ca(2+) ionophore A23187, was inhibited by dominant negative MEKK2 mutants

291 and to a lesser extent the calcium ionophore A23187 were highly variable and correlated with the numb

292 Also, vasoconstrictions to A23187 were reversed to dilations (-18.7+/-2.2 versus 18

293 ow levels of H2O2 (75-100 microM), VP-16 and A23187 were unable to induce apoptosis in these cells.

294 osure of the cells to the calcium ionophore, A23187, were resolved at the level of individual exocyto

295 er, the D93N mutant is fully functional with A23187, whereas the D43N mutant is nearly inactive.

296 ld be immediately and completely released by A23187, whereas the sequestered Ca2+ was remarkably resi

297 Treatment with the calcium ionophore A23187, which increases Ca(2+)-calmodulin binding to nNO

298 othelial growth factor, and Ca(2+) ionophore A23187, which is corroborated in isolated perfused mouse

299 acrosome reactions induced by the ionophore A23187, zona binding was extended to a broad area coveri

300 anoid production induced by stimuli that do (A23187, zymosan) or do not (phorbol myristate acetate (P