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 d repression of AP1LUC reporter induction by phorbol myristate acetate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

22 -dimethyl benzanthracene when applied before phorbol myristate acetate.

23 IL-1alpha, tumor necrosis factor-alpha, and phorbol myristate acetate.

24 investigated by treating blood samples with phorbol myristate acetate.

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

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

27 ERK2 phosphorylation induced by exposure to phorbol myristate acetate.

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

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

30 37 cells were induced to differentiate using phorbol myristate acetate (100 nM for 48 h) and then wer

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

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

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

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

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

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

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

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

39 Forskolin and phorbol myristate acetate acted synergistically to enhan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 However, in response to phorbol myristate acetate and ionomycin, duodenal LPLs f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 Phorbol myristate acetate enhanced fibroblast minocyclin

87 Moreover, phorbol myristate acetate enhanced Nedd4-2 phosphorylati

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

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

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

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

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

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

94 TLC and phorbol myristate acetate increased cytosolic pMARCKS an

95 Both high Pi and phorbol myristate acetate increased the phosphorylation

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

97 Phorbol myristate acetate induced a dramatic increase of

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

99 Phorbol myristate acetate induced TTF1 protein degradati

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

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

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

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

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

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

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

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

108 Phorbol myristate acetate-induced phosphorylation of p22

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

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

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

112 Phorbol-myristate-acetate-induced formation of neutrophi

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

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

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

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

117 Following ex vivo stimulation with phorbol myristate acetate/ionomycin, PSC patients showed

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

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

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

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

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

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

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

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

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

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

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

129 he cutaneous inflammation induced by topical phorbol myristate acetate or imiquimod, reduced the infl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 Phorbol myristate acetate (PMA) activated alphaIIbbeta3

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

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

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

150 Phorbol myristate acetate (PMA) and bacterial lipopolysa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 14 cell surface expression; however, neither phorbol myristate acetate (PMA) or A23187 increased rece

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

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

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

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

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

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

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

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

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

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

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

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

185 Phorbol myristate acetate (PMA) treatment of U937 human

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

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

188 kappaB2, while activation of NF-kappaB2 with phorbol myristate acetate (PMA) upregulated fermentative

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 Phorbol myristate acetate (PMA)-induced differentiation

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

221 Phorbol myristate acetate (PMA)-induced translocation of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 m neutrophil extracellular traps (NETs) with phorbol myristate acetate released high concentrations o

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

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

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

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

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

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

261 The PKC activator phorbol myristate acetate significantly increased vascul

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

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

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

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

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

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

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

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

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

271 Assays using phorbol myristate acetate-stimulated transfected B lymph

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

273 Phorbol myristate acetate stimulates neutrophils to disc

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

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

276 Furthermore, phorbol myristate acetate stimulation of the NADPH oxida

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

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

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

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

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

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

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

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

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

286 ATGAM synergized with phorbol myristate acetate to produce strong proliferatio

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