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

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

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

5 e, KCl-dependent membrane depolarization and phorbol 12,13-dibutyrate (PDBu).

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

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

8 10R/L20R) compared to the wild-type, whereas phorbol 12,13-dibutyrate showed a 6000-fold loss of affi

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

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

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

12 Ionomycin and phorbol 12-myristate 13 acetate (PMA) are used to trigge

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

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

18 48-hour exposure to the potent PKC activator phorbol 12-myristate 13-acetate (PMA) at 10 nM concentra

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

20 rect activation of PKC via the phorbol ester phorbol 12-myristate 13-acetate (PMA) mimics CXCL12-medi

21 that SOPD-Pep mitigated toxicity induced by phorbol 12-myristate 13-acetate (PMA) more effectively t

22 stigated the effects of PKC activation using phorbol 12-myristate 13-acetate (PMA) on hERG channels e

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

24 Phorbol 12-myristate 13-acetate (PMA) promotes skin canc

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

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

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

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

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

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

31 However, following treatment with phorbol 12-myristate 13-acetate (PMA), ASP translocates

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

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

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

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

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

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

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

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

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

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

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

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

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

45 BACH2 expression resulted in suppression of phorbol 12-myristate 13-acetate (PMA)/ionomycin-driven a

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

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

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

49 Phorbol 12-myristate 13-acetate and ionomycin stimulated

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

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

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

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

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

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

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

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

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

59 Phorbol 12-myristate 13-acetate increased intracellular

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

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

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

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

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

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 signalling in lipin1 deficient myoblasts by phorbol 12-myristate 13-acetate transiently activated PK

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

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

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

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

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

79 by the protein kinase C (PKC) activator PMA (phorbol 12-myristate 13-acetate) in Xenopus oocytes.

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

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

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

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

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

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

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

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 of AJH-836 and a prototypical phorbol ester (phorbol 12-myristate 13-acetate, PMA) to induce changes

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 ed macrophages, human monocytic THP-1 cells, phorbol 12-myristate 13-acetate-differentiated human mac

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

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

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

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

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

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

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

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

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

103 oxidative burst was preserved in response to phorbol 12-myristate 13-acetate.

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

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

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

107 s (mAbs), phytohaemagglutinin/interleukin-2, phorbol 12-myristate 13-acetate/ionomycin, prostratin, p

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

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

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

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

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

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

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

115 Human THP-1 monocytes were activated with phorbol-12-myristate-13-acetate (PMA) and differentiated

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

117 line that can be differentiated in vitro by phorbol-12-myristate-13-acetate (PMA) treatment to produ

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

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

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

121 2) depletion, whereas activation of PKC with phorbol-12-myristate-13-acetate potentiated the Ci-VSP-i

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

123 he inflammatory processes in THP-1 cells and phorbol-12-myristate-13-acetate-differentiated macrophag

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

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

129 ene, and then promoted by 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 n with vasoactive intestinal peptide (V) and phorbol ester (P) synergistically activated viral infect

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

145 ed the ability of AJH-836 and a prototypical phorbol ester (phorbol 12-myristate 13-acetate, PMA) to

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

147 sion after induction of differentiation with phorbol ester (PMA) and transduction with the full-lengt

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

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

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

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

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

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

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

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

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

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

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

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

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

161 Phorbol ester and RTA transgene induction were used to i

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

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

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

165 identified as a genomic region important for phorbol ester biosynthesis.

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

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

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

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

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

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

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

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

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

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

176 strate that direct activation of PKC via the phorbol ester phorbol 12-myristate 13-acetate (PMA) mimi

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

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

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

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

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

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

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

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

185 duced at the plasma membrane (PM) induced by phorbol ester stimulation of PLD were rapidly internaliz

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

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

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

189 nd impaired stratum corneum thickening after phorbol ester treatment.

190 econd messenger diacylglycerol (DAG) and the phorbol ester tumor promoters.

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

192 ition of HSF1 attenuated latency reversal by phorbol ester+ionomycin but not by anti-CD3+anti-CD28.

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

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

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

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

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

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

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

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

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

202 Phorbol ester-induced sequential phosphorylation of both

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

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

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

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

207 Diacylglycerol (DAG)/phorbol ester-regulated protein kinase C (PKC) isozymes

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

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

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

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

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

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

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

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

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

217 matory lesions after topical applications of phorbol ester.

218 , and displayed translocation in response to phorbol ester.

219 kat and primary human T cells activated with phorbol ester/ionomycin or antibodies against CD3/CD28.

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

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

222 ds diacylglycerol as well as tumor-promoting phorbol esters and a catalytic GAP domain that inactivat

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

224 Phorbol esters and Group I metabotropic glutamate recept

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

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

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

228 Both phorbol esters and tetanic stimulation potentiate synapt

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

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

231 Interestingly, phorbol esters did not accelerate endocytosis of axonal

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

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

234 e to the limitation posed by the presence of phorbol esters in toxic varieties.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

250 This signature was normalized by specific phorbol esters, making them promising therapeutic candid

251 s of lysosomal function showed that specific phorbol esters, such as PEP005, reduced alpha-synuclein

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

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

254 ubiquitination or endocytosis in response to phorbol esters.

255 ow extracellular calcium and facilitation by phorbol esters.

256 cal structure and the medicinal potential of phorbol esters.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 Moreover, phorbol myristate acetate enhanced Nedd4-2 phosphorylati

273 TLC and phorbol myristate acetate increased cytosolic pMARCKS an

274 Phorbol myristate acetate induced TTF1 protein degradati

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

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

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

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

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

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

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

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

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

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

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

286 -dimethyl benzanthracene when applied before phorbol myristate acetate.

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

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

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

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

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

292 TE), and stimulated with lipopolysaccharide, phorbol myristate and ionomycin (agonists).

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

294 Phorbol-myristate-acetate-induced formation of neutrophi

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