ライフサイエンスコーパス: tetradecanoylphorbol

1 ent with the protein kinase C activator 12-O-tetradecanoylphorbol 12-acetate (TPA) enables radiation-

2 neous measurement of miR155 and CD69 in 12-O-tetradecanoylphorbol 13-acetate (PMA) and Ionomycin stim

3 tion of FR-beta in KG-1 cells treated with O-tetradecanoylphorbol 13-acetate (TPA) was accompanied by

4 The phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA), a potent stimulat

5 ry culture were treated with 0.2 microM 12-O-tetradecanoylphorbol 13-acetate (TPA), and c-jun mRNA wa

6 in combination with the tumor promoter 12-O-tetradecanoylphorbol 13-acetate (TPA), did not result in

7 potentiated by the phorbol ester 4beta-12-O-tetradecanoylphorbol 13-acetate (TPA), the potency of wh

8 In addition, the compound inhibits 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced ornithine

9 nucleophosmin) significantly suppresses 12-O-tetradecanoylphorbol 13-acetate (TPA)-mediated apoptosis

10 ation of reporter constructs containing 12-O-tetradecanoylphorbol 13-acetate (TPA)-responsive element

11 nt phosphorylation after treatment with 12-O-tetradecanoylphorbol 13-acetate (TPA).

12 have examined the regulation of PS1 by 12-O-tetradecanoylphorbol 13-acetate (TPA).

13 induction of osteopontin in response to 12-O-tetradecanoylphorbol 13-acetate and okadaic acid.

14 monocytic differentiation and enhanced 12-O-tetradecanoylphorbol 13-acetate induced macrophage diffe

15 12-dimethylbenz[a]anthracene-initiation/12-O-tetradecanoylphorbol 13-acetate promotion, that produce

16 ent with the protein kinase C activator 12-O-tetradecanoylphorbol 13-acetate reduced junctional condu

17 essor in 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol 13-acetate skin carcinogenesis and

18 formation, we treated THP-1 cells with 12-O-tetradecanoylphorbol 13-acetate to differentiate them in

19 tresses (heat shock, osmotic shock, and 12-O-tetradecanoylphorbol 13-acetate), agents causing mainly

20 rentiation, all-trans-retinoic acid and 12-O-tetradecanoylphorbol 13-acetate, increased PTEN expressi

21 l line is induced to differentiate with 12-O-tetradecanoylphorbol 13-acetate, overexpression of MKL1

22 60 induced by 1,25-(OH)2 vitamin D3 and 12-O-tetradecanoylphorbol 13-acetate, respectively.

23 as demonstrated by the observation that 12-O-tetradecanoylphorbol 13-acetate-activated cell adhesion

24 goblet cell lineage, in forskolin- and 12-O-tetradecanoylphorbol 13-acetate-induced HT29 cells, and

25 sed sensitivity of Pglyrp2(-/-) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like i

26 re more sensitive to the development of 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like i

27 itive application of the tumor promoter 12-O-tetradecanoylphorbol 13-acetate.

28 with the PKC activating phorbol ester, 12-O-tetradecanoylphorbol 13-acetate.

29 ylation induced by an activator of PKC (12-O-tetradecanoylphorbol 13-acetate; TPA) versus agents that

30 thelial cells using c-Jun, acting via a 12-O-tetradecanoylphorbol-13 acetate response element located

31 n in the 7,12-Dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA) model of skin

32 two-step 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA) skin carcinog

33 tible to 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA)-induced skin

34 ene alone (complete carcinogen) or with 12-O-tetradecanoylphorbol-13-acetate (TPA) (initiation/promot

35 The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) activates a geneti

36 ypes of experiments: (i) application of 12-O-tetradecanoylphorbol-13-acetate (TPA) and (ii) full-thic

37 d with epidermal growth factor (EGF) or 12-O-tetradecanoylphorbol-13-acetate (TPA) and a constitutive

38 Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal grow

39 Human myeloid leukemia cells respond to 12-tetradecanoylphorbol-13-acetate (TPA) and other activato

40 nfected keratinocytes were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) and RT-PCR was per

41 helial cell differentiation, as well as 12-O-tetradecanoylphorbol-13-acetate (TPA) and sodium butyrat

42 arrying these viruses were induced with 12-O-tetradecanoylphorbol-13-acetate (TPA) and sodium butyrat

43 the stimulation of IRF-7 expression by 12-O-tetradecanoylphorbol-13-acetate (TPA) and tumor necrosis

44 ive effects of the skin tumor promoter, 12-0-tetradecanoylphorbol-13-acetate (TPA) and were more sens

45 mor promoters such as the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) are proinflammator

46 er in wild-type mouse skin treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) as compared with P

47 lbenz(a)anthracene as the initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as the promoter.

48 thylbenz(a)anthracene as carcinogen and 12-O-tetradecanoylphorbol-13-acetate (TPA) as tumor promoter.

49 K5-AZ mice treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) at 0 and 24 h exhi

50 owing treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) because of a defec

51 flammatory hypersensitivity to a single 12-O-tetradecanoylphorbol-13-acetate (TPA) challenge.

52 Here we found that 12-O-tetradecanoylphorbol-13-acetate (TPA) could induce cell

53 c mice treated with the promoting agent 12-O-tetradecanoylphorbol-13-acetate (TPA) developed papillom

54 ed to the proinflammatory phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) exhibited higher t

55 hracene (DMBA), mice were promoted with 12-O-tetradecanoylphorbol-13-acetate (TPA) for 20 weeks.

56 followed by twice weekly application of 12-O-tetradecanoylphorbol-13-acetate (TPA) for 27 weeks.

57 12-O-tetradecanoylphorbol-13-acetate (TPA) has been shown to

58 transcriptional regulation of fra-1 by 12-O-tetradecanoylphorbol-13-acetate (TPA) in human bronchial

59 expression was up- or down-regulated by 12-O-tetradecanoylphorbol-13-acetate (TPA) in mouse skin kera

60 activated by the tumor promoting agent, 12-O-tetradecanoylphorbol-13-acetate (TPA) in normal human or

61 We further show that 12-O-tetradecanoylphorbol-13-acetate (TPA) increases BCSG1 mR

62 RA treatment suppresses 12-O-tetradecanoylphorbol-13-acetate (TPA) induced AP-1 activ

63 topical treatment of K14-RIP4 mice with 12-O-tetradecanoylphorbol-13-acetate (TPA) induced dramatic,

64 Topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA) induced strong VEG

65 fected reporter constructs, and mediates 2-O-tetradecanoylphorbol-13-acetate (TPA) induced transcript

66 pesvirus-8 [HHV-8]) with agents such as 12-O-tetradecanoylphorbol-13-acetate (TPA) induces a lytic vi

67 dies demonstrate that the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) induces translocat

68 12-O-Tetradecanoylphorbol-13-acetate (TPA) induction of the F

69 The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is a potent induce

70 human U-937 myeloid leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with

71 12-O-Tetradecanoylphorbol-13-acetate (TPA) is widely used as

72 e 7,12-dimethylbenz(a)anthracene (DMBA)/12-o-tetradecanoylphorbol-13-acetate (TPA) model of mouse ski

73 r 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) models].

74 e 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) mouse skin carcino

75 d to a two-stage dimethylbenzanthracene/12-O-tetradecanoylphorbol-13-acetate (TPA) mouse skin carcino

76 of tumor-promoting phorbol esters like 12-O-tetradecanoylphorbol-13-acetate (TPA) on Ras pathways in

77 protein and mRNA expression induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) or EGF in human pr

78 vation by hypoxia or using the chemical 12-O-tetradecanoylphorbol-13-acetate (TPA) or sodium butyrate

79 imethylbenz(a)anthracene initiation and 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion protocol

80 hylbenz(a)anthracene (DMBA) initiation, 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion skin car

81 age 12-dimethylbenz(a)anthracene (DMBA)/12-o-tetradecanoylphorbol-13-acetate (TPA) protocol for skin

82 Selective activation of PKC by 12-O-tetradecanoylphorbol-13-acetate (TPA) reduced phospho-Se

83 ulation of ErbB-4-expressing cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) results in the pro

84 ermine the sensitivity of these mice to 12-O-tetradecanoylphorbol-13-acetate (TPA) skin tumor promoti

85 19-fold greater phosphatidylserine and 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulated kinase

86 12-O-Tetradecanoylphorbol-13-acetate (TPA) suppresses the pro

87 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment of Chine

88 Topical 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment of K5-PK

89 ng cultures and to study the effects of 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment on the d

90 d increased inflammation in response to 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment.

91 rol mice regressed after termination of 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment; whereas

92 levated extracellular calcium and acute 12-O-tetradecanoylphorbol-13-acetate (TPA) treatments induced

93 a 7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) two-stage carcinog

94 LNCaP human prostate carcinoma cells by 12-O-tetradecanoylphorbol-13-acetate (TPA) was examined.

95 e multiplicity of papillomas induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) was lower than tha

96 sistently, endogenous SAG is induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) with an induction

97 cells with phorbol ester (2 micrometer 12-O-tetradecanoylphorbol-13-acetate (TPA)) gives rise to a n

98 lation of NCC by the phorbol ester (PE) 12-O-tetradecanoylphorbol-13-acetate (TPA), a diacylglycerol

99 eavage was stimulated by phorbol ester (12-O-tetradecanoylphorbol-13-acetate (TPA), a mimic of diacyl

100 eatment of cells with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), a PKC activator,

101 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase

102 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase

103 proteins and the phorbol ester, 4 beta-12-O-tetradecanoylphorbol-13-acetate (TPA), but lacking lipid

104 uced by the protein kinase C activator, 12-O-tetradecanoylphorbol-13-acetate (TPA), did not affect it

105 and IL-1alpha production by IL-1alpha, 12-O-tetradecanoylphorbol-13-acetate (TPA), epidermal growth

106 ulated adult feline cardiomyocytes with 12-O-tetradecanoylphorbol-13-acetate (TPA), insulin, or forsk

107 ormation induced by the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), is suppressed in

108 t classes of tumor promoters, including 12-O-tetradecanoylphorbol-13-acetate (TPA), okadaic acid, and

109 93 cells with either the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), or insulin result

110 ion (338)SSYY(341) in response to 4beta-12-O-tetradecanoylphorbol-13-acetate (TPA), or mutation of Y3

111 uch as epidermal growth factor (EGF) or 12-O-tetradecanoylphorbol-13-acetate (TPA), phosphorylation o

112 12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA), respectively) is

113 in the skin upon topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA), resulting in a dr

114 pical treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA), resulting in epid

115 lls and its expression was inducible by 12-O-tetradecanoylphorbol-13-acetate (TPA), sensitive to cycl

116 activation of protein kinase C (PKC) by 12-O-tetradecanoylphorbol-13-acetate (TPA), the ErbB-4 ectodo

117 nse to epidermal growth factor (EGF) or 12-O-tetradecanoylphorbol-13-acetate (TPA), the promotion-sen

118 tment of promyelocytic HL-60 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA), which triggers di

119 It is thought that the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced AP-1 activ

120 Previously, we reported that 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced apoptosis

121 t Smad3 knockout mice were resistant to 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced epidermal

122 K5.PRAS40(T246A) mice were resistant to 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced epidermal

123 icated that chlorogenic acid suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced neoplastic

124 /ml and 40 mum, respectively, inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced neoplastic

125 Here we report that equol inhibits 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced neoplastic

126 ere, we report that MSK1 is involved in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced or epiderm

127 In these cells, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced phosphoryl

128 ion of PACSIN3 in HT1080 cells enhanced 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced proHB-EGF

129 udy identifies genes expressed early in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin carci

130 (Dex) could not efficiently suppress a 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin infla

131 Using acute and chronic models of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin infla

132 red wine flavonoid quercetin inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced transforma

133 The mechanism of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor prom

134 1) was previously identified as a novel 12-O-tetradecanoylphorbol-13-acetate (TPA)-inducible gene wit

135 Murine 8S-lipoxygenase (8S-LOX) is a 12-O-tetradecanoylphorbol-13-acetate (TPA)-inducible lipoxyge

136 al hyperplasia/hyperkeratosis and novel 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted papilloma

137 imethylbenz(a)anthracene-initiation and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promotion protocol

138 benz(a)anthracene (DMBA)-initiation and 12-O-tetradecanoylphorbol-13-acetate (TPA)-promotion protocol

139 pitation assays were used to identify a 12-O-tetradecanoylphorbol-13-acetate (TPA)-response element (

140 ed the vIRF core promoter and defined a 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive region

141 The role of 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated polyami

142 LCLs and abrogating gp350 expression in 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated B95-8 cell

143 s of neomycin-treated BCBL-1 cells than 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated cells.

144 llowing exposure to the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA).

145 owing treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA).

146 hours) when treated with tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA).

147 l cells treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA).

148 n kinase C activator and tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA).

149 and mediate inflammation in response to 12-O-tetradecanoylphorbol-13-acetate (TPA).

150 r follicles when treated topically with 12-O-tetradecanoylphorbol-13-acetate (TPA).

151 ved by treatment with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA).

152 methyl-1,2-benz[a]anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA).

153 expression induced by the phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA).

154 lowing treatment with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA).

155 ties induced by the phorbol ester 4beta-12-O-tetradecanoylphorbol-13-acetate (TPA).

156 ole of NEP in PC cell susceptibility to 12-O-tetradecanoylphorbol-13-acetate (TPA).

157 treated with the differentiating agent, 12-O-tetradecanoylphorbol-13-acetate (TPA).

158 ed in epidermal differentiation induced by O-tetradecanoylphorbol-13-acetate (TPA).

159 nduced by treatment of B95-8 cells with 12-O-tetradecanoylphorbol-13-acetate (TPA).

160 by the potent differentiating stimulus, 12-O-tetradecanoylphorbol-13-acetate (TPA).

161 perplasia in response to application of 12-O-tetradecanoylphorbol-13-acetate (TPA).

162 ced proliferation following exposure to 12-O-tetradecanoylphorbol-13-acetate (TPA).

163 a when PKCalpha is activated by topical 12-O-tetradecanoylphorbol-13-acetate (TPA).

164 rosis factor-alpha) or a phorbol ester [12-O-tetradecanoylphorbol-13-acetate (TPA)] only induced p16,

165 e [7,12-dimethylbenz(a)-anthracene plus 12-O-tetradecanoylphorbol-13-acetate (TPA)] skin carcinogenes

166 [7,12-dimethylbenz(a)anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)] skin carcinogenes

167 with the addition of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA, also known as PMA)

168 Clinically achievable concentrations of 12-O-tetradecanoylphorbol-13-acetate (TPA; 0.16-0.32 nM) and

169 ibroblasts, epidermal growth factor and 12-O-tetradecanoylphorbol-13-acetate activated the MAPK casca

170 12-O-tetradecanoylphorbol-13-acetate activation of p42/p44 MA

171 her analysis demonstrated that serum or 12-O-tetradecanoylphorbol-13-acetate activation of several im

172 D3 and anti-CD28 antibodies, but not by 12-O-tetradecanoylphorbol-13-acetate and Ca(2+) ionophore A23

173 th keratinocyte-differentiating agents, 12-O-tetradecanoylphorbol-13-acetate and calcium via a mechan

174 (2+)-free conditions in the presence of 12-O-tetradecanoylphorbol-13-acetate and forskolin.

175 ociation is greatly stimulated by 4beta-12-O-tetradecanoylphorbol-13-acetate and nocodazole and by ex

176 inc finger mutant Raf by both EGF/4beta-12-O-tetradecanoylphorbol-13-acetate and nocodazole.

177 in mouse ears by topical treatment with 12-O-tetradecanoylphorbol-13-acetate and oxazalone, respectiv

178 lymphoma cell lines in the presence of 12-O-tetradecanoylphorbol-13-acetate and phosphonoformic acid

179 ation of human erythroleukemia cells by 12-O-tetradecanoylphorbol-13-acetate and primary megakaryocyt

180 293T BAC-stop45 cells were induced with 12-O-tetradecanoylphorbol-13-acetate and sodium butyrate, no

181 From various stimuli tested, 12-O-tetradecanoylphorbol-13-acetate and tunicamycin affected

182 or linoleic acid, 45 min and 4 h after 12-O-tetradecanoylphorbol-13-acetate application, resulted in

183 he mice were treated with 2.5 microg of 12-O-tetradecanoylphorbol-13-acetate applied weekly to the sh

184 uced by 7,12-dimethylbenz(a)-anthracene/12-O-tetradecanoylphorbol-13-acetate at the early stage of ca

185 classic 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate cancer model in which a

186 wo-stage 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate chemical skin carcinogen

187 cting them to a standard two-stage DMBA/12-O-tetradecanoylphorbol-13-acetate cutaneous carcinogenesis

188 Treatment of melanoma cells with 12-O-tetradecanoylphorbol-13-acetate downregulated zyxin expr

189 Activation of PKC by 12-O-tetradecanoylphorbol-13-acetate dramatically decreased M

190 We report that tumor promoter 12-O-tetradecanoylphorbol-13-acetate exposure decreases prote

191 n of 7,12-dimethylbenz(a)anthracene and 12-O-tetradecanoylphorbol-13-acetate for 3 wk increased epide

192 AP-1) induced by ultraviolet B (UVB) or 12-O-tetradecanoylphorbol-13-acetate in mouse epidermal JB6 c

193 rt the induction of IRF-7 expression by 12-O-tetradecanoylphorbol-13-acetate in U937 and HL60 cells a

194 nt of the corneal epithelial cells with 12-O-tetradecanoylphorbol-13-acetate increased hINV gene expr

195 EGF and 12-O-tetradecanoylphorbol-13-acetate induce Stat3 mitochondri

196 ever, treatment with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate induced tumors in 18 and

197 rst demonstrate that AP-1 activation by 12-O-tetradecanoylphorbol-13-acetate induces PTPROt expressio

198 The protective activity of 12-O-tetradecanoylphorbol-13-acetate is abrogated by pretreat

199 tic leukemia cells to the phorbol ester 12-O-tetradecanoylphorbol-13-acetate mimics several features

200 e 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate mouse skin carcinogenesi

201 Specific activation of PKC with 12-O-tetradecanoylphorbol-13-acetate or bryostatin-1 induced

202 ation of 7,12-Dimethylbenz(a)anthracene/12-O-Tetradecanoylphorbol-13-acetate or by Myc/Ras overexpres

203 y PKC either in vitro or in response to 12-O-tetradecanoylphorbol-13-acetate or epidermal growth fact

204 ErbB-4 very similar to that induced by 12-O-tetradecanoylphorbol-13-acetate or pervanadate (each of

205 c extracts from adipocytes treated with 12-O-tetradecanoylphorbol-13-acetate or PKC alpha antisense o

206 late cyclase-activating polypeptide and 12-O-tetradecanoylphorbol-13-acetate plus dbcAMP) and were en

207 that the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate prevents DNA damage-indu

208 a]anthracene (DMBA) initiation with 12-ortho-tetradecanoylphorbol-13-acetate promotion), K14.MCM7 mic

209 However, within 15-20 weeks of 12-O-tetradecanoylphorbol-13-acetate promotion, 40% of T7-PKC

210 o ceramide synthesis, or phorbol ester, 12-O-tetradecanoylphorbol-13-acetate reduced endogenous ceram

211 ediated by the Tax-responsive CD28RE-3'-12-O-tetradecanoylphorbol-13-acetate response element (AP1) e

212 A 12-O-tetradecanoylphorbol-13-acetate response element (TRE) l

213 while treatment with the PKC stimulator 12-O-tetradecanoylphorbol-13-acetate restored TG activity in

214 arization could be partially rescued by 12-O-tetradecanoylphorbol-13-acetate skin treatment.

215 s exposed to epidermal growth factor or 12-O-tetradecanoylphorbol-13-acetate stimulation compared wit

216 t c-JUN at the PED/PEA-15 promoter upon 12-O-tetradecanoylphorbol-13-acetate stimulation of the cells

217 proteases in response to the ligand or 12-O-tetradecanoylphorbol-13-acetate stimulation resulting in

218 ity-based lymphoma 1 cells induced with 12-O-tetradecanoylphorbol-13-acetate to obtain HHV-8 capsids

219 Treatment of cells with 12-O-tetradecanoylphorbol-13-acetate to phosphorylate NKX3.1

220 ificantly alter ear thickness following 12-O-tetradecanoylphorbol-13-acetate treatment in peroxisome

221 ein kinase C (PKC) depletion by chronic 12-O-tetradecanoylphorbol-13-acetate treatment nearly abolish

222 ollowing 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate treatment of mice, sugge

223 12-O-Tetradecanoylphorbol-13-acetate treatment or expression

224 As expected, 12-O-tetradecanoylphorbol-13-acetate treatment resulted in a

225 12-O-tetradecanoylphorbol-13-acetate treatment resulted in an

226 al keratinocytes with 0.12 mm Ca(2+) or 12-O-tetradecanoylphorbol-13-acetate treatment resulted in th

227 els in BCBL-1 cells were increased upon 12-O-tetradecanoylphorbol-13-acetate treatment, with kinetics

228 served after epidermal growth factor or 12-O-tetradecanoylphorbol-13-acetate treatment.

229 anced inflammatory response to ear skin 12-O-tetradecanoylphorbol-13-acetate treatment.

230 enz[a]anthracene; promotion with 5 nmol 12-O-tetradecanoylphorbol-13-acetate twice weekly).

231 the 7,12-dimethylbenzanthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate two-stage skin carcinoge

232 whole blood with lipopolysaccharide or 12-0 tetradecanoylphorbol-13-acetate up-regulated plasminogen

233 f lytic cycle genes were expressed when 12-O-tetradecanoylphorbol-13-acetate was added to the HMVEC-d

234 e 1/2 inhibitor U0126 and phorbol ester 12-O-tetradecanoylphorbol-13-acetate) and compared the patter

235 muli (serum, EGF, and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate) that alter skin keratin

236 ,12-dimethylbenz[alpha]anthracene)/TPA (12-O-tetradecanoylphorbol-13-acetate) two-stage carcinogenesi

237 ioassay (7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-acetate) were significantly enha

238 or phorbol 12-myristate 13-acetate (PMA/12-O-tetradecanoylphorbol-13-acetate), suggesting that p38 mi

239 s did not modulate either basal or TPA (12-O-tetradecanoylphorbol-13-acetate)-stimulated transcriptio

240 In contrast, 12-O-tetradecanoylphorbol-13-acetate, a mitogen for melanocyt

241 tment of multidrug-resistant cells with 12-O-tetradecanoylphorbol-13-acetate, a phorbol ester that in

242 1alpha, comparable with that induced by 12-O-tetradecanoylphorbol-13-acetate, a potent tumor promoter

243 vation in response to the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, a well-known mouse skin

244 ers, such as epidermal growth factor or 12-O-tetradecanoylphorbol-13-acetate, and that kaempferol, a

245 ld-type mice after tumor promotion with 12-O-tetradecanoylphorbol-13-acetate, and this effect was dim

246 12-O-tetradecanoylphorbol-13-acetate, but not 1,25(OH)(2)D(3)

247 ith the keratinocyte regulatory agents, 12-O-tetradecanoylphorbol-13-acetate, calcium, and okadaic ac

248 tion of 133-224 (2C), whereas TNFalpha, 12-O-Tetradecanoylphorbol-13-acetate, human T-cell leukemia v

249 ical applications of the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, in the absence of tumor

250 nd 293T-DeltagBBAC36 cells were induced with tetradecanoylphorbol-13-acetate, infectious virus was de

251 Cx43, by tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate, is associated with an u

252 nning in response to the tumor promoter 12-O-tetradecanoylphorbol-13-acetate, phenocopying the reduce

253 differentiation-inducing agents such as 12-O-tetradecanoylphorbol-13-acetate, retinoic acid or dimeth

254 ted by cell treatment with heregulin or 12-O-tetradecanoylphorbol-13-acetate, the fragment associates

255 , which activate adenylate cyclase, and 12-O-tetradecanoylphorbol-13-acetate, which activates protein

256 with 7,12-dimethylbenz[alpha]anthracene/12-o-tetradecanoylphorbol-13-acetate, which typically generat

257 inase, and MAPK kinase 4 induced by UVB/12-O-tetradecanoylphorbol-13-acetate, yet higher doses were r

258 ow that PRMT5 inhibits the PKCdelta- or 12-O-tetradecanoylphorbol-13-acetate-dependent increase in hu

259 ignal-regulated kinase (ERK) signaling, 12-O-tetradecanoylphorbol-13-acetate-independent growth, and

260 could effectively inhibit phorbol ester 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 activity an

261 UP-TF strongly inhibited tumor promoter 12-O-tetradecanoylphorbol-13-acetate-induced AP-1 transactiva

262 ored the ability of trans-RA to inhibit 12-O-tetradecanoylphorbol-13-acetate-induced c-Jun expression

263 ese COX-2 inhibitors could also inhibit 12-O-tetradecanoylphorbol-13-acetate-induced cell transformat

264 mRNA in erythroleukemia K562 cells upon 12-O-tetradecanoylphorbol-13-acetate-induced differentiation.

265 ce showed an enhanced responsiveness to 12-O-tetradecanoylphorbol-13-acetate-induced epidermal hyperp

266 n respond to proliferative stress, with 12-O-tetradecanoylphorbol-13-acetate-induced epidermal hyperp

267 ed receptor-alpha, had no effect on the 12-O-tetradecanoylphorbol-13-acetate-induced inflammation.

268 on in vitro and, in addition, inhibited 12-O-tetradecanoylphorbol-13-acetate-induced proliferation an

269 pment of 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate-induced skin papillomas,

270 quired for heregulin-dependent, but not 12-O-tetradecanoylphorbol-13-acetate-induced, ErbB-4 ectodoma

271 Thus, in K562 cells, 12-O-tetradecanoylphorbol-13-acetate-inducible expression of

272 echanism of this PI3-kinase inhibition, 12-O-tetradecanoylphorbol-13-acetate-matured U937 cells were

273 ures displayed a decreased capacity for 12-O-tetradecanoylphorbol-13-acetate-mediated p16 induction.

274 imethylbenz(a)anthracene initiation and 12-O-tetradecanoylphorbol-13-acetate-promotion or by repeated

275 indicated that BAD is localized at the 12-O-tetradecanoylphorbol-13-acetate-response element (TRE) a

276 duced expression of an AP-1 target gene in a tetradecanoylphorbol-13-acetate-response element (TRE)-d

277 /-94 bp enhancer harboring two critical 12-O-tetradecanoylphorbol-13-acetate-responsive elements (TRE

278 with histone deacetylase (HDAC) 1/2 in 12-O-tetradecanoylphorbol-13-acetate-stimulated BCBL-1 lympho

279 1 to suppress both the constitutive and 12-O-tetradecanoylphorbol-13-acetate-stimulated expression of

280 Three cell types (MCF-10A, MCF-7, and 12- O-tetradecanoylphorbol-13-acetate-treated MCF-7) with diff

281 reduce the levels of these cytokines in 12-O-tetradecanoylphorbol-13-acetate-treated skin.

282 12-O-Tetradecanoylphorbol-13-acetate-type tumor promoters, su

283 ither amphetamine or the PKC activator, 12-O-tetradecanoylphorbol-13-acetate.

284 stimulated directly with phorbol ester, 12-O-tetradecanoylphorbol-13-acetate.

285 with 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-13-acetate.

286 treatment of 3T3-F442A adipocytes with 12-O-tetradecanoylphorbol-13-acetate.

287 ed by IL-1beta, lipopolysaccharide, and 12-O-tetradecanoylphorbol-13-acetate.

288 ylhydroquinone, beta-naphthoflavone, or 12-O-tetradecanoylphorbol-13-acetate.

289 ce and were inducible by treatment with 12-O-tetradecanoylphorbol-13-acetate.

290 lication initiated by the viral inducer 12-O-tetradecanoylphorbol-13-acetate.

291 leviating acute dermatitis triggered by 12-O-tetradecanoylphorbol-13-acetate.

292 lowing promotion with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate.

293 ng PKC stimulation by the phorbol ester 12-O-tetradecanoylphorbol-3-acetate (PMA) and by bryostatin-1

294 that activation of PKC by the phorbol ester tetradecanoylphorbol acetate (TPA) inhibits cell death v

295 f cells with HNE dose-dependently suppresses tetradecanoylphorbol acetate (TPA)/ionomycin (IM)-induce

296 ollowing exposure to the tumor promoter 12-O-tetradecanoylphorbol acetate than in P+ cells.

297 However, in TPA (tetradecanoylphorbol acetate)-treated cells, TLK16998 bu

298 both AP-1 transcriptional activity and 12-O-tetradecanoylphorbol-induced transcriptional transactiva

299 12-dimethylbenz(alpha)anthracene (DMBA)/12-O-tetradecanoylphorbol-l3-acetate (TPA) multistage skin ca

300 edding of M-CSFR elicited by phorbol esters (tetradecanoylphorbol myristate acetate (TPA)) or LPS in