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1  (phorbol 12-myristate 13-acetate [PMA] plus ionomycin).
2 -CD28 or phorbol-12-myristate-13-acetate and ionomycin.
3 ion with phorbol 12-myristate 13-acetate and ionomycin.
4 3 + anti-CD28 monoclonal antibodies or PMA + ionomycin.
5 , or Ca(2+) mobilization by thapsigargin and ionomycin.
6  cells by provision of calcium signals using ionomycin.
7 pamycin/FRB/FKBP system or by treatment with ionomycin.
8 tivated protein kinase (AMPK) in response to ionomycin.
9 arkedly different from the rapid response to ionomycin.
10 ollowing stimulation with either anti-IgM or ionomycin.
11 ted with phorbol 12-myristate 13-acetate and ionomycin.
12  also by the pharmacological stimuli PMA and ionomycin.
13 of Nox5 in response to low concentrations of ionomycin.
14  increased activity at low concentrations of ionomycin.
15 anti-CD3 and anti-CD28 antibodies or PMA and ionomycin.
16 ol 12-myristate 13-acetate (PMA), but not by ionomycin.
17 jority make IFN-gamma in response to PMA and ionomycin.
18 ulation with phorbol myristate acetate (PMA)/ionomycin.
19 tion and was greater than that observed with ionomycin.
20 osed to H(2)O(2) but not in cells exposed to ionomycin.
21 such as angiotensin-II and a Ca2+ ionophore, ionomycin.
22 n nonneuronal cells on Ca2+ entry induced by ionomycin.
23 w-derived cultured mast cells in response to ionomycin.
24 oubled the amplitude of transients evoked by ionomycin.
25 n stimulation with ionophores, nigericin, or ionomycin.
26  overload (1.6 mM) after permeabilization by ionomycin.
27 e cells were activated by phorbol ester plus ionomycin.
28 inhibitors prevented E-cad(100) induction by ionomycin.
29 t were absent after exposure to either FN or ionomycin.
30 amma when Th cells were treated with PMA and ionomycin.
31 croM ionomycin and was reversed by 50 microM ionomycin.
32 liminated L. amazonensis when incubated with ionomycin.
33  and without phorbol 12-myristate 13-acetate/ionomycin.
34 e antibacterial peptide LL-37 in response to ionomycin.
35 onses to phorbol 12-myristate 13-acetate and ionomycin.
36  in vitro mitogenic stimulation with PMA and ionomycin.
37  and actinomycin D and with necrosis inducer ionomycin.
38 ion with phorbol 12-myristate 13-acetate and ionomycin.
39 oss-linking antibodies or phorbol ester plus ionomycin.
40 ulation with epidermal growth factor (EGF) + ionomycin.
41 induces Treg proliferation in the absence of ionomycin.
42 on with phorbol 12-myristate 13-acetate plus ionomycin.
43 lated by phorbol 12-myristate 13-acetate and ionomycin.
44 ocation was rescued by the Ca(2+) ionophore, ionomycin.
45  active calcineurin or the calcium ionophore ionomycin.
46 n with ouabain versus Ca(2+) modulation with ionomycin.
47 mal concentration of the strong secretagogue ionomycin (1 microM), for which there was a delay betwee
48 res, stimulation (S2) of the same cells with ionomycin (10 microM), in the absence of extracellular c
49 After stimulation with the calcium ionophore ionomycin, 2-AG levels in MGL-silenced cells were compar
50  inhibitor), histamine (cAMP activator), and ionomycin (a Ca(2+) ionophore) to tissue-engineered cons
51 es revealed that basal and evoked IK(ATP) by ionomycin, a Ca(2+) ionophore, is activated by CaMKII.
52 yristate 13-acetate (PMA) to activate PKC or ionomycin, a Ca(2+) ionophore.
53                                    Moreover, Ionomycin, a Ca(2+)-dependent pathway activator, stimula
54                                              Ionomycin, a calcium ionophore, causes rapid mitochondri
55         Stimulation of mouse astrocytes with ionomycin, a calcium ionophore, enhanced the production
56  AVP-dependent desensitization of NPR-B, and ionomycin, a calcium ionophore, mimics the AVP effect.
57                Stimulation of VSM cells with ionomycin, a calcium ionophore, resulted in activation o
58                         As with monensin and ionomycin, a minor fraction of activity may be electroge
59                        CD300f also binds PMA/ionomycin-activated splenocytes and Ag-stimulated T cell
60 to the SUMO-1 bodies, whereas treatment with ionomycin alone induced nuclear translocation of NFAT1 b
61           In contrast, treatment with PMA or ionomycin alone induces chromatin remodeling at far fewe
62                               We report that ionomycin alone induces IL-4 and IFN-gamma, but not IL-2
63  whereas anergic transcription stimulated by ionomycin alone may occur without recruitment into the S
64 ation with PMA and ionomycin, but not PMA or ionomycin alone, induces cyclin D2 expression and cell-c
65                                              Ionomycin also activates CaMKIV, which, together with p3
66                        The calcium ionophore ionomycin also induced a rapid hyperpolarization.
67                           The Ca2+ ionophore ionomycin also inhibited bTREK-1 currents through channe
68 diation, H(2)O(2), and the Ca(2+) ionophore, ionomycin, also stimulated NOS activity, and this was as
69          Treatment of Wnt4(-/-) kidneys with Ionomycin, an activator of the pathway, partially rescue
70 astly, the activation of AMPK in response to ionomycin and 2-deoxyglucose is not impaired in LKB1(-/-
71 maximum depletion produced by the ionophores ionomycin and A23187.
72 rescued SOCE in response to thapsigargin and ionomycin and abrogated IFN-alpha/beta-induced apoptosis
73  H2O2 generated by DeltakatG likely oxidizes ionomycin and alters its ability to transport Ca(2+).
74        Using phorbol myristate acetate (PMA)/ionomycin and anti-CD3 activation of CD4(+)CD25(-) cells
75 their PBMCs by phorbol-myristate acetate and ionomycin and both IFN-gamma and IL-4 deficiencies in V(
76 on with both phorbol 12-myristate 13-acetate/ionomycin and CMV-peptide-loaded antigen-presenting cell
77  studied in mouse keratinocytes treated with ionomycin and during the wound-healing process.
78                The calcium mobilizing agents ionomycin and glutamate stimulate endogenous HO2 activit
79 nal activation with anti-CD3 or with PMA and ionomycin and in both C57BL/6 and BALB/c mice.
80 go autophosphorylation in cells treated with ionomycin and is likely also targeted by PKA.
81  mRNA and protein after stimulation with PMA/ionomycin and latency-reversing agents (LRAs).
82  induced in unfertilized mouse eggs by using ionomycin and manipulating extracellular calcium.
83 enhanced IFN-gamma expression in response to ionomycin and phorbol 12-myristate 13-acetate and weakly
84 rthermore, we found that treatment with both ionomycin and phorbol 12-myristate 13-acetate ensured ef
85                                              Ionomycin and phorbol 12-myristate 13-acetate further in
86 l activity of NFAT1 upon co-stimulation with ionomycin and phorbol 12-myristate 13-acetate, whereas a
87                   Using protease inhibitors, ionomycin and phorbol myristate acetate stimulation, sma
88  Ag-free protocol that included bryostatin 1/ionomycin and sequential common gamma-chain cytokines (I
89  this, BMP2 gene expression was increased by ionomycin and suppressed by the calcineurin inhibitor, c
90 acity and IL-2 production in response to PMA/ionomycin and T cell receptor cross-linking.
91                                              Ionomycin and thapsigargin increased intracellular Ca2+
92                         The Ca(2+) ionophore ionomycin and the excitotoxin glutamate induced producti
93 2-myristate 13-acetate and calcium ionophore ionomycin and was blocked by the NFAT antagonist cyclosp
94 q-coupled [Ca(2+)]i increase was mimicked by ionomycin and was not affected by inhibition of protein
95 he DMSO effect was counteracted by 10 microM ionomycin and was reversed by 50 microM ionomycin.
96   In this study, using the calcium ionophore ionomycin and/or PMA on Jurkat T cells, we show that the
97 istinct consequences on caspase-independent (ionomycin) and -dependent (ABT-263) cell death.
98 with different stimuli, including Con A, PMA/ionomycin, and allogeneic spleen cells.
99 ty to mobilize calcium upon stimulation with ionomycin, and BCR-induced calcium mobilization from int
100 dence on store depletion by thapsigargin and ionomycin, and differential sensitivity to inhibition by
101 , including purinergic receptor stimulation, ionomycin, and increases in cell volume, each activated
102 +) pools remained sensitive to thapsigargin, ionomycin, and inositol trisphosphate.
103 activity that is activated by phorbol ester, ionomycin, and okadaic acid.
104 l responses to phorbol myristate acetate and ionomycin, and possessed decreased levels of CD3zeta.
105 on of Pyk2 and ERK than the Ca(2+) ionophore ionomycin, and the effects of PMA and Ang II were abolis
106 2-myristate 13-acetate, the Ca(2+) ionophore ionomycin, and the serine/threonine phosphatase inhibito
107  more vulnerable to the cytotoxic effects of ionomycin- and 2,5-di-(t-butyl)-1,4-hydroquinone-induced
108 reover, anthrax LT specifically inhibits PMA/ionomycin- and anti-CD3-induced IL-2 production in Jurka
109 ntly enhance phorbol 12-myristate 13-acetate/ionomycin- and anti-CD3-stimulated lymphocyte apoptosis.
110 by dimethylsphingosine blocks thapsigargin-, ionomycin-, and platelet-activating factor-mediated SOCE
111 splayed limited Ca(2+) influx in response to ionomycin, as a result of ionophore H2O2 sensitivity.
112                 Conversely, thapsigargin and ionomycin attenuated the BAPTA-AM effects and promoted N
113 stimulation by phorbol myristate acetate and ionomycin but not IL-2 or IL-12, and could be induced to
114 nd A549 cells, mannitol, 2-deoxyglucose, and ionomycin, but not 5-aminoimidazole-4-carboxamide-1-beta
115 ing (G0) B cells, costimulation with PMA and ionomycin, but not PMA or ionomycin alone, induces cycli
116 erent localized [Ca2+] upon stimulation with ionomycin, but rather differences in phosphorylation sta
117 a production in T(H)2 cells activated by PMA-ionomycin, but weakly increased IFN-gamma production in
118 of Pasteurella multocida toxin by 2-fold and ionomycin by 3-fold.
119 function was examined by treating cells with ionomycin (calcium influx), thapsgargin (endoplasmic ret
120                                 Furthermore, ionomycin (calcium ionophore) and TPA augmented the enha
121                                      PMA and ionomycin cause T cell cytokine production.
122                                  Exposure to ionomycin caused an increase in I sc 2-fold greater than
123                                 H(2)O(2) and ionomycin caused cell death in a dose-dependent manner,
124                                       Higher ionomycin concentrations induce a stochastic failure of
125 ar Ca(2+) inhibited both A(2B) receptor- and ionomycin-dependent IL-4 secretion.
126               Topical lingual application of ionomycin did not affect the phasic part of the CT respo
127                       Ca(2+) mobilization by ionomycin did not permit dGal-1 to mobilize PS, indicati
128 imulation with phorbol myristate acetate and ionomycin did not restore the production of IFN-gamma.
129                               In response to ionomycin, EGFP-cPLA(2)zeta translocated to ruffles and
130               Moreover, complement and EGF + ionomycin enhanced phosphorylation of Ser-511.
131 e, after treatment with the Ca(2+) ionophore ionomycin, ER microsomes from NT1 cells overproducing CR
132 e channels, in HEK293 cells expressing CLCAs ionomycin-evoked increases in intracellular calcium stim
133                          Although agonist or ionomycin exposure can raise bulk [Ca(2+)](i) to levels
134  contrast to wild type cells, treatment with ionomycin failed to increase GlcAT-I promoter activity i
135 n ex vivo with phorbol myristate acetate and ionomycin for 5 hours.
136 r stimulation with phorbol myristate acetate-ionomycin, high gamma interferon and low IL-4 levels wer
137 ed with phorbol 12-myristate 13-acetate plus ionomycin, IL-25 plus IL-33 (IL-25/IL-33), or a mixture
138 onse to phorbol 12-myristate 13-acetate plus ionomycin, IL-25/IL-33, or a mixture of TLR ligands.
139 e RGC-5 following 24 h of exposure to 250 nM ionomycin (IMN) or 300 units/ml interferon-gamma (IFN-ga
140  lymphocyte proliferation induced by PMA and ionomycin in an IL-2-independent manner.
141 eased by the combination of thapsigargin and ionomycin in Ca2+-free solution and the Ca2+ influx comp
142 lar Ca2+ to saturating levels with 10 microM ionomycin in the presence of 10 mM extracellular Ca2+ eq
143 Cells were stimulated with phorbol ester and ionomycin in the presence of brefeldin A and stained for
144                A suboptimal concentration of ionomycin in the presence of PMA fully activates Tgfb1(-
145 rtantly, activation of the RCAN1 promoter by ionomycin, in control and FHL2 knockdown cells, was abol
146                     In the presence of cAMP, ionomycin increased sensory adaptation to HCl, CO(2), an
147 s expressing TF(C186S/C209S) with HgCl(2) or ionomycin increased the cell-surface TF activity to the
148 n, with phorbol myristate acetate (PMA) plus ionomycin increasing E3-directed transcription 100-fold.
149 increasing intracellular calcium levels with ionomycin induced pyk2/RAFTK phosphorylation, and adenov
150                       The calcium ionophore, ionomycin, induced chondrogenesis through activation of
151  mutation displayed increased area under the ionomycin-induced [Ca(2+)](i) versus time curve (AI) com
152  also partially resistant to calcineurin- or ionomycin-induced apoptosis.
153 d mode of NCX, evaluated in experiments with ionomycin-induced Ca(2+) influx into neurons, was strong
154                                              Ionomycin-induced Ca(2+) influx promoted p-Akt, an effec
155                                  One and two ionomycin-induced Ca(2+) transients resulted in 39 and 4
156 itor of Mek1,2, had no appreciable effect on ionomycin-induced calpain activation.
157        However, it had minimal effect on PMA/ionomycin-induced CD69 up-regulation in Jurkat cells, on
158 nd rescued Nrf2-/- neurons from rotenone- or ionomycin-induced cell death.
159 II activity with KN93 abolished thrombin- or ionomycin-induced CREB phosphorylation on Ser(142) witho
160                                              Ionomycin-induced cytokine production requires NFAT, p38
161            However, both proteins attenuated ionomycin-induced cytosolic free calcium ([Ca(2+) ](i)),
162 mast cells eliminates both IgE-dependent and ionomycin-induced degranulation and causes a significant
163 psilonRI-mediated degranulation, but not PMA/ionomycin-induced degranulation, as shown by beta-hexosa
164 e formin INF2 reduces both un-stimulated and ionomycin-induced Drp1 accumulation and mitochondrial fi
165 tory to phorbol 12-myristate 13-acetate plus ionomycin-induced ERK1/2 phosphorylation (referred to as
166 vity in an assay measuring inhibition of PMA/ionomycin-induced human PBMC proliferation.
167                           Both the basal and ionomycin-induced I sc were inhibited by basolateral Ba
168              ARTS-1 expression also enhances ionomycin-induced IL-1RII shedding.
169 G protein-coupled receptor activation, or by ionomycin-induced intracellular calcium release.
170              Phorbol-12-myristate-13-acetate/ionomycin-induced MAPK signaling was measured by whole-b
171                             At the opposite, ionomycin-induced NFAT activity allows survival of nonre
172  chelators (BAPTA, EGTA) inhibited basal and ionomycin-induced NO production, they failed to inhibit
173                  Knocking down ASK1 inhibits ionomycin-induced p38 phosphorylation and IL-4 productio
174 ARC down-regulation was further confirmed as ionomycin-induced PARC down-regulation in both chemosens
175 d found that phorbol 12-myristate 13-acetate/ionomycin-induced transcription was augmented by IL-2 tr
176 horing protein (AKAP) 79 and interferes with ionomycin-induced translocation of conventional PKC to t
177 timulation of Tgfb1(-/-) T cells by PMA plus ionomycin induces IL-2 production and mitogenic response
178                                              Ionomycin induces p38 phosphorylation through a calcium-
179 uorophores following activation with calcium-ionomycin, ionomycin, or hPLCzeta cRNA microinjection.
180 psigargin, or phorbol myristate acetate plus ionomycin, leading to persistent NFAT (nuclear factor of
181                Treatment of MCF-7 cells with ionomycin led to increased accumulation of beta-cat(75)
182 isplay a concentration-dependent response to ionomycin: low concentrations mimic nigericin by hyperpo
183                                  Ouabain and ionomycin may be useful pharmacologic agents for increas
184 hancement of phorbol 12-myristate 13-acetate/ionomycin-mediated activation signals.
185 m sequestration since neither treatment with ionomycin nor endothelin-1, both of which elevated the i
186 , stimulating internal Ca(2+) by exposure to ionomycin not only caused greater stimulation of K(+) ((
187 mutant and prevents the inhibitory effect of ionomycin on NHE3 activity as well as the oligomerizatio
188 tinin-4 potentiates the inhibitory effect of ionomycin on NHE3 activity by accelerating the oligomeri
189 mice following treatment with either PMA and ionomycin or anti-CD3 was markedly inhibited.
190 The Ca2+-dependent changes in CBF induced by ionomycin or ATP were not affected by KT5823.
191 hyperpolarization; however, Ca(2+) influx by ionomycin or Ca(2+) release from intracellular stores by
192          In the presence of rCIL-2, PMA plus ionomycin or Con A stimulated CD4(+)CD25(+) cell prolife
193 t by mitogen phorbol 12-myristate 13-acetate/ionomycin or cytokine tumor necrosis factor alpha, two w
194 eatment with phorbol 12-myristate 13-acetate/ionomycin or lipopolysaccharide, and unique sensitivity
195             Whole-cell currents activated by ionomycin or methacholine were anion-selective and showe
196 vity of nigericin for Pb(2+) exceeds that of ionomycin or monensin and arises, at least in part, from
197 ow sodium conditions, and in the presence of ionomycin or monensin, which enhanced pneumococcal sensi
198 ulated proliferation, which was corrected by ionomycin or reconstitution of Bid, particularly an ER-t
199 gglutinin P or with Ca(2+)-mobilizing agents ionomycin or thapsigargin induced accumulation of FM1-43
200 f TRP-3/SPE-41 in spe-38 mutant spermatozoa, ionomycin or thapsigargin induced influx of Ca(2+) remai
201 lation with either phorbol myristate acetate/ionomycin or the Vdelta2 gammadelta T-cell receptor agon
202 ntrast in human dermal fibroblasts, TPA plus ionomycin or TPA did not significantly alter the proport
203 00) was generated by treatment of cells with ionomycin or TPA.
204  stimulating bypassing surface proteins (PMA:ionomycin) or through the TCR (e.g., viral Ags).
205 lular calcium by the P2-purinergic receptor, ionomycin, or a direct activator of phospholipase C, ind
206 n A (Con A), phorbol myristate acetate (PMA)/ionomycin, or anti-CD3/anti-CD28 before comparing the pr
207 mounts of TNFalpha in response to Con A, PMA/ionomycin, or anti-CD3/anti-CD28.
208 -linking or by phorbol-myristate acetate and ionomycin, or by phytohemagglutinin.
209 following activation with calcium-ionomycin, ionomycin, or hPLCzeta cRNA microinjection.
210               Stimulation with CD3/CD28, PMA/ionomycin, or latency reversing agents prostratin and SA
211 stimulation with platelet activating factor, ionomycin, or phorbol 12-myristate 13-acetate was signif
212        Downregulation was not induced by PMA-ionomycin, or prevented by PI3K inhibition, implicating
213  (LPS), phorbol myristate acetate (PMA) plus ionomycin, or purified protein derivative (PPD) was stud
214 ts showed that 20 microM ouabain, 0.3 microM ionomycin, or their combination increased the tensile mo
215 as degraded after 10 min exposure to PMA and ionomycin, or TNF and was maximally degraded by 30 min.
216 additional 379% after short-term exposure to ionomycin (P < 0.05).
217  induced in the Th2 clone D10 after PMA plus ionomycin (P/I) stimulation; however we found that the I
218 nduced with chemical activators of shedding (ionomycin, phorbol 12-myristate 13-acetate, and 4-aminop
219 ed (U), with phorbol 12-myristate 13-acetate/ionomycin (PI) or lipopolysaccharide (LPS), and stained
220 ints by the intra-articular Ca(2+) ionophore ionomycin, prostaglandin E(2), cAMP-raising agents, seri
221 sue with phorbol-12-myristate-13-acetate and ionomycin, recapitulating CAVD microenvironment, resulte
222 lin, or stimulating calmodulin activity with ionomycin, reduces Smad2 levels.
223 1 in N2a cells reduced the Ca(2+) content of ionomycin-releasable intracellular stores and decreased
224  to induction by E1A, activation by PMA plus ionomycin requires the two E3 NF-kappaB binding sites.
225  signalosome and can be activated by PMA and ionomycin, respectively.
226 -21 cells with phorbol myristate acetate and ionomycin resulted in a small increase in the amount of
227         Treatment with the calcium ionophore ionomycin resulted in increased GlcAT-I expression, wher
228 es with phorbol 12-myristate 13-acetate plus ionomycin results in transcriptional repression of TdT e
229                      Exposure to basolateral ionomycin, reversibly increased TRC Ca(2+), resting pH(i
230                                      PMA and ionomycin significantly increased the activation of MAPK
231                       Treatment with PMA and ionomycin significantly prevented the decrease in IL-17
232               Treatment of intact cells with ionomycin stimulated a rapid increase in FAK phosphoryla
233 ted CD4+ T cells and immune responses of PMA/ionomycin stimulated CD4+ T cells by FACS analysis purif
234          Phorbol 12-myristate 13-acetate and ionomycin stimulated ectodomain shedding of meprin beta
235 -O-tetradecanoylphorbol 13-acetate (PMA) and Ionomycin stimulated Jurkat cells.
236 ously demonstrated that ATP is released from ionomycin-stimulated airway epithelial goblet cells coor
237             Furthermore, 2-deoxyglucose- and ionomycin-stimulated AMPK activity, alphaThr-172 phospho
238 roduction in phorbol 12-myristate 13-acetate/ionomycin-stimulated human CD4+ T cells isolated from he
239 ion of phorbol 12-myristate 13-acetate (PMA)/ionomycin-stimulated human peripheral blood mononuclear
240 sal and phorbol 12-myristate 13-acetate plus ionomycin-stimulated interferon-gamma, IL-4, and tumor n
241                        Complement- and EGF + ionomycin-stimulated iPLA(2)gamma activity was attenuate
242 ne (PP2) abrogates 17beta-estradiol- but not ionomycin-stimulated NO release.
243 he sheddase responsible for constitutive and ionomycin-stimulated processing of the PDGFRbeta.
244 and were the primary source for histamine or ionomycin-stimulated secretion of these molecules.
245 utive, phorbol 12-myristate 13-acetate-, and ionomycin-stimulated shedding of meprin beta and meprin
246 e ADAM10 substrate betacellulin, whereas the ionomycin-stimulated shedding of the ADAM17 substrates C
247 ACScan flow cytometry, the proportion of PMA/ionomycin-stimulated T cells expressing cytokines ex viv
248                      Both naive and PMA plus ionomycin-stimulated thymic CD4(+)CD25(+) cells suppress
249 his drug did not have any effect on PMA plus ionomycin stimulation (CsA-sensitive pathway).
250 ing cell phorbol 12-myristate 13-acetate and ionomycin stimulation and calcineurin activation.
251 - mice respond to anti-CD3/anti-CD28 and PMA/ionomycin stimulation and produce IL-2 similar to WT.
252 conventional CD4+CD25- T cells following PMA/ionomycin stimulation demonstrated no differences in ind
253                               LPS, PMA, plus ionomycin stimulation in vitro for 5 h induced B10 cells
254 higher [Ca2+] in unstimulated cells but upon ionomycin stimulation, the probes experienced equal amou
255  B cells to express IL-10 following PMA plus ionomycin stimulation.
256  peptide-coated cells, CD3/CD28 Abs, and PMA/ionomycin stimulation.
257 rimary human CD14(+) monocytes after PMA and ionomycin stimulation.
258 to phorbol 12-myristate 13-acetate (PMA) and ionomycin stimulation.
259                                              Ionomycin studies indicated that intracellular Ca2+ stor
260 by global Ca(2+) signals induced by IP(3) or ionomycin, suggesting that critical, local Ca(2+) nanodo
261                                              Ionomycin, thapsigargin, and dialysis of the cell with i
262  Abeta secretion induced by thapsigargin and ionomycin (that elevate intracellular calcium concentrat
263 ulated by compounds (forskolin, epinephrine, ionomycin) that raise cellular cAMP or calcium levels.
264 in alpha-latrotoxin, or the Ca(2+)-ionophore ionomycin), the homo- and heteromultimerization of synap
265 aive animals stimulated with LPS or PMA plus ionomycin, the levels were significantly enhanced after
266 ide pathway, including the calcium ionophore ionomycin, the nitric oxide donor S-nitroso-N-acetylpeni
267  with cPLA2 and mutants were stimulated with ionomycin, the wild type and S505E translocated to the p
268  during apical or basolateral application of ionomycin to increase [Ca(2+)]i near the apical or basol
269 vity was demonstrated by using the ionophore ionomycin to mimic sumatriptan action.
270  blocks the ability of the calcium ionophore ionomycin to promote neurite outgrowth.
271 ase in intact human red cells by introducing ionomycin to raise cytoplasmic Ca++, phosphatidylserine
272 ure of the parasites to a calcium ionophore (ionomycin), to an inhibitor of the V-H(+)-ATPase (bafilo
273                    This association requires ionomycin together with a phorbol ester, which also sugg
274 -tetradecanoyl-phorbol-13-acetate (TPA) plus ionomycin, TPA, and raised extracellular calcium, induce
275 chol and caffeine responses but only reduced ionomycin transients by 30 %, suggesting that blockade o
276 er 20 min of IL-4 (50 ng/ml), but not IL-13, ionomycin transients were decreased to 0.50 +/- 0.16 (S2
277 vation under phorbol 12-myristate 13-acetate/ionomycin treatment conditions.
278                   Inhibition of Cn following ionomycin treatment did not block GlcAT-I and tauT, a To
279 imulation or phorbol 12-myristate 13-acetate/ionomycin treatment enhances P2 promoter activity.
280                                          PMA/Ionomycin treatment of DOCK8-deficient NK cells rescued
281 rial [Ca(2+)] and cell death after prolonged ionomycin treatment, as a model of Ca(2+) overload, were
282  by alphaCD3/alphaCD28 cross-linking and PMA/ionomycin treatment, but not by TNFalpha or dsRNA.
283                          Moreover, following ionomycin treatment, fibroblasts from CnAalpha and CnAbe
284        Elevation of intracellular calcium by ionomycin treatment, or activation of acetylcholine rece
285 into fragments when the ER was fragmented by ionomycin treatment.
286  subset of cells also secreted IL-4 with PMA/ionomycin treatment.
287  confirmed calpain activation in response to ionomycin treatment.
288  elevation of cytoplasmic Ca(2+) levels with ionomycin upregulated FN-binding activity, demonstrating
289 l activity was decreased, and sensitivity to ionomycin was abolished.
290 g induced by TCR cross-linking, IL-2, or PMA/ionomycin was found to be blunted within all T cell subp
291       However, calcium mobilization alone by ionomycin was insufficient for IRF3 phosphorylation.
292 horbol 12-myristate 13-acetate combined with ionomycin, was inhibited.
293 nd Jurkat CD4(+) T cells stimulated with PMA/ionomycin, we demonstrate activation (phosphorylation) o
294 imulation with phorbol myristate acetate and ionomycin, we examined gamma interferon (IFN-gamma), IL-
295 everal possible mechanisms for the effect of ionomycin were considered.
296 ed necrosis mediated by the Ca(2+) ionophore ionomycin, whereas apoptosis mediated by the Bcl-2 inhib
297 ce of extracellular Ca2 and 2) the effect of ionomycin, which could not take Ca2+ out of acidic organ
298 f-function of Calfacilitin can be rescued by ionomycin, which increases intracellular calcium.
299 s, phorbol 12-myristate 13-acetate (PMA) and ionomycin, which mobilize elements of the phospholipase
300 th phorbol 12-myristate 13-acetate (PMA) and ionomycin, which signal via protein kinase C (PKC) and c
301  were first stimulated in vitro with PMA and ionomycin, which yielded IFN-gamma in 25% of cells.

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