ライフサイエンスコーパス: phorbol

1 that PMA, but not its inactive analog 4alpha-phorbol 12, 13-didecanoate (4alpha-PDD), caused phosphor

2 nd that extracellular activation of PKC with phorbol 12,13-diacetate induced a pharmacological potent

3 A phorbol ester phorbol 12,13-dibutyrate (PDBu) (a diacylglycerol analog

4 We also show that PKC activation with phorbol 12,13-dibutyrate (PDBu) causes a 4-fold slowing

5 By activating PKC with the phorbol ester phorbol 12,13-dibutyrate (PDBu) or a natural stimulant,

6 In addition, the PKC activator phorbol 12,13-dibutyrate (PDBu), a PKC catalytic subunit

7 pidermal growth factor (ErbB1 activation) or phorbol 12,13-dibutyrate (PKC activation).

8 quirement for anionic phospholipid for [(3)H]phorbol 12,13-dibutyrate binding was determined; it decr

9 10R/L20R) compared to the wild-type, whereas phorbol 12,13-dibutyrate showed a 6000-fold loss of affi

10 rolonged treatment of native thymocytes with phorbol 12,13-dibutyrate together with the calcium ionop

11 ing affinity (Kd = 2890 +/- 240 nm for [(3)H]phorbol 12,13-dibutyrate.

12 potonicity and heat but responsive to 4alpha-phorbol 12,13-didecanoate, an agonist that binds directl

13 1 pre-monocyte macrophages (MDM) obtained by phorbol 12-myristate 13 acetate (PMA) treatment.

14 essin (100 and 500 pm) and the PKC activator phorbol 12-myristate 13-acetate (1 nm) each inhibited hu

15 lowing UVB or 7,12-dimethylbenz(a)anthracene/phorbol 12-myristate 13-acetate (DMBA/PMA) treatment dev

16 protein kinase Cepsilon (PKCepsilon), while phorbol 12-myristate 13-acetate (PMA) activation of PKCe

17 nd produced IFN-gamma ex vivo in response to phorbol 12-myristate 13-acetate (PMA) and ionomycin stim

18 L-22 suppression, PP cells were treated with phorbol 12-myristate 13-acetate (PMA) and ionomycin, whi

19 d prevents activated platelet supernatant or phorbol 12-myristate 13-acetate (PMA) from inducing NETo

20 In this model, we show that phorbol 12-myristate 13-acetate (PMA) immediately activa

21 We show that treatment with a combination of phorbol 12-myristate 13-acetate (PMA) plus ionophore A23

22 ith HIV (JLat cells) were more responsive to phorbol 12-myristate 13-acetate (PMA) reactivation in th

23 The PKC activator phorbol 12-myristate 13-acetate (PMA) stimulated apoE se

24 lastase (NE) release following activation by phorbol 12-myristate 13-acetate (PMA) than cells isolate

25 studies with pharmacological agonists (e.g. phorbol 12-myristate 13-acetate (PMA)) indicate that pro

26 In the current work we used phorbol 12-myristate 13-acetate (PMA), a well recognized

27 cells were stimulated with thrombopoietin or phorbol 12-myristate 13-acetate (PMA), alphaIIbbeta3 bec

28 nduced by stimulation with the phorbol ester phorbol 12-myristate 13-acetate (PMA), but not by ionomy

29 nts or the protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate (PMA), in primary HUVECs

30 ion with adenosine-5'-triphosphate (ATP) and phorbol 12-myristate 13-acetate (PMA), results in a cati

31 ith p38 kinase inducer, hydrogen peroxide or phorbol 12-myristate 13-acetate (PMA), U6 promoter activ

32 tubes were treated with the PKC/D1 activator phorbol 12-myristate 13-acetate (PMA), which acts as a D

33 ibition of NF-kappaB reversed both H2O2- and phorbol 12-myristate 13-acetate (PMA)-induced decrease i

34 Here we studied the role of PK in phorbol 12-myristate 13-acetate (PMA)-induced megakaryoc

35 Ankrd1 deletion enhanced both basal and phorbol 12-myristate 13-acetate (PMA)-induced MMP13 prom

36 Both basal and phorbol 12-myristate 13-acetate (PMA)-induced NADPH oxid

37 nsfer (BRET), we detected a constitutive and phorbol 12-myristate 13-acetate (PMA)-induced ubiquitina

38 leukocyte protease profiles under naive and phorbol 12-myristate 13-acetate (PMA)-stimulated conditi

39 n PC1(lo) cells when stimulated with LPS and phorbol 12-myristate 13-acetate (PMA).

40 ator of conventional and novel PKC isoforms, phorbol 12-myristate 13-acetate (PMA).

41 ) was combined with human PMN induced with 4-phorbol 12-myristate 13-acetate (PMA).

42 inhibitor, TAPI-1, while it was promoted by phorbol 12-myristate 13-acetate (PMA).

43 ct on proinflammatory cytokine production of phorbol 12-myristate 13-acetate (PMA)/ionomycin-stimulat

44 the expression of K-Rta or by treatment with phorbol 12-myristate 13-acetate (TPA) and/or n-butyrate.

45 a by TCR-independent polyclonal stimulation (phorbol 12-myristate 13-acetate [PMA] plus ionomycin).

46 Phorbol 12-myristate 13-acetate and ionomycin stimulated

47 this effect is only detected following cell phorbol 12-myristate 13-acetate and ionomycin stimulatio

48 ficantly reduced NK- and T-cell responses to phorbol 12-myristate 13-acetate and ionomycin.

49 on of MEK and ERK following stimulation with phorbol 12-myristate 13-acetate and ionomycin.

50 , T-plastin-negative PBLs were stimulated by phorbol 12-myristate 13-acetate and ionomycin.

51 Isoproterenol also blocked ERK downstream of phorbol 12-myristate 13-acetate and the P2X(7) and epide

52 Similar results were obtained with phorbol 12-myristate 13-acetate as well as activation of

53 y several microorganism membrane components, phorbol 12-myristate 13-acetate as well as by amyloid fi

54 Epidermal growth factor or the phorbol ester phorbol 12-myristate 13-acetate caused rapid phosphoryla

55 tion of T cells with concanavalin A, but not phorbol 12-myristate 13-acetate combined with ionomycin,

56 hat treatment with the inflammatory stimulus phorbol 12-myristate 13-acetate downregulates meprin alp

57 ro and membrane translocation in response to phorbol 12-myristate 13-acetate in LNCaP cells.

58 Phorbol 12-myristate 13-acetate increased intracellular

59 or rottlerin treatment versus activation by phorbol 12-myristate 13-acetate indicated that 2B15 unde

60 the activity of ADAM17, activated by either phorbol 12-myristate 13-acetate or EGF.

61 Treatment of BMT or HSCT neutrophils with phorbol 12-myristate 13-acetate or rapamycin resulted in

62 ILC2s were then stimulated with phorbol 12-myristate 13-acetate plus ionomycin, IL-25 pl

63 reover, ILC2s expressed CD154 in response to phorbol 12-myristate 13-acetate plus ionomycin, IL-25/IL

64 ied a subset of CD8(+) T cells refractory to phorbol 12-myristate 13-acetate plus ionomycin-induced E

65 MB-231 and MDA-MB-435, upon stimulation with phorbol 12-myristate 13-acetate plus ionomycin.

66 ressing PKCdelta followed by incubation with phorbol 12-myristate 13-acetate resulted in an increase

67 We found that acute activation of PKC with phorbol 12-myristate 13-acetate shortened carbachol-evok

68 ound that activation of the PKC pathway with phorbol 12-myristate 13-acetate significantly increased

69 Phorbol 12-myristate 13-acetate stimulation of both cell

70 way in lymphocytes after antigen receptor or phorbol 12-myristate 13-acetate stimulation, whereas CD4

71 pidly phosphorylated at Ser31 in response to phorbol 12-myristate 13-acetate stimulation.

72 that addition of the NADPH oxidase activator phorbol 12-myristate 13-acetate to nitric oxide-producin

73 and insulinoma cells, either with or without phorbol 12-myristate 13-acetate treatment.

74 cation of PKCdelta to the plasma membrane by phorbol 12-myristate 13-acetate was enhanced in p23-depl

75 S) in response to angiotensin II (Ang II) or phorbol 12-myristate 13-acetate was markedly reduced in

76 th platelet activating factor, ionomycin, or phorbol 12-myristate 13-acetate was significantly enhanc

77 The increases by strain, PGE2, Wnt-3a, and phorbol 12-myristate 13-acetate were attenuated by inhib

78 increased relative basal and phorbol ester (phorbol 12-myristate 13-acetate)-induced PKC activity bu

79 ERK1/2 are also activated in most cells by phorbol 12-myristate 13-acetate, a classical inhibitor o

80 phosphorylation at Ser(430) is stimulated by phorbol 12-myristate 13-acetate, an activator of classic

81 chemical activators of shedding (ionomycin, phorbol 12-myristate 13-acetate, and 4-aminophenylmercur

82 The pharmacologic inhibitors chlorpromazine, phorbol 12-myristate 13-acetate, and cytochalasin D caus

83 nteractions among carbachol, PKC inhibitors, phorbol 12-myristate 13-acetate, and thapsigargin to mod

84 on by serotonin showed a similar response to phorbol 12-myristate 13-acetate, implicating a potential

85 Exogenously added diacylglycerol or phorbol 12-myristate 13-acetate, known activators of PKC

86 hibited NF-kappaB activation induced by TNF, phorbol 12-myristate 13-acetate, lipopolysaccharide, and

87 by N-formyl-methionyl-leucyl-phenylalanine, phorbol 12-myristate 13-acetate, or grass pollen allerge

88 low-density lipoprotein, 7-ketocholesterol, phorbol 12-myristate 13-acetate, or macrophage colony-st

89 eceptor mimetic carbachol, the phorbol ester phorbol 12-myristate 13-acetate, the Ca(2+) ionophore io

90 ent of pancreatoids with (-)-Indolactam-V or phorbol 12-myristate 13-acetate, two protein kinase C ac

91 s most effective in preventing constitutive, phorbol 12-myristate 13-acetate-, and ionomycin-stimulat

92 t of Vpr on monocyte-derived macrophages and phorbol 12-myristate 13-acetate-activated THP1 macrophag

93 )-induced PKC activity but were defective in phorbol 12-myristate 13-acetate-induced actin cytoskelet

94 ed proliferation, and provided resistance to phorbol 12-myristate 13-acetate-induced apoptosis in LNC

95 ved GC synthesis protected skin from topical phorbol 12-myristate 13-acetate-induced inflammatory ass

96 cked by PKC inhibitors, unlike carbachol- or phorbol 12-myristate 13-acetate-initiated phosphorylatio

97 Only SFHFKSGSL, in PKCdelta-transfected phorbol 12-myristate 13-acetate-stimulated cells, caused

98 signal of O2[Symbol: see text] generated by phorbol 12-myristate 13-acetate-stimulated neutrophils.

99 the L-selectin tail with cell extracts from phorbol 12-myristate 13-acetate-stimulated Raw 264.7 mac

100 MMP-9 transcription was decreased in phorbol 12-myristate 13-acetate-stimulated THP-1 macroph

101 kines IL-1beta and TNF-alpha were reduced in phorbol 12-myristate 13-acetate-treated MCs developed fr

102 arget genes, c-fos and egr-1, in response to phorbol 12-myristate 13-acetate.

103 N-formyl-methionyl-leucyl-phenylalanine, or phorbol 12-myristate 13-acetate.

104 KCdelta downstream effectors ROCK and JNK by phorbol 12-myristate 13-acetate.

105 twice weekly application of proinflammatory phorbol 12-myristate 13-acetate.

106 r cells were cultured unstimulated (U), with phorbol 12-myristate 13-acetate/ionomycin (PI) or lipopo

107 tokine production upon stimulation with both phorbol 12-myristate 13-acetate/ionomycin and CMV-peptid

108 but also accelerated T cell activation under phorbol 12-myristate 13-acetate/ionomycin treatment cond

109 l activation through CD3/CD28 stimulation or phorbol 12-myristate 13-acetate/ionomycin treatment enha

110 ic knockdown of GIMAP6 led to enhancement of phorbol 12-myristate 13-acetate/ionomycin-mediated activ

111 CPIP1 by MG132 abrogated HIV-1 production in phorbol 12-myristate 13-acetate/ionomycin-stimulated hum

112 lls were cultured overnight with and without phorbol 12-myristate 13-acetate/ionomycin.

113 and conversely, direct activation of PKC by phorbol 12-myristate,13-acetate potentiated GluK2/GluK5.

114 on of receptor G-protein coupling induced by phorbol 12-myristate.

115 ures after stimulation with a phorbol ester, phorbol-12,13-dibutyrate (PDBu).

116 The PKC activator phorbol-12,13-dibutyrate mimicked the effect of ethanol,

117 During phorbol-12-myristate 13-acetate-induced differentiation

118 iR-21 are induced by common stimuli, such as phorbol-12-myristate-13-acetate (PMA) and androgens, but

119 directly on-chip and free radical release by phorbol-12-myristate-13-acetate (PMA) stimulation was de

120 isolated human monocytes pre-activated with phorbol-12-myristate-13-acetate (PMA) were added back in

121 or without UDCA and further activated using phorbol-12-myristate-13-acetate (PMA).

122 The stimulation of tissue with phorbol-12-myristate-13-acetate and ionomycin, recapitul

123 , or the PKCalpha-activator and TJ-disruptor phorbol-12-myristate-13-acetate, similarly reduced TJ in

124 -transformed B-cell lines partially restored phorbol-12-myristate-13-acetate-induced cell death.

125 Phorbol-12-myristate-13-acetate/ionomycin-induced MAPK s

126 by repeated treatments of 12-O-tetradecanoyl phorbol 13-acetate (TPA).

127 with the chemical inducer 12-O-tetradecanoyl-phorbol-13-acetate (TPA) led to much greater activation

128 kdown of BLIMP1 inhibited 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced lytic reactivation in N

129 uced by the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA).

130 12-dimethylbenzanthracene/12-O-tetradecanoyl-phorbol-13-acetate induction.

131 dimethylbenz[a]anthracene/12-O-tetradecanoyl-phorbol-13-acetate resulted in delayed and reduced papil

132 skin and after short-term 12-O-tetradecanoyl-phorbol-13-acetate treatment and acute UVB exposure.

133 marked resistance to TPA (12-O-tetradecanoyl-phorbol-13-acetate)-induced keratinocyte proliferation,

134 12-dimethylbenzanthracene/12-O-tetradecanoyl-phorbol-13-acetate-induced tumors from Er/+ skin.

135 osis factor alpha (TNF-alpha), tetradecanoyl phorbol acetate (TPA), and trichostatin A (TSA), in U1 m

136 in Raji cells, in response to tetradecanoyl phorbol acetate (TPA), was also inhibited by VPA.

137 Tetradecanoyl phorbol acetate (TPA)-induced CD44 cleavage requires dep

138 fection and after spontaneous, tetradecanoyl phorbol acetate-, or open reading frame 50 (ORF50)/repli

139 Access to useful quantities of phorbol and related analogues has relied on isolation fr

140 We solved the structure of the phorbol-binding domain (C1B) of PKCdelta complexed with

141 molecule in a surface pocket adjacent to the phorbol-binding site, making van der Waals contacts with

142 rous skin condition (actinic keratosis), and phorbol derivatives such as resiniferatoxin and prostrat

143 Cleavage was stimulated by phorbol ester (12-O-tetradecanoylphorbol-13-acetate (TPA

144 n with vasoactive intestinal peptide (V) and phorbol ester (P) synergistically activated viral infect

145 lasts displayed increased relative basal and phorbol ester (phorbol 12-myristate 13-acetate)-induced

146 PKC activation by phorbol ester (phorbol myristate acetate [PMA]) reduced

147 ciates upon activation of gene expression by phorbol ester (PMA).

148 sing ex vivo retinal explants, we found that phorbol ester 12-myristate 13-acetate and insulin-like g

149 surface localization of GLUT1 induced by the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA

150 -)/Tg.AC mice exposed to the proinflammatory phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA)

151 on that is reversed with the addition of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA,

152 o extracellular stimuli (serum, EGF, and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate) that

153 Forced depletion of Cx43, by tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate, is a

154 otein kinase C activity, whose activation by phorbol ester also promoted ERRalpha protein loss.

155 PKCdelta upon stimulation by ligands of the phorbol ester and bryostatin classes.

156 e depressed in mice in vivo and in humans to phorbol ester and calcium ionophore stimulation in vitro

157 tained oxidative burst upon stimulation with phorbol ester and fMLP, Gsr-deficient neutrophils displa

158 Cells were stimulated with phorbol ester and ionomycin in the presence of brefeldin

159 a and endotoxin) or tumor promoters (such as phorbol ester and okadaic acid), 3-FC suppressed NF-kapp

160 Phorbol ester and RTA transgene induction were used to i

161 We show that stolonidiol binds to the phorbol ester binding site of protein kinase C (PKC), in

162 th the mutated C1 domains also showed strong phorbol ester binding, albeit modestly weaker than that

163 ta C1b (deltaC1b) conferred high potency for phorbol ester binding.

164 l-length RasGRP2 with the mutated C1 domain, phorbol ester enhanced the ability of the mutated RasGRP

165 that the activation of viral replication by phorbol ester in latently infected monocytic cells requi

166 IGF-1 and phorbol ester increased hBVR/PKCdelta binding; hBVR was

167 Angiotensin II and phorbol ester increased superoxide/H2O2 generation in PM

168 In addition, PKC activation by phorbol ester induced agonist-independent KOPR phosphory

169 ressing the IL-1 family member, IL-1F6, with phorbol ester leads to an inflammatory condition with ma

170 We show here that phorbol ester or angiotensin II-induced proteolytic rele

171 out 30%), but increases after application of phorbol ester or during PTP.

172 Treatment of cells with phorbol ester or histone deacetylase inhibitors triggere

173 a release upon pro-inflammatory priming with phorbol ester or Toll-like receptor stimulation.

174 A phorbol ester phorbol 12,13-dibutyrate (PDBu) (a diacylg

175 By activating PKC with the phorbol ester phorbol 12,13-dibutyrate (PDBu) or a natur

176 f IL-23R was induced by stimulation with the phorbol ester phorbol 12-myristate 13-acetate (PMA), but

177 Epidermal growth factor or the phorbol ester phorbol 12-myristate 13-acetate caused rap

178 d muscarinic receptor mimetic carbachol, the phorbol ester phorbol 12-myristate 13-acetate, the Ca(2+

179 l receptor (TCR) cross-linking antibodies or phorbol ester plus ionomycin.

180 activation of protein kinase C (PKC) by the phorbol ester PMA has been shown to down-regulate cell s

181 al transactivator region is inducible by the phorbol ester PMA, a potent activator of the protein kin

182 In contrast, the PKC-activating phorbol ester PMA, often used as a strong inducer of ADA

183 ucleotide exchange factor and diacylglycerol/phorbol ester receptor expressed in mast cells (MCs) and

184 rsistent activation of PKC family members by phorbol ester stimulation in cells leads to phosphorylat

185 We show that complexinI/II deficiency or phorbol ester stimulation indeed affects responses to hy

186 ancer cells undergo apoptosis in response to phorbol ester stimulation via PKCdelta-mediated release

187 orm in controlling the induction of genes by phorbol ester stimulation, whereas PKCepsilon predominan

188 in cells growing in serum or in response to phorbol ester stimulation.

189 Consistent with the ability of phorbol ester to induce translocation of the full-length

190 nd impaired stratum corneum thickening after phorbol ester treatment.

191 lastic and inflammatory responses to topical phorbol ester were significantly suppressed, suggesting

192 y, spermatozoa exposed to calcium ionophore, phorbol ester, or H(2)O(2) exhibited superoxide anion pr

193 ome-like structures after stimulation with a phorbol ester, phorbol-12,13-dibutyrate (PDBu).

194 ort induced by unprocessed PKCs activated by phorbol ester, PKCalpha-CT directly drives HDAC cytosoli

195 Activating PKC with the phorbol ester, PMA, enhanced Ca(2+) entry, and potentiat

196 Upon cell stimulation with phorbol ester, the NF-kappaB soluble complex exchanges F

197 Phorbol ester- and TNF-alpha-dependent activation of the

198 e gene encoding Munc13-2, which has calcium-/phorbol ester-binding domains and controls presynaptic f

199 on of a melanocyte-lineage signature, drives phorbol ester-independent growth in vitro, and promotes

200 sphorylation sites (S396A, S402A) were used, phorbol ester-induced desensitization of the calcium res

201 orter degradation fragments and to increased phorbol ester-induced down-regulation, further supportin

202 urnover is further slowed in the presence of phorbol ester-induced ERK activation, resulting in Mcl-1

203 a unique and critical role in wound healing, phorbol ester-induced hyperplasia, and tumor development

204 Phorbol ester-induced sequential phosphorylation of both

205 Mouse CD163 resisted endotoxin- and phorbol ester-induced shedding, and ex vivo analysis of

206 ponse, however, does not distinguish between phorbol ester-like and bryostatin-like behavior.

207 eration and cell attachment assays displayed phorbol ester-like and/or toxic behavior, including WN-8

208 infection of fibroblast cells and following phorbol ester-mediated reactivation from a latently infe

209 array using RNAi depletion of diacylglycerol/phorbol ester-regulated PKCs.

210 Cepsilon (PKCepsilon), a diacyglycerol- and phorbol ester-responsive serine-threonine kinase, has be

211 ping yet distinct from clusters based on the phorbol ester-stimulated B cell reactivation time course

212 during de novo fibroblast infection and upon phorbol ester-stimulated B cell reactivation, highlighti

213 ase activities were successfully detected in phorbol ester-stimulated neutrophils and eosinophils usi

214 CAT-1 ubiquitination and endocytosis in phorbol ester-stimulated porcine aorthic endothelial and

215 nts, only the C1B domain is required for the phorbol ester-stimulated translocation of PKCdelta to ot

216 cell rounding and/or decreased apoptosis in phorbol ester-treated LNCaP, LNCaP-C4-2, and MAT-LyLu pr

217 mbrane-sensing role of the C2 domain, causes phorbol ester-triggered redistribution of PKCalpha to ot

218 arkers and was not slowed in the presence of phorbol ester.

219 RI or combination of Ca (2)(+) ionophore and phorbol ester.

220 matory lesions after topical applications of phorbol ester.

221 , and displayed translocation in response to phorbol ester.

222 ab downregulates cell-surface CD33 by 80% in phorbol-ester differentiated U937 cells, at concentratio

223 Cyclopropylmethanol inhibited phorbol-ester-induced PKCdelta activity, but failed to d

224 s independent of Src and can be triggered by phorbol esters and 2) agonist-stimulated activation in t

225 PKC isozymes and responsible for binding of phorbol esters and diacylglycerol, interact with the Gol

226 Phorbol esters and Group I metabotropic glutamate recept

227 otection was enhanced by PKD activation with phorbol esters and limited by PKD inhibition with CID756

228 ometry of ~50% and was strongly increased by phorbol esters and protein phosphatase inhibitors, demon

229 enous Pcyt2 were dramatically increased with phorbol esters and reduced by specific PKC inhibitors.

230 internalization was observed in response to phorbol esters and sphingosine 1-phosphate.

231 we used the stimulation of MLP29 cells with phorbol esters and the in vivo activation after partial

232 hage-like cells (D-U1) by costimulation with phorbol esters and urokinase-type plasminogen activator.

233 Interestingly, phorbol esters did not accelerate endocytosis of axonal

234 fibrosarcoma cells and that proinflammatory phorbol esters further enhanced this effect.

235 he recognition module for diacylglycerol and phorbol esters in protein kinase C, Ras guanine nucleoti

236 C (PKC) attendant to prolonged activation by phorbol esters is a widely described property of this ke

237 rticipation in the action of tumor-promoting phorbol esters like 12-O-tetradecanoylphorbol-13-acetate

238 nated following activation induced by either phorbol esters or natural agonists.

239 and BCL2A1, mediate the apoptotic effect of phorbol esters or the chemotherapeutic agent etoposide i

240 Phorbol esters or the engagement of the T cell antigen r

241 tor molecules constitutively, in response to phorbol esters or through bystander activation by innate

242 with mitochondria following stimulation with phorbol esters or, in L6 myocytes, with insulin via a me

243 Although phorbol esters promote a strong apoptotic response in LN

244 The non-tumor-inducing phorbol esters prostratin and 12-deoxyphorbol-13-phenyla

245 we found that short-term exposure of CAFs to phorbol esters reduced the number of stress fibers and t

246 nducing agents, like activating cytokines or phorbol esters that stimulate host cell signal transduct

247 phosphorylated in response to high glucose, phorbol esters, and analogs of cAMP, all key insulin sec

248 promoting function of their potent ligands, phorbol esters, and the prevalence of their mutations.

249 e second messenger diacylglycerol and of the phorbol esters, are classified as typical (ligand-respon

250 rotein kinase C regulator, and plant-derived phorbol esters, but each ligand induces different activi

251 inases are major targets for tumor-promoting phorbol esters, G protein-coupled receptors, and activat

252 Na(+)/H(+) exchange activity in response to phorbol esters, growth factors or protein phosphatase in

253 mulated by growth factors or tumor-promoting phorbol esters, we analyzed its role in amino acid-depen

254 d in the absence of promoting agents such as phorbol esters.

255 ubiquitination or endocytosis in response to phorbol esters.

256 rotein kinase C (PKC)-Ras-Erk signaling with phorbol esters.

257 y inhibit the dephosphorylation triggered by phorbol esters.

258 lation and down-regulation of PKC induced by phorbol esters.

259 n but also as a consequence of activation by phorbol esters.

260 kinase activation and cannot be triggered by phorbol esters.

261 through a heterologous mechanism mediated by phorbol esters.

262 ow extracellular calcium and facilitation by phorbol esters.

263 cal structure and the medicinal potential of phorbol esters.

264 Purely synthetic enantiopure phorbol has remained elusive, and biological synthesis h

265 hieve enantiospecific total synthesis of (+)-phorbol in only 19 steps from the abundant monoterpene (

266 nction, the des-B-ring analogues displayed a phorbol-like biological function in cells.

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

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

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

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

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

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

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

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

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

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

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

278 Moreover, phorbol myristate acetate enhanced Nedd4-2 phosphorylati

279 TLC and phorbol myristate acetate increased cytosolic pMARCKS an

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

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

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

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

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

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

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

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

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

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

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

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

292 tivated protein (MAP) kinases in response to phorbol myristate acid (PMA), H(2)O(2), UV, and anisomyc

293 latelet-free plasma (PFP) or in buffer using phorbol myristate actetate or calcium ionophore.

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

295 In human cells, phorbol myristic acid induces syndecan-1 shedding, resul

296 Phorbol myristic acid stimulation significantly decrease

297 C or 25 degrees C and in the presence of 1) phorbol myristic acid, forskolin and 3-isobutyl-1-methyl

298 n kinase C (PKC) by the diacylglycerol mimic phorbol-myristic acid resulted in specific and dose-resp

299 dynamics of cPKC activation upon receptor or phorbol stimulation.

300 Phorbol, the flagship member of the tigliane diterpene f