ライフサイエンスコーパス: phorbol myristate acetate

1 fibroblast growth factor, and phorbol ester (phorbol myristate acetate).

2 phorylation of p47(phox) upon stimulation by phorbol myristate acetate.

3 de after stimulation by opsonized zymosan or phorbol myristate acetate.

4 ice produced superoxide after stimulation by phorbol myristate acetate.

5 blocking CD4 down-modulation in response to phorbol myristate acetate.

6 (MIP)-2/platelet-aggregating factor (PAF) or phorbol myristate acetate.

7 hanical strain in the presence or absence of phorbol myristate acetate.

8 cal substrate of MAP kinases, in response to phorbol myristate acetate.

9 in which H(2)O(2) production was induced by phorbol myristate acetate.

10 ly with changes in CR1 expression induced by phorbol myristate acetate.

11 unts of O(2) in response to fMet-Leu-Phe and phorbol myristate acetate.

12 urkat-T-4) and stimulated with anti-CD3 plus phorbol myristate acetate.

13 er rHuIL-1alpha pretreatment was mimicked by phorbol myristate acetate.

14 vascular endothelial cell growth factor, and phorbol myristate acetate.

15 ysaccharide, tumor necrosis factor alpha, or phorbol myristate acetate.

16 erin can be regulated by divalent cations or phorbol myristate acetate.

17 fect mimicked by treatment of the cells with phorbol myristate acetate.

18 long term incubation with the phorbol ester, phorbol myristate acetate.

19 stimulation of these cells with thrombin or phorbol myristate acetate.

20 d, through the T-cell receptor, CD28, and/or phorbol myristate acetate.

21 investigated by treating blood samples with phorbol myristate acetate.

22 d was not enhanced upon cell activation with phorbol myristate acetate.

23 edium with 0.1 mg/mL cycloheximide and 10 nM phorbol myristate acetate.

24 ERK2 phosphorylation induced by exposure to phorbol myristate acetate.

25 d repression of AP1LUC reporter induction by phorbol myristate acetate.

26 tor-alpha but were enhanced up to 20-fold by phorbol myristate acetate.

27 bacteria than NETs induced by bacteria or by phorbol-myristate acetate.

28 37 cells were induced to differentiate using phorbol myristate acetate (100 nM for 48 h) and then wer

29 ked by the protein kinase C (PKC) activator, phorbol myristate acetate (100 nM), but was not altered

30 We generated T-cell clones deficient in phorbol myristate acetate (a surrogate for DAG)-induced

31 tment of luteinized rat granulosa cells with phorbol myristate acetate, a known activator of PKC, pro

32 Phorbol myristate acetate, a known stimulator of NF-kapp

33 medium on the [Ca2+]i response to both 12,13-phorbol myristate acetate, a protein kinase C activator,

34 se enzyme activity can also be stimulated by phorbol myristate acetate, a synergism between arsenic a

35 in MF, we found that CTLA-4 is stimulated by phorbol myristate acetate/A23187 to a greater level when

36 to TRAIL-induced apoptosis, stimulation with phorbol myristate acetate abrogated the ligand-independe

37 Forskolin and phorbol myristate acetate acted synergistically to enhan

38 ed with their cognate growth factors or with phorbol myristate acetate, activation of mTORC1 required

39 ggered by fMet-Leu-Phe, immune complexes, or phorbol myristate acetate, an activator of PKC.

40 The addition of phorbol myristate acetate, an activator of protein kinas

41 gism between arsenic and the clinically used phorbol myristate acetate analog, bryostatin 1, through

42 on, but not PEEC secretion, was activated by phorbol myristate acetate and blocked by an inhibitor (m

43 -regulated with inflammation and in vitro by phorbol myristate acetate and interleukin 1beta.

44 ssion in the Jurkat T-cell line treated with phorbol myristate acetate and ionomycin (P/I), pharmacol

45 lated perforin in response to stimulation by phorbol myristate acetate and ionomycin but not IL-2 or

46 n combination with IL-12 or stimulation with phorbol myristate acetate and ionomycin did not restore

47 subjects, following stimulation ex vivo with phorbol myristate acetate and ionomycin for 5 hours.

48 eatment of Tax-transfected BHK-21 cells with phorbol myristate acetate and ionomycin resulted in a sm

49 nti-CD3 [TcR], anti-CD28, exogenous IL-2, or phorbol myristate acetate and ionomycin).

50 ll receptor antibodies or a combination of a phorbol myristate acetate and ionomycin, an increase in

51 tor stimulation, despite normal responses to phorbol myristate acetate and ionomycin, and possessed d

52 lar cytokine staining after stimulation with phorbol myristate acetate and ionomycin, we examined gam

53 roduced IL-13 protein in response to IL-2 or phorbol myristate acetate and ionomycin.

54 -color flow cytometry after stimulation with phorbol myristate acetate and ionomycin.

55 After stimulation of MM6 cells by phorbol myristate acetate and ionophore A23187, a perinu

56 a plasmid encoding FSTL1 and stimulated with phorbol myristate acetate and lipopolysaccharide.

57 Furthermore, phorbol myristate acetate and membrane-targeted HIV-1 Ne

58 igarette smoke condensate), tumor promoters (phorbol myristate acetate and okadaic acid), and an infl

59 increased 8- to 12-fold after treatment with phorbol myristate acetate and phytohemagglutinin (PMA/PH

60 abolished the phosphorylation of RAFTK upon phorbol myristate acetate and stem cell factor stimulati

61 mulation and inhibition of PKC activity with phorbol myristate acetate and with staurosporine, respec

62 after in vitro stimulation of their PBMCs by phorbol-myristate acetate and ionomycin and both IFN-gam

63 ls were activated by CD3 cross-linking or by phorbol-myristate acetate and ionomycin, or by phytohema

64 , doxorubicin, lipopolysaccharide, H(2)O(2), phorbol myristate acetate, and cigarette smoke; the supp

65 ), okadaic acid, cigarette smoke condensate, phorbol myristate acetate, and H2O2 and that the suppres

66 ase following protein kinase C activation by phorbol myristate acetate, and importantly, this effect

67 bits p70s6k activation in response to serum, phorbol myristate acetate, and increased amino acid leve

68 n of conventional or novel classes of PKC by phorbol myristate acetate; and (3) ribozymes specific fo

69 lls with MAPK stimulators, such as serum and phorbol myristate acetate, as well as by coexpression of

70 and found Abeta(1-42) to be as effective as phorbol myristate acetate at differentiating THP-1 monoc

71 utrophils activated by the soluble stimulus, phorbol myristate acetate, both chlorinated fluorescein

72 vation of apoptosis, which was suppressed by phorbol myristate acetate but not by inhibitors of ceram

73 th the protein kinase inhibitor H-8, whereas phorbol myristate acetate caused an increase to 4.50 x 1

74 Activation of the NADPH oxidase by phorbol myristate acetate caused oxidative stress as sho

75 Although short term stimulation with phorbol myristate acetate caused PKC-dependent phosphory

76 th hyaluronan oligosaccharides, IL-1beta, or phorbol myristate acetate, CD44 fragmentation was enhanc

77 with the nonselective PKC isozyme activator phorbol myristate acetate could not emulate IPC, but blo

78 ith factors such as epidermal growth factor, phorbol myristate acetate, cyclic AMP, or KCI had no sig

79 let activating factor, calcium ionophore, or phorbol myristate acetate, develops within 120 minutes i

80 Stimulation via protein kinase C (0.1 microM phorbol myristate acetate) did not.

81 he present study evaluated the potential for phorbol myristate acetate-differentiated THP-1 cells to

82 dose dependently increased TNF production in phorbol myristate acetate-differentiated U937 cells in t

83 /HS lymph incubation also increased (p <.05) phorbol myristate acetate elicited respiratory burst com

84 Phorbol myristate acetate enhanced fibroblast minocyclin

85 Moreover, phorbol myristate acetate enhanced Nedd4-2 phosphorylati

86 Stimulation by phorbol myristate acetate enhanced WT channel gating, an

87 Moreover, phorbol myristate acetate-enhanced in vitro invasion was

88 ermore, the incubation of HCT116 or RKO with phorbol myristate acetate for 16 h, which down-regulated

89 Treatment of cells with phorbol myristate acetate for 60 min led to the formatio

90 that activation of protein kinase C (PKC) by phorbol myristate acetate, Gq/11-coupled GPCR, or epider

91 sis was induced by activation with ionomycin/phorbol myristate acetate (in the presence of Brefeldin

92 TLC and phorbol myristate acetate increased cytosolic pMARCKS an

93 Treatment of Jurkat cells with phorbol myristate acetate increased the expression of si

94 Both high Pi and phorbol myristate acetate increased the phosphorylation

95 Similar assays with the phorbol ester phorbol myristate acetate indicate that it could effecti

96 Phorbol myristate acetate induced a dramatic increase of

97 Stimulation of neutrophils with phorbol myristate acetate induced secretion of BNBD-12,

98 ficant antiinflammatory activity in the PMA (phorbol myristate acetate)-induced mouse ear edema model

99 The same conditioned media also inhibit phorbol myristate acetate-induced activation of the HIV-

100 Protein kinase C inhibitors blocked phorbol myristate acetate-induced and spontaneous sheddi

101 otransfection of TACE in EC-2 cells enhanced phorbol myristate acetate-induced but not constitutive s

102 acity of K562 cells nor their sensitivity to phorbol myristate acetate-induced cytostasis and megakar

103 not formylmethionyl-leucylphenylalanine- or phorbol myristate acetate-induced LPL phosphorylation an

104 resulted in the almost complete reduction of phorbol myristate acetate-induced MMP-9 secretion but no

105 ive for T-cell antigen receptor/CD28- or Akt/phorbol myristate acetate-induced NF-kappa B induction,

106 Phorbol myristate acetate-induced phosphorylation of p22

107 related component of oxidative stress in the phorbol myristate acetate-induced response, we pretreate

108 In the 7,12-dimethyl-benzanthracene plus phorbol myristate acetate-induced skin chemical carcinog

109 sed CD11b expression and augmentation of the phorbol myristate acetate-induced superoxide response.

110 PKC-zeta(mut) to interfere with the basal or phorbol myristate acetate-inducible CREB- or AP1-depende

111 se of intracellular Ca(2+) stores but not on phorbol myristate acetate-insensitive activation of Ca(2

112 After stimulation with phorbol myristate acetate-ionomycin, high gamma interfer

113 on following ex vivo stimulation with either phorbol myristate acetate/ionomycin or the Vdelta2 gamma

114 Exposure of PASMC to phorbol myristate acetate, lipopolysaccharide, tumor nec

115 exposure of microvessels to a PKC activator (phorbol myristate acetate) markedly reduced tracer coupl

116 nsfected with the PKC betaII, hBVR augmented phorbol myristate acetate-mediated c-fos expression, and

117 ch as interleukin-1beta, lipopolysaccharide, phorbol myristate acetate, okadaic acid, hydrogen peroxi

118 so abolished NF-kappaB activation induced by phorbol myristate acetate, okadaic acid, lipopolysacchar

119 ology, although it does block the effects of phorbol myristate acetate on cell morphology.

120 re we show that several neutrophil agonists (phorbol myristate acetate, opsonized zymosan, and N-form

121 n of cytokines by these cells in response to phorbol myristate acetate or anti-CD3-anti-CD28 stimulat

122 of p47(phox) to the membrane in response to phorbol myristate acetate or fMet-Leu-Phe was reduced in

123 from luteinized granulosa cells treated with phorbol myristate acetate or following in vitro activati

124 double mutant T29A/S97A failed to respond to phorbol myristate acetate or GF109203X.

125 d cells we found that treatments (e.g., with phorbol myristate acetate or MnCl2) that increased adhes

126 superoxide production in response to either phorbol myristate acetate or opsonized Candida albicans

127 Artificially activating PKC with phorbol myristate acetate or poisoning the calcium pump

128 (IL-1beta), hyaluronan oligosaccharides, or phorbol myristate acetate or were passaged and subcultur

129 Treatment of eggs with phorbol myristate acetate or with the actin disrupting a

130 induced by the calcium ionophore A23187, by phorbol myristate acetate, or by stimulation of G-protei

131 allenge with the protein kinase C activator, phorbol myristate acetate, or the calcium ionophore, A23

132 ast to CAF, alpha-defensin-1 did not inhibit phorbol myristate acetate- or Tat-mediated HIV-1 LTR act

133 erferon (IFN)-gamma per ml over 3 d and 1 nM phorbol myristate acetate over 24 h resulted in the expr

134 and adenosine antagonist, 10 micromol/L) and phorbol myristate acetate (phorbol ester, 10 micromol/L)

135 agents, including anti-CD3/CD28 antibodies, phorbol myristate acetate/phytohemagglutinin, and prostr

136 on in response to anti-CD3, thapsigargin, or phorbol myristate acetate plus ionomycin, leading to per

137 type 2 cytokine IL-13 in response to IL-2 or phorbol myristate acetate plus ionomycin.

138 mortalized keratinocytes were incubated with phorbol myristate acetate (PMA) (50 ng/ml) for 24 h.

139 beta-agonist and PGE2 also inhibited phorbol myristate acetate (PMA) + calcimycin-stimulated

140 inflammatory cytokines and a combination of phorbol myristate acetate (PMA) + ionomycin.

141 Phorbol myristate acetate (PMA) activated alphaIIbbeta3

142 In intact HL-60 cells, phorbol myristate acetate (PMA) activated PLD as measure

143 ses on an improved biofuel cell operating on phorbol myristate acetate (PMA) activated THP-1 human mo

144 hown that stimulation of T cells via CD28 or phorbol myristate acetate (PMA) activation is highly res

145 Phorbol myristate acetate (PMA) also activated host PLD,

146 Phorbol myristate acetate (PMA) and bacterial lipopolysa

147 human pleural mesothelioma (MS-1) cells with phorbol myristate acetate (PMA) and cycloheximide result

148 tory burst of human PMN stimulated with both phorbol myristate acetate (PMA) and formyl-methionyl-leu

149 anergy and can be overcome by treatment with phorbol myristate acetate (PMA) and ionomycin or by high

150 Signaling induced by phorbol myristate acetate (PMA) and ionomycin was not si

151 tivity can be bypassed by the combination of phorbol myristate acetate (PMA) and ionomycin, suggestin

152 ce of EL4 cells increases with activation by phorbol myristate acetate (PMA) and ionomycin.

153 block platelet aggregation by ristocetin or phorbol myristate acetate (PMA) and only slightly attenu

154 Here we show that phorbol myristate acetate (PMA) and tert-butylhydroquino

155 Topical application of phorbol myristate acetate (PMA) elicits intense local in

156 nce of Ie in human eosinophils stimulated by phorbol myristate acetate (PMA) from room temperature to

157 minin (ECL) attachment matrix or exposure to phorbol myristate acetate (PMA) further enhanced the adh

158 Phorbol myristate acetate (PMA) has long been known as a

159 sine 3', 5'-cyclic monophosphate (cAMP), and phorbol myristate acetate (PMA) in primary rat hepatocyt

160 t T cells were stimulated with anti-CD28 and phorbol myristate acetate (PMA) in the presence of dexam

161 ciated MAPK activity in trans by the mitogen phorbol myristate acetate (PMA) increased viral infectiv

162 n surface expression of alphaMbeta2, whereas phorbol myristate acetate (PMA) induced extensive change

163 The protein kinase C (PKC) agonist phorbol myristate acetate (PMA) induced KDR mRNA express

164 Phorbol myristate acetate (PMA) is a potent agonist for

165 ble tie-1 receptor from endothelial cells by phorbol myristate acetate (PMA) is mediated through prot

166 eatment of endothelial cells in culture with phorbol myristate acetate (PMA) led to upregulation of P

167 ne interaction using bisfunctional (dimeric) phorbol myristate acetate (PMA) molecules.

168 14 cell surface expression; however, neither phorbol myristate acetate (PMA) or A23187 increased rece

169 K cells produce large amounts of CXCL8 after phorbol myristate acetate (PMA) or cytokine treatment.

170 for sensitization of HUVEC to Shiga toxin by phorbol myristate acetate (PMA) or LPS but not by TNF or

171 ressing rPLD1-V5, PLD activity stimulated by phorbol myristate acetate (PMA) or lysophosphatidic acid

172 to ionomycin treatment, exposure of cells to phorbol myristate acetate (PMA) plus anti-CD28 did not i

173 tremely sensitive to T-cell activation, with phorbol myristate acetate (PMA) plus ionomycin increasin

174 th concanavalin A, lipopolysaccharide (LPS), phorbol myristate acetate (PMA) plus ionomycin, or purif

175 Treatment with phorbol myristate acetate (PMA) resulted in approximatel

176 udied in the perforated-patch configuration, phorbol myristate acetate (PMA) stimulation elicited NAD

177 -linking, phytohemagglutinin stimulation, or phorbol myristate acetate (PMA) stimulation of periphera

178 in vitro with either IL-1beta, TNFalpha, or phorbol myristate acetate (PMA) to assess their potentia

179 FLNB K1147 to interfere with the ability of phorbol myristate acetate (PMA) to promote FLNB-mediated

180 rventions: Lung injury was induced by adding phorbol myristate acetate (PMA) to the blood perfusing t

181 Phorbol myristate acetate (PMA) treatment of U937 human

182 sitized cells to apoptosis, especially after phorbol myristate acetate (PMA) treatment to induce diff

183 l-derived wild-type blood vessels exposed to phorbol myristate acetate (PMA) underwent extensive aber

184 Treatment of B95-8CR with phorbol myristate acetate (PMA) was able to bypass the I

185 tory burst assays following stimulation with phorbol myristate acetate (PMA) was detected in neutroph

186 yers stimulated by interleukin (IL)-1beta or phorbol myristate acetate (PMA) were assayed for the nuc

187 gocytes possessing many of the activities of phorbol myristate acetate (PMA) with notable functional

188 re exposed within the microfluidic device to phorbol myristate acetate (PMA), a known promoter of oxi

189 In contrast, treatment with phorbol myristate acetate (PMA), a protein kinase C acti

190 tumor necrosis factor alpha (TNF-alpha) and phorbol myristate acetate (PMA), an epithelial cell acti

191 kat cells activated their JNK in response to phorbol myristate acetate (PMA), and the response of the

192 in vivo was stimulated by the PKC activator phorbol myristate acetate (PMA), and this process could

193 ctivity in Jurkat T cells in the presence of phorbol myristate acetate (PMA), but activated Rho (V14R

194 se values were modulated by stimulation with phorbol myristate acetate (PMA), but not interleukin-8 (

195 yl-methionyl-leucyl-phenylalanine (FMLP), or phorbol myristate acetate (PMA), caused increased releas

196 release by neutrophils upon stimulation with phorbol myristate acetate (PMA), formylmethionyl-leucyl-

197 luated in cultures of THP-1 cells exposed to phorbol myristate acetate (PMA), M. fermentans incognitu

198 erol analogue 1,2-dioctanoyl-sn-glycerol and phorbol myristate acetate (PMA), mimicked the effect of

199 When stimulated with phorbol myristate acetate (PMA), neutrophils generated s

200 vity required the protein kinase C activator phorbol myristate acetate (PMA), Nox3 activity was alrea

201 stimuli that do (A23187, zymosan) or do not (phorbol myristate acetate (PMA), okadaic acid) mobilize

202 verse agonists including calcium ionophores, phorbol myristate acetate (PMA), okadaic acid, and the p

203 not block neuregulin release in response to phorbol myristate acetate (PMA), suggesting that other p

204 nse to agents such as cytochalasin B (CB) or phorbol myristate acetate (PMA), which are strong stimul

205 When cells were treated with phorbol myristate acetate (PMA), which down-modulates a

206 levels did not change following exposure to phorbol myristate acetate (PMA), which induces FV replic

207 Interestingly, purified PlcHR decreased phorbol myristate acetate (PMA)- but not formyl methiony

208 oplasmic tails of various length also showed phorbol myristate acetate (PMA)-dependent phosphorylatio

209 ts, rat basophilic leukemia (RBL) cells, and phorbol myristate acetate (PMA)-differentiated HL-60 mye

210 We studied the undifferentiated and phorbol myristate acetate (PMA)-differentiated human mon

211 veolar macrophages were analyzed ex vivo for phorbol myristate acetate (PMA)-driven superoxide releas

212 GF-induced activation but enables a vigorous phorbol myristate acetate (PMA)-induced activation.

213 to 80% of that of human neutrophils, and of phorbol myristate acetate (PMA)-induced activity up to 2

214 hat NMDA receptor activity was necessary for phorbol myristate acetate (PMA)-induced differentiation

215 Phorbol myristate acetate (PMA)-induced differentiation

216 se and time dependently downregulated during phorbol myristate acetate (PMA)-induced monocyte-to-macr

217 Phorbol myristate acetate (PMA)-induced translocation of

218 us was sufficient for converting Nox4 into a phorbol myristate acetate (PMA)-inducible phenotype, whi

219 Here, using a novel, highly phorbol myristate acetate (PMA)-responsive variant of th

220 Sources for O2-. and H2O2 included phorbol myristate acetate (PMA)-stimulated neutrophils a

221 necrosis, phagocytosis, and spontaneous and phorbol myristate acetate (PMA)-stimulated production of

222 In phorbol myristate acetate (PMA)-treated Jurkat T cells,

223 it an increased sensitivity to inhibition by phorbol myristate acetate (PMA).

224 an eosinophils and neutrophils stimulated by phorbol myristate acetate (PMA).

225 tients and controls and then stimulated with phorbol myristate acetate (PMA).

226 silon) PKC isozymes that can be activated by phorbol myristate acetate (PMA).

227 t was after unphysiological stimulation with phorbol myristate acetate (PMA).

228 cells was also stimulated with forskolin and phorbol myristate acetate (PMA).

229 be induced to interact with fibrinogen using phorbol myristate acetate (PMA).

230 glycerol analogue DiC8 or the phorbol ester, phorbol myristate acetate (PMA).

231 ctor (PDGF) and the protein kinase C agonist phorbol myristate acetate (PMA).

232 not suppress oxidative burst in response to phorbol myristate acetate (PMA).

233 ed by a combination of human neutrophils and phorbol myristate acetate (PMA).

234 oxidative burst when elicited in vitro with phorbol myristate acetate (PMA).

235 riety of NADPH oxidase activators, including phorbol myristate acetate (PMA).

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

237 myl-methionyl-leucyl-phenylalanine (FMLP) or phorbol myristate acetate (PMA).

238 Using phorbol myristate acetate (PMA)/ionomycin and anti-CD3 a

239 sence or presence of concanavalin A (Con A), phorbol myristate acetate (PMA)/ionomycin, or anti-CD3/a

240 tored to normal levels by restimulation with phorbol myristate acetate (PMA)/ionomycin.

241 y via protein kinase C (PKC), the effects of phorbol myristate acetate (PMA, 10 nM for 24 h) and aden

242 ell lines following a 24-hour treatment with phorbol myristate acetate (PMA, 10(-8) mol/L) or tumor n

243 Rho, nor was upregulation of adhesion using phorbol myristate acetate (PMA; 10 ng/ml) or Mn++ (1 mM)

244 Phorbol myristate acetate (PMA; 200 nM) enhanced secreti

245 only used animal model of acute lung injury, phorbol-myristate acetate (PMA), to see if it would atte

246 ivators (IgE-activated mast cell supernates, phorbol myristate acetate [PMA; to activate TACE], TNFal

247 PKC activation by phorbol ester (phorbol myristate acetate [PMA]) reduced insulin-induced

248 after stimulation by either a phorbol ester (phorbol myristate acetate [PMA]), a potent protein kinas

249 expression is up-regulated in phorbol ester (phorbol myristate acetate, PMA)-differentiated human U93

250 Treatment of LGI1-expressing cells with phorbol myristate acetate prevents the inhibition of MMP

251 ia intracellular Ca(2+) rise using ionomycin/phorbol myristate acetate promoted survival in the absen

252 Differentiation of the cells induced by phorbol myristate acetate resulted in a 75% reduction of

253 Exposure to phorbol myristate acetate resulted in an increase in VZV

254 Although treatment with the phorbol myristate acetate resulted in ERK activation and

255 s induced to differentiate by treatment with phorbol myristate acetate revealed three major proteins

256 n was dependent on intracellular calcium and phorbol myristate acetate-sensitive protein kinase Cs.

257 t 9-cis retinoic acid-induced apoptosis, but phorbol myristate acetate significantly decreased the ap

258 The PKC activator phorbol myristate acetate significantly increased vascul

259 d by either epidermal growth factor (EGF) or phorbol myristate acetate specifically phosphorylates Se

260 ttractant fMet-Leu-Phe and the phorbol ester phorbol myristate acetate stimulate formation of Rac-GTP

261 e demonstration that 2-BrHDA was produced by phorbol myristate acetate-stimulated eosinophils and by

262 the preparation of granule lysate and during phorbol myristate acetate-stimulated granule secretion f

263 nd LDL plasmalogen pools was demonstrated in phorbol myristate acetate-stimulated human monocytes, re

264 oneal neutrophils exhibited an inhibition of phorbol myristate acetate-stimulated hydrogen peroxide g

265 -chloro fatty aldehydes were not produced in phorbol myristate acetate-stimulated mouse monocytes.

266 can detect H2O2 release from as few as 2000 phorbol myristate acetate-stimulated neutrophils with a

267 ected by flow cytometry in 12.3% +/- 0.9% of phorbol myristate acetate-stimulated peripheral blood ne

268 ived cells displayed significantly increased phorbol myristate acetate-stimulated release of superoxi

269 Assays using phorbol myristate acetate-stimulated transfected B lymph

270 nse of phosphatidic acid (PA), decreased the phorbol myristate acetate-stimulated Tyr phosphorylation

271 Phorbol myristate acetate stimulates neutrophils to disc

272 In contrast, activating macrophages with phorbol-myristate-acetate stimulates degradation of aggr

273 In addition, phorbol myristate acetate stimulation of the NADPH oxida

274 Furthermore, phorbol myristate acetate stimulation of the NADPH oxida

275 rated a decreased aggregation potential upon phorbol myristate acetate stimulation, decreased platele

276 After antigen-receptor ligation or phorbol myristate acetate stimulation, FcmuR expression

277 Using protease inhibitors, ionomycin and phorbol myristate acetate stimulation, small interfering

278 llowing tumor necrosis factor (TNF)-alpha or phorbol myristate acetate stimulation.

279 he tyrosine phosphorylation of paxillin upon phorbol myristate acetate stimulation.

280 P-3 was induced; however, in the presence of phorbol myristate acetate, strain augmented MMP-1 expres

281 ression of MIF in eosinophils in response to phorbol myristate acetate suggest the participation of M

282 After cells were stimulated with phorbol myristate acetate, the amount of phosphorylated

283 in untransfected cells, upon treatment with phorbol myristate acetate, the PKC translocated to the p

284 ATGAM synergized with phorbol myristate acetate to produce strong proliferatio

285 es of collagenase messenger RNA in IL-1- and phorbol myristate acetate-treated fibroblasts.

286 However, phorbol myristate acetate treatment alone induced LAK pp

287 e, RhoH is dramatically down regulated after phorbol myristate acetate treatment and in Th1 cells aft

288 r, after ex vivo CD8(+) T cell depletion and phorbol myristate acetate treatment, FIV could be reacti

289 The oncogene v-reland phorbol myristate acetate, two known inhibitors of bursa

290 Accordingly, the PKC activator phorbol myristate acetate up-regulated LAT expression.

291 To create inflammatory ECs, phorbol myristate acetate was added 4.5 h before perfusi

292 nhibit the neutrophil respiratory burst when phorbol myristate acetate was added.

293 of TNFRSF1A in response to stimulation with phorbol myristate acetate was assessed in leukocytes and

294 Electron current stimulated by PMA (phorbol myristate acetate) was recorded in both perforat

295 ed by formylmethionyl-leucylphenylalanine or phorbol myristate acetate were not affected by PKA inhib

296 of megakaryocytes and their progenitors, and phorbol myristate acetate, which causes differentiation

297 R from other proteins, or by incubation with phorbol myristate acetate, which is known to decrease th

298 n early oxidative burst when stimulated with phorbol myristate acetate, which was fully abrogated by

299 tion of monoclonal anti-Edg-4 R antibody and phorbol myristate acetate, which were inactive separatel

300 /=250 microm) inhibit p70(s6k) activation by phorbol myristate acetate, while higher salicylate conce