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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.
56 AVP-dependent desensitization of NPR-B, and ionomycin, a calcium ionophore, mimics the AVP effect.
60 to the SUMO-1 bodies, whereas treatment with ionomycin alone induced nuclear translocation of NFAT1 b
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
68 diation, H(2)O(2), and the Ca(2+) ionophore, ionomycin, also stimulated NOS activity, and this was as
70 astly, the activation of AMPK in response to ionomycin and 2-deoxyglucose is not impaired in LKB1(-/-
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+).
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
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
86 l activity of NFAT1 upon co-stimulation with ionomycin and phorbol 12-myristate 13-acetate, whereas a
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
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
96 In this study, using the calcium ionophore ionomycin and/or PMA on Jurkat T cells, we show that the
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
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.
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
119 function was examined by treating cells with ionomycin (calcium influx), thapsgargin (endoplasmic ret
128 imulation with phorbol myristate acetate and ionomycin did not restore the production of IFN-gamma.
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
134 contrast to wild type cells, treatment with ionomycin failed to increase GlcAT-I promoter activity i
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
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
145 rtantly, activation of the RCAN1 promoter by ionomycin, in control and FHL2 knockdown cells, was abol
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
151 mutation displayed increased area under the ionomycin-induced [Ca(2+)](i) versus time curve (AI) com
153 d mode of NCX, evaluated in experiments with ionomycin-induced Ca(2+) influx into neurons, was strong
159 II activity with KN93 abolished thrombin- or ionomycin-induced CREB phosphorylation on Ser(142) witho
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
172 chelators (BAPTA, EGTA) inhibited basal and ionomycin-induced NO production, they failed to inhibit
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
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
182 isplay a concentration-dependent response to ionomycin: low concentrations mimic nigericin by hyperpo
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
191 hyperpolarization; however, Ca(2+) influx by ionomycin or Ca(2+) release from intracellular stores by
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
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
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
211 stimulation with platelet activating factor, ionomycin, or phorbol 12-myristate 13-acetate was signif
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.
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
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.
226 -21 cells with phorbol myristate acetate and ionomycin resulted in a small increase in the amount of
228 es with phorbol 12-myristate 13-acetate plus ionomycin results in transcriptional repression of TdT e
233 ted CD4+ T cells and immune responses of PMA/ionomycin stimulated CD4+ T cells by FACS analysis purif
236 ously demonstrated that ATP is released from ionomycin-stimulated airway epithelial goblet cells coor
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
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
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
254 higher [Ca2+] in unstimulated cells but upon ionomycin stimulation, the probes experienced equal amou
260 by global Ca(2+) signals induced by IP(3) or ionomycin, suggesting that critical, local Ca(2+) nanodo
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
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
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
281 rial [Ca(2+)] and cell death after prolonged ionomycin treatment, as a model of Ca(2+) overload, were
288 elevation of cytoplasmic Ca(2+) levels with ionomycin upregulated FN-binding activity, demonstrating
290 g induced by TCR cross-linking, IL-2, or PMA/ionomycin was found to be blunted within all T cell subp
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-
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
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
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