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1 matory lesions after topical applications of phorbol ester.
2 , and displayed translocation in response to phorbol ester.
3 ve to Rol, while retaining responsiveness to phorbol ester.
4 , a mediator of the cell death effect by the phorbol ester.
5 ive C1 domains and has been reported to bind phorbol ester.
6 of the two MRCK isoforms alpha and beta with phorbol ester.
7 tion as well as a weaker initial response to phorbol ester.
8 y 30% at baseline and after stimulation with phorbol ester.
9 ercome by signals bypassing the TCR, such as phorbol ester.
10 in the deltaC1b domain conferred response to phorbol ester.
11 arkers and was not slowed in the presence of phorbol ester.
12 RI or combination of Ca (2)(+) ionophore and phorbol ester.
13 rotein kinase C (PKC)-Ras-Erk signaling with phorbol esters.
14 y inhibit the dephosphorylation triggered by phorbol esters.
15 lation and down-regulation of PKC induced by phorbol esters.
16 n but also as a consequence of activation by phorbol esters.
17 kinase activation and cannot be triggered by phorbol esters.
18 through a heterologous mechanism mediated by phorbol esters.
19 P1 KO cells even after 60 min of exposure to phorbol esters.
20 affinity to diacylglycerol analogs like the phorbol esters.
21 in the absence of chemical inducers such as phorbol esters.
22 ow extracellular calcium and facilitation by phorbol esters.
23 cal structure and the medicinal potential of phorbol esters.
24 second messenger diacylglycerol (DAG) or the phorbol esters.
25 lglycerol and its ultrapotent analogues, the phorbol esters.
26 lglycerol and its ultrapotent analogues, the phorbol esters.
27 ated the levels of isozymes that cannot bind phorbol esters.
28 cytes induced to differentiate by calcium or phorbol esters.
29 europeptide signalling and responsiveness to phorbol esters.
30 d in the absence of promoting agents such as phorbol esters.
31 ubiquitination or endocytosis in response to phorbol esters.
32 0 micromol/L) and phorbol myristate acetate (phorbol ester, 10 micromol/L), and inhibited by H-89 (pr
33 sing ex vivo retinal explants, we found that phorbol ester 12-myristate 13-acetate and insulin-like g
34 surface localization of GLUT1 induced by the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA
35 -)/Tg.AC mice exposed to the proinflammatory phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA)
36 on that is reversed with the addition of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA,
37 o extracellular stimuli (serum, EGF, and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate) that
38 an mediate Ras activation in response to the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, a we
39 Forced depletion of Cx43, by tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate, is a
42 and current responses to the TRPV4 agonists phorbol ester 4alpha-phorbol 12,13-didecanoate (4alphaPD
43 dulatory domains, including a diacylglycerol/phorbol ester [4beta-phorbol-12, 13-dibutyrate (PDBu)] b
47 the alpha-subtype of PKC as the mediator of phorbol ester action on FR recycling and provide evidenc
53 ) and erbB2/4-Akt pathways was mimicked by a phorbol ester and blocked by pharmacological inhibition
55 e depressed in mice in vivo and in humans to phorbol ester and calcium ionophore stimulation in vitro
56 re-B cells are inhibited by a combination of phorbol ester and calcium ionophore, agents that bypass
58 gh levels of superoxide when stimulated with phorbol ester and efficiently ingest immunoglobulin (Ig)
59 tained oxidative burst upon stimulation with phorbol ester and fMLP, Gsr-deficient neutrophils displa
62 factor alpha gene expression in response to phorbol ester and ionophore, while signal-responsive gen
64 a and endotoxin) or tumor promoters (such as phorbol ester and okadaic acid), 3-FC suppressed NF-kapp
66 tic cycle in EBV-positive AGS/BX1 cells with phorbol ester and sodium butyrate treatment led to a tra
67 s independent of Src and can be triggered by phorbol esters and 2) agonist-stimulated activation in t
71 in alpha2-chimaerin that restricts access of phorbol esters and DAG, thereby limiting its activation.
72 PKC isozymes and responsible for binding of phorbol esters and diacylglycerol, interact with the Gol
74 otection was enhanced by PKD activation with phorbol esters and limited by PKD inhibition with CID756
75 ometry of ~50% and was strongly increased by phorbol esters and protein phosphatase inhibitors, demon
76 enous Pcyt2 were dramatically increased with phorbol esters and reduced by specific PKC inhibitors.
77 cells undergo apoptosis upon treatment with phorbol esters and related analogs, an effect primarily
80 we used the stimulation of MLP29 cells with phorbol esters and the in vivo activation after partial
81 ta2-chimaerin is that it can be activated by phorbol esters and the lipid second messenger diacylglyc
82 erins possess a C1 domain capable of binding phorbol esters and the lipid second messenger diacylglyc
83 hage-like cells (D-U1) by costimulation with phorbol esters and urokinase-type plasminogen activator.
84 eceptor-mediated signaling pathways (but not phorbol esters) and differs from signaling at plasma mem
85 aB activation induced by lipopolysaccharide, phorbol ester, and cigarette smoke, was also abolished i
86 s (C1A and C1B) that bind diacylglycerol and phorbol ester, and the C2 domain that is responsible for
87 phosphorylated in response to high glucose, phorbol esters, and analogs of cAMP, all key insulin sec
88 promoting function of their potent ligands, phorbol esters, and the prevalence of their mutations.
91 assays to study directional cell migration, phorbol esters are frequently used as a chemotactic agen
93 e second messenger diacylglycerol and of the phorbol esters, are classified as typical (ligand-respon
94 e vesicles for fusion, which are targeted by phorbol esters, are different for the spontaneous and ev
95 if the C1 domains of MRCK are to respond to phorbol ester at concentrations comparable with those th
96 lacental trophoblast cells revealed that the phorbol ester (beta-PMA)-induced phosphorylation of NET
99 th the mutated C1 domains also showed strong phorbol ester binding, albeit modestly weaker than that
103 e gene encoding Munc13-2, which has calcium-/phorbol ester-binding domains and controls presynaptic f
105 rotein kinase C regulator, and plant-derived phorbol esters, but each ligand induces different activi
106 deltaC1a and deltaC1b domains potently bound phorbol esters, but the binding of [(3)H]phorbol 12,13-d
107 ent signaling response to diacylglycerol and phorbol esters by protein kinase C (PKC) and by several
108 ctroscopy, we dissect the contribution of DG/phorbol esters (C1 ligand) and PS in driving the associa
109 -delta, and -epsilon) were down-regulated by phorbol ester, cells remained responsive to FGF2 with Er
116 ab downregulates cell-surface CD33 by 80% in phorbol-ester differentiated U937 cells, at concentratio
117 diacylglycerol (DAG) signaling pathways with phorbol esters dramatically enhances Ca2+-triggered exoc
119 l-length RasGRP2 with the mutated C1 domain, phorbol ester enhanced the ability of the mutated RasGRP
120 equired 50-100-fold higher concentrations of phorbol ester for induction of membrane translocation.
121 activation, as did calcium ionophore A23187, phorbol ester, forskolin, 8-bromo-cyclic AMP, and the Ep
123 inases are major targets for tumor-promoting phorbol esters, G protein-coupled receptors, and activat
126 Na(+)/H(+) exchange activity in response to phorbol esters, growth factors or protein phosphatase in
127 PKC) activators including diacylglycerol and phorbol ester have previously been reported to increase
129 that the activation of viral replication by phorbol ester in latently infected monocytic cells requi
130 he recognition module for diacylglycerol and phorbol esters in protein kinase C, Ras guanine nucleoti
131 decreased effectiveness of DG compared with phorbol esters in retaining the C1 domain on membranes c
133 enylephrine or direct activation of PKC with phorbol ester increased HERG channel protein abundance a
134 ng cells expressing low levels of Wnt5A with phorbol ester increased Snail expression inhibiting PKC
136 on of a melanocyte-lineage signature, drives phorbol ester-independent growth in vitro, and promotes
137 ular production of HOCl when stimulated with phorbol ester, indicating that CF neutrophils had the no
139 ) as well as the protein kinase C activator, phorbol ester, induce rapid phosphorylation of hSphK2 wh
144 e known biological actions of PKD1 including phorbol ester-induced class IIa histone deacetylase 5 nu
146 sphorylation sites (S396A, S402A) were used, phorbol ester-induced desensitization of the calcium res
148 Ets-2 also increased dramatically following phorbol ester-induced differentiation of the v-Myb-trans
149 mechanism to protect cells from ischemia and phorbol ester-induced down-regulation of channel conduct
150 orter degradation fragments and to increased phorbol ester-induced down-regulation, further supportin
151 In cell-based assays, CID755673 blocked phorbol ester-induced endogenous PKD1 activation in LNCa
152 urnover is further slowed in the presence of phorbol ester-induced ERK activation, resulting in Mcl-1
154 a cells was associated with constitutive and phorbol ester-induced expression and secretion of active
155 this report, we show that PKCdelta mediates phorbol ester-induced G1 arrest in lung adenocarcinoma c
156 a unique and critical role in wound healing, phorbol ester-induced hyperplasia, and tumor development
157 UNX-1-containing multiprotein complexes from phorbol ester-induced L8057 murine megakaryoblastic cell
158 miR-34a is strongly up-regulated during phorbol ester-induced megakaryocyte differentiation, but
160 armacologic inhibition of Akt also abrogated phorbol ester-induced O(2)(-) production, which was unaf
165 ely, activation of myosin II or treatment of phorbol ester induces macropinocytosis in the axons and
168 C (PKC) attendant to prolonged activation by phorbol esters is a widely described property of this ke
169 collagen XVII shedding was not stimulated by phorbol esters, known activators of ADAM17, (b) constitu
170 ressing the IL-1 family member, IL-1F6, with phorbol ester leads to an inflammatory condition with ma
171 d stimulation of protein kinase C (PKC) with phorbol esters led to sequestration of recycling endosom
172 rticipation in the action of tumor-promoting phorbol esters like 12-O-tetradecanoylphorbol-13-acetate
174 eration and cell attachment assays displayed phorbol ester-like and/or toxic behavior, including WN-8
175 iated TGF-beta activation can be enhanced by phorbol esters, likely because of the increased activity
177 etic depletion of RINCK had no effect on the phorbol ester-mediated down-regulation and, additionally
178 n of PKC occurs independently of the classic phorbol ester-mediated down-regulation: genetic depletio
179 ucture-function studies of this inhibitor of phorbol ester-mediated ornithine decarboxylase induction
180 infection of fibroblast cells and following phorbol ester-mediated reactivation from a latently infe
190 racellular release of superoxide elicited by phorbol ester or formyl-methionyl-leucyl-phenylalanine (
193 rved that the remnant induced in response to phorbol ester or platelet-derived growth factor has a re
197 and BCL2A1, mediate the apoptotic effect of phorbol esters or the chemotherapeutic agent etoposide i
199 tor molecules constitutively, in response to phorbol esters or through bystander activation by innate
200 with mitochondria following stimulation with phorbol esters or, in L6 myocytes, with insulin via a me
201 i of ectodomain cleavage--hypertonic stress, phorbol ester, or activation of G-protein-coupled recept
202 y, spermatozoa exposed to calcium ionophore, phorbol ester, or H(2)O(2) exhibited superoxide anion pr
203 n with vasoactive intestinal peptide (V) and phorbol ester (P) synergistically activated viral infect
205 o study the complex regulation of NCC by the phorbol ester (PE) 12-O-tetradecanoylphorbol-13-acetate
208 SOCs stimulated by CPA, BAPTA-AM and the phorbol ester phorbol 12,13-dibutyrate (PDBu) were reduc
209 inhibitor chelerythrine and activated by the phorbol ester phorbol 12,13-dibutyrate (PDBu), the diacy
210 f IL-23R was induced by stimulation with the phorbol ester phorbol 12-myristate 13-acetate (PMA), but
211 s in which PKC was directly activated by the phorbol ester phorbol 12-myristate 13-acetate (PMA).
213 d muscarinic receptor mimetic carbachol, the phorbol ester phorbol 12-myristate 13-acetate, the Ca(2+
214 on in B95-8 marmoset lymphoblastoid cells by phorbol ester phorbol-12-myristate-13-acetate (TPA).
215 Activation of protein kinase C (PKC) by the phorbol ester (phorbol 12-myristate 13-acetate) induces
216 lasts displayed increased relative basal and phorbol ester (phorbol 12-myristate 13-acetate)-induced
218 ort that COX-2 expression is up-regulated in phorbol ester (phorbol myristate acetate, PMA)-different
220 increase in NP(o) of SOCs stimulated by the phorbol ester, phorbol 12,13-dibutyrate (PDBu) in inside
222 ort induced by unprocessed PKCs activated by phorbol ester, PKCalpha-CT directly drives HDAC cytosoli
224 r187 in the enhancement of exocytosis by the phorbol ester PMA (phorbol 12-myristate 13-acetate).
226 activation of protein kinase C (PKC) by the phorbol ester PMA has been shown to down-regulate cell s
227 al transactivator region is inducible by the phorbol ester PMA, a potent activator of the protein kin
230 promoter activity was stimulated by IBMX and phorbol ester (PMA) in Raw264.7 monocytes, but only by I
232 regulated in a rapid and transient manner in phorbol ester (PMA)-stimulated B-1a cells, whereas cycli
239 upon sustained stimulation (30-60 min) with phorbol esters, protein kinase C (PKC) alpha and betaII
240 As the predominant cellular receptor for phorbol esters, protein kinase C (PKC) is assumed to pla
242 ucleotide exchange factor and diacylglycerol/phorbol ester receptor expressed in mast cells (MCs) and
244 we found that short-term exposure of CAFs to phorbol esters reduced the number of stress fibers and t
248 ntial homology to that of the diacylglycerol/phorbol ester-responsive C1 domains and has been reporte
249 endently of p53 by activating an alternative phorbol ester-responsive promoter to produce a longer pr
250 Cepsilon (PKCepsilon), a diacyglycerol- and phorbol ester-responsive serine-threonine kinase, has be
257 ion is integrin mediated, but in contrast to phorbol ester-stimulated adhesion, it is not dependent o
258 ping yet distinct from clusters based on the phorbol ester-stimulated B cell reactivation time course
259 during de novo fibroblast infection and upon phorbol ester-stimulated B cell reactivation, highlighti
260 ase activities were successfully detected in phorbol ester-stimulated neutrophils and eosinophils usi
261 CAT-1 ubiquitination and endocytosis in phorbol ester-stimulated porcine aorthic endothelial and
262 ADAM17, even though ADAM17 is essential for phorbol ester-stimulated shedding of these EGFR-ligands.
263 nts, only the C1B domain is required for the phorbol ester-stimulated translocation of PKCdelta to ot
264 h NHERF-1 in live cells that is triggered by phorbol ester stimulation and, importantly, differs stri
265 rsistent activation of PKC family members by phorbol ester stimulation in cells leads to phosphorylat
266 We show that complexinI/II deficiency or phorbol ester stimulation indeed affects responses to hy
268 ancer cells undergo apoptosis in response to phorbol ester stimulation via PKCdelta-mediated release
269 orm in controlling the induction of genes by phorbol ester stimulation, whereas PKCepsilon predominan
271 a) had no apparent effect on the response to phorbol esters, suggesting that the specific position of
272 D (PKD) is a family of novel diacylglycerol/phorbol ester targets that regulate many important cellu
273 latent virus can occur by treatment with the phorbol ester tetradecanoyl phorbol acetate (TPA) or wit
274 the second messenger diacylglycerol and the phorbol esters that is yet poorly characterized, particu
275 nducing agents, like activating cytokines or phorbol esters that stimulate host cell signal transduct
278 nger sn-1,2-diacylglycerol (DAG) and for the phorbol esters, the C1 domain has been an important targ
280 stitutions was reduced in cells treated with phorbol ester to the levels detected in nonstimulated ce
281 veral JNK upstream activators, including the phorbol ester TPA, anisomycin and MAPK kinase kinase-1 (
283 cell rounding and/or decreased apoptosis in phorbol ester-treated LNCaP, LNCaP-C4-2, and MAT-LyLu pr
285 for APP when TACE activity was enhanced via phorbol ester treatment or if APP was modified such that
286 trigger compensation by the other form, and phorbol ester treatment rescued the endocytotic activity
291 down of PHLPP expression reduces the rate of phorbol ester-triggered dephosphorylation of the hydroph
292 mbrane-sensing role of the C2 domain, causes phorbol ester-triggered redistribution of PKCalpha to ot
295 mulated by growth factors or tumor-promoting phorbol esters, we analyzed its role in amino acid-depen
296 lastic and inflammatory responses to topical phorbol ester were significantly suppressed, suggesting
298 e protein kinase C pathway by treatment with phorbol ester, which has been shown previously to result
299 active compounds were identified, including phorbol esters, which likely act through protein kinase
300 lycerol-binding site, such as bryostatin and phorbol esters, which produce prolonged down-regulation,
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