PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 3005408-4 1986 This response, which is also induced by phorbol myristate acetate and lipolysaccharide, is detectable within 1 min of mIg cross-linking and is followed within 4 min by additional translocation of PKCa to a Triton-insoluble particulate compartment. Tetradecanoylphorbol Acetate 40-65 protein kinase C alpha Homo sapiens 196-200 2790038-7 1989 Chronic exposure to TPA resulted in down-regulation of PKC enzyme activity in both cell lines, and a selective decrease in PKC-beta RNA transcripts in both cell types. Tetradecanoylphorbol Acetate 20-23 protein kinase C alpha Homo sapiens 55-58 33760219-0 2021 Bruton"s agammaglobulinemia tyrosine kinase (Btk) regulates TPA-induced breast cancer cell invasion via PLCgamma2/PKCbeta/NF-kappaB/AP-1-dependent matrix metalloproteinase-9 activation. Tetradecanoylphorbol Acetate 60-63 protein kinase C alpha Homo sapiens 114-121 3005408-2 1986 Specifically, the pharmacologic PKC activator phorbol myristate acetate mimics the biologic effects of mIg cross-linking ligands, and cross-linking of membrane Ig (mIg) induces polyphosphoinositide hydrolysis generating diacylglycerol, a potent activator of PKC. Tetradecanoylphorbol Acetate 46-71 protein kinase C alpha Homo sapiens 32-35 33528492-6 2021 Furthermore, we also demonstrated that inhibiting the PKCalpha/ERK signaling pathway reversed the reduction of C7ORF41 in TPA-induced keratinocytes, indicating that C7ORF41 expression could be regulated by upstream PKCalpha/ERK signaling pathway during keratinocyte differentiation. Tetradecanoylphorbol Acetate 122-125 protein kinase C alpha Homo sapiens 54-62 33760219-8 2021 BTK inhibitors [ibrutinib (10 microM), CNX-774 (10 microM)] significantly attenuated TPA-induced cell invasion and migration in MCF-7 cells and inhibited the activation of the phospholipase Cgamma2/PKCbeta signaling pathways. Tetradecanoylphorbol Acetate 85-88 protein kinase C alpha Homo sapiens 198-205 33528492-6 2021 Furthermore, we also demonstrated that inhibiting the PKCalpha/ERK signaling pathway reversed the reduction of C7ORF41 in TPA-induced keratinocytes, indicating that C7ORF41 expression could be regulated by upstream PKCalpha/ERK signaling pathway during keratinocyte differentiation. Tetradecanoylphorbol Acetate 122-125 protein kinase C alpha Homo sapiens 215-223 33443102-7 2021 Finally, we found that silencing of PKCalpha, but not PKCdelta, inhibits phorbol-12-myristate-13-acetate (PMA)-induced cytoplasmic enrichment of KRIT1, suggesting a major role for PKCalpha in regulating KRIT1 nucleocytoplasmic shuttling. Tetradecanoylphorbol Acetate 73-104 protein kinase C alpha Homo sapiens 36-44 33443102-7 2021 Finally, we found that silencing of PKCalpha, but not PKCdelta, inhibits phorbol-12-myristate-13-acetate (PMA)-induced cytoplasmic enrichment of KRIT1, suggesting a major role for PKCalpha in regulating KRIT1 nucleocytoplasmic shuttling. Tetradecanoylphorbol Acetate 73-104 protein kinase C alpha Homo sapiens 180-188 33443102-7 2021 Finally, we found that silencing of PKCalpha, but not PKCdelta, inhibits phorbol-12-myristate-13-acetate (PMA)-induced cytoplasmic enrichment of KRIT1, suggesting a major role for PKCalpha in regulating KRIT1 nucleocytoplasmic shuttling. Tetradecanoylphorbol Acetate 106-109 protein kinase C alpha Homo sapiens 36-44 33443102-7 2021 Finally, we found that silencing of PKCalpha, but not PKCdelta, inhibits phorbol-12-myristate-13-acetate (PMA)-induced cytoplasmic enrichment of KRIT1, suggesting a major role for PKCalpha in regulating KRIT1 nucleocytoplasmic shuttling. Tetradecanoylphorbol Acetate 106-109 protein kinase C alpha Homo sapiens 180-188 30776542-3 2019 To further reveal the mediated mechanism that Nrf2 active state was affected by protein kinase C (PKC), here we evaluated SVCV replication in host cells by treated with a strong activator of PKC phorbol-12-myristate-13-acetate (PMA) and an inhibitor staurosporine. Tetradecanoylphorbol Acetate 228-231 protein kinase C alpha Homo sapiens 98-101 32179476-5 2020 Significantly, activation of PKCalpha with other activating or inflammatory agents, including phorbol 12-myristate 13-acetate and histamine, modulates Golgi structure in a similar fashion. Tetradecanoylphorbol Acetate 94-125 protein kinase C alpha Homo sapiens 29-37 31111899-4 2019 ABCG1 phosphorylation was enhanced by treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C (PKC) activator. Tetradecanoylphorbol Acetate 53-89 protein kinase C alpha Homo sapiens 117-120 32171817-6 2020 Activating PKCalpha with phorbol 12-myristate 13-acetate (PMA), a phorbol ester binds and activates PKCalpha) promoted SCs proliferation and migration. Tetradecanoylphorbol Acetate 25-56 protein kinase C alpha Homo sapiens 11-19 32171817-6 2020 Activating PKCalpha with phorbol 12-myristate 13-acetate (PMA), a phorbol ester binds and activates PKCalpha) promoted SCs proliferation and migration. Tetradecanoylphorbol Acetate 25-56 protein kinase C alpha Homo sapiens 100-108 32171817-6 2020 Activating PKCalpha with phorbol 12-myristate 13-acetate (PMA), a phorbol ester binds and activates PKCalpha) promoted SCs proliferation and migration. Tetradecanoylphorbol Acetate 58-61 protein kinase C alpha Homo sapiens 11-19 32171817-6 2020 Activating PKCalpha with phorbol 12-myristate 13-acetate (PMA), a phorbol ester binds and activates PKCalpha) promoted SCs proliferation and migration. Tetradecanoylphorbol Acetate 58-61 protein kinase C alpha Homo sapiens 100-108 31407399-4 2020 Here we report that the action potential (AP) firing activity of ARC neurons in culture was up-regulated by application of the adenylate cyclase activator forskolin or the PKC activator PMA, and that the forskolin or PMA application-induced up-regulation of AP firing activity could be blocked by pre-application of the SFK inhibitor PP2. Tetradecanoylphorbol Acetate 186-189 protein kinase C alpha Homo sapiens 172-175 31407399-6 2020 Furthermore, we identified that forskolin or PMA application caused increases in the phosphorylation not only in PKAs at T197 or PKCs at S660 and PKCalpha/betaII at T638/641, but also in SFKs at Y416. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 146-154 30645596-4 2019 Phorbol-12-myristate-13-acetate (PMA), a PKCalpha activator, significantly increased the activity and expression of matrix metalloproteinases (MMP) -2 and -9 in human (late outgrowth) EPCs in vitro. Tetradecanoylphorbol Acetate 0-31 protein kinase C alpha Homo sapiens 41-49 31111899-4 2019 ABCG1 phosphorylation was enhanced by treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C (PKC) activator. Tetradecanoylphorbol Acetate 91-94 protein kinase C alpha Homo sapiens 117-120 31111899-5 2019 PKC activation by TPA increased ABCG1 protein levels and promoted ABCG1-dependent cholesterol efflux to HDL. Tetradecanoylphorbol Acetate 18-21 protein kinase C alpha Homo sapiens 0-3 30645596-4 2019 Phorbol-12-myristate-13-acetate (PMA), a PKCalpha activator, significantly increased the activity and expression of matrix metalloproteinases (MMP) -2 and -9 in human (late outgrowth) EPCs in vitro. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 41-49 30645596-11 2019 PMA could activate PKCalpha and promote the angiogenesis capacity of human EPCs via NADPH oxidase-mediated, redox-related, MMP-2 and MMP-9 pathways. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 19-27 30466990-0 2018 Orientin inhibits invasion by suppressing MMP-9 and IL-8 expression via the PKCalpha/ ERK/AP-1/STAT3-mediated signaling pathways in TPA-treated MCF-7 breast cancer cells. Tetradecanoylphorbol Acetate 132-135 protein kinase C alpha Homo sapiens 76-84 30466990-7 2018 TPA-induced membrane translocation of protein kinase C alpha (PKCalpha), phosphorylation of extracellular signal regulated kinase (ERK), and nuclear translocations of activator protein-1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) were downregulated by orientin. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 38-60 30466990-7 2018 TPA-induced membrane translocation of protein kinase C alpha (PKCalpha), phosphorylation of extracellular signal regulated kinase (ERK), and nuclear translocations of activator protein-1 (AP-1) and signal transducer and activator of transcription 3 (STAT3) were downregulated by orientin. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 62-70 30466990-9 2018 CONCLUSION: Orientin inhibits migratory and invasive responses by suppressing MMP-9 and IL-8 expression through mitigation of TPA-induced PKCalpha and ERK activation, as well as the nuclear translocation of AP-1 and STAT3. Tetradecanoylphorbol Acetate 126-129 protein kinase C alpha Homo sapiens 138-146 29452158-8 2018 However, direct activation of PKC by phorbol 12-myristate 13-acetate (PMA) increased the cloned human IKs in HEK293 cells. Tetradecanoylphorbol Acetate 37-68 protein kinase C alpha Homo sapiens 30-33 30133131-6 2018 TPA-induced membrane translocation of PKCalpha, phosphorylation of JNK, and the nuclear translocations of AP-1 and NF-kappaB were downregulated by mLU8C-PU in MCF-7 cells. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 38-46 30133131-8 2018 These results indicate that mLU8C-PU inhibits migratory and invasive responses in MCF-7 breast cancer cells by suppressing MMP-9 and IL-8 expression through mitigating TPA-induced PKCalpha, JNK activation, and the nuclear translocation of AP-1 and NF-kappaB. Tetradecanoylphorbol Acetate 168-171 protein kinase C alpha Homo sapiens 180-188 29452158-8 2018 However, direct activation of PKC by phorbol 12-myristate 13-acetate (PMA) increased the cloned human IKs in HEK293 cells. Tetradecanoylphorbol Acetate 70-73 protein kinase C alpha Homo sapiens 30-33 27717886-4 2017 We observed that PKC activation with tetradecanoylphorbol acetate (TPA) increases the migration and invasion capacity of two human glioblastoma derived human cell lines (U251 MG and U87) and that the treatment with the PR receptor antagonist RU486 blocks these processes. Tetradecanoylphorbol Acetate 37-65 protein kinase C alpha Homo sapiens 17-20 28513986-7 2017 TPA markedly downregulated the expression of PKCalpha, PKCdelta, and PKCepsilon, suggesting that PKCdelta or PKCepsilon activation could contribute to inhibition of glucose transport by FFA. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 45-53 28926616-4 2017 Here, we report that mTORC1 activation by phorbol 12,13-myristate acetate (PMA) requires both classic, cPKC, and novel PKC (nPKC) isoforms, specifically PKCeta, acting through distinct pathways. Tetradecanoylphorbol Acetate 75-78 protein kinase C alpha Homo sapiens 104-107 27717886-4 2017 We observed that PKC activation with tetradecanoylphorbol acetate (TPA) increases the migration and invasion capacity of two human glioblastoma derived human cell lines (U251 MG and U87) and that the treatment with the PR receptor antagonist RU486 blocks these processes. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 17-20 28008134-8 2017 Activating PKC-alpha and EGFR directly with the combination of phorbol 12-myristate 13-acetate (PMA) and EGF potentiated MMP1 gene and protein expression, and cell invasion. Tetradecanoylphorbol Acetate 63-94 protein kinase C alpha Homo sapiens 11-20 26033110-4 2015 PKC activation by phorbol 12-myristate 13-acetate causes cortactin phosphorylation, filopodial retraction and F-actin-bundle loss. Tetradecanoylphorbol Acetate 18-49 protein kinase C alpha Homo sapiens 0-3 26769967-2 2016 However, studies with pharmacological agonists (e.g. phorbol 12-myristate 13-acetate (PMA)) indicate that prolonged stimulation leads to PKCalpha desensitization via dephosphorylation and/or degradation. Tetradecanoylphorbol Acetate 53-84 protein kinase C alpha Homo sapiens 137-145 26769967-2 2016 However, studies with pharmacological agonists (e.g. phorbol 12-myristate 13-acetate (PMA)) indicate that prolonged stimulation leads to PKCalpha desensitization via dephosphorylation and/or degradation. Tetradecanoylphorbol Acetate 86-89 protein kinase C alpha Homo sapiens 137-145 29911380-8 2017 In addition, knockdown of PKCalpha, NF-kappaB or PXR can significantly attenuate PMA-induced P-gp suppression. Tetradecanoylphorbol Acetate 81-84 protein kinase C alpha Homo sapiens 26-34 26912086-2 2016 Upon TPA treatment, protein kinase C (PKC) alpha and PKCbeta1 exerted differential effects on the nuclear translocation of cytoplasmic pErk1/2, a protein which maintains senescence. Tetradecanoylphorbol Acetate 5-8 protein kinase C alpha Homo sapiens 20-48 26912086-6 2016 Thus, PKCalpha downregulation is accompanied by in vivo cell proliferation, as evidenced in 7, 12-dimethylbenz(a)anthracene (DMBA)-TPA-mediated carcinogenesis. Tetradecanoylphorbol Acetate 131-134 protein kinase C alpha Homo sapiens 6-14 26912086-7 2016 The ability of TPA to reverse senescence was further demonstrated in old HDF cells using RNA-sequencing analyses in which TPA-induced nuclear PKCalpha degradation freed nuclear pErk1/2 to induce cell proliferation and facilitated the recovery of mitochondrial energy metabolism. Tetradecanoylphorbol Acetate 15-18 protein kinase C alpha Homo sapiens 142-150 26912086-7 2016 The ability of TPA to reverse senescence was further demonstrated in old HDF cells using RNA-sequencing analyses in which TPA-induced nuclear PKCalpha degradation freed nuclear pErk1/2 to induce cell proliferation and facilitated the recovery of mitochondrial energy metabolism. Tetradecanoylphorbol Acetate 122-125 protein kinase C alpha Homo sapiens 142-150 26912086-9 2016 Loss of PKCalpha expression following TPA treatment reduces pErk1/2-activated SP1 biding to the p21(WAF1) gene promoter, thus preventing senescence onset and overcoming G1/S cell cycle arrest in senescent cells. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 8-16 26796274-4 2016 The short term exposure (3 days) of MCF-7 cells to TPA exhibited significant induction of Wnt5a expression, along with the enhanced expression of PKC-alpha, to promote cell migration, which suggested that activation of noncanonical Wnt signaling pathway is associated with PKC-alpha. Tetradecanoylphorbol Acetate 51-54 protein kinase C alpha Homo sapiens 146-155 26796274-4 2016 The short term exposure (3 days) of MCF-7 cells to TPA exhibited significant induction of Wnt5a expression, along with the enhanced expression of PKC-alpha, to promote cell migration, which suggested that activation of noncanonical Wnt signaling pathway is associated with PKC-alpha. Tetradecanoylphorbol Acetate 51-54 protein kinase C alpha Homo sapiens 273-282 26542395-6 2016 Currents demonstrated outward rectification and reversal at 0 mV (properties consistent with TMEM16A) and were inhibited by either molecular (siRNA) or pharmacologic (PMA or Go6976) inhibition of PKCalpha. Tetradecanoylphorbol Acetate 167-170 protein kinase C alpha Homo sapiens 196-204 27771709-9 2016 RESULTS: The percentage of RBCs showing PS exposure after activation with LPA, PMA, or A23187 is significantly reduced after inhibition of the scramblase using the specific inhibitor R5421 as well as after the inhibition of the PKCalpha using chelerythrine chloride or calphostin C. Tetradecanoylphorbol Acetate 79-82 protein kinase C alpha Homo sapiens 228-236 26717978-8 2016 The results indicated that the PJT-mediated inhibition of TPA-induced MMP-9 expression and cell invasion involved the suppression of the PKCalpha/NF-kappaB pathway in MCF-7 cells. Tetradecanoylphorbol Acetate 58-61 protein kinase C alpha Homo sapiens 137-145 26404773-8 2015 In contrast, activation of the PKC system by phorbol 12-myristate 13-acetate (PMA) exerted inhibitory actions on TRPC6 and suppressed its expression. Tetradecanoylphorbol Acetate 45-76 protein kinase C alpha Homo sapiens 31-34 26404773-8 2015 In contrast, activation of the PKC system by phorbol 12-myristate 13-acetate (PMA) exerted inhibitory actions on TRPC6 and suppressed its expression. Tetradecanoylphorbol Acetate 78-81 protein kinase C alpha Homo sapiens 31-34 26404773-9 2015 Importantly, PMA treatment markedly down-regulated the expression levels of PKCalpha, PKCbeta, and PKCeta reflecting their activation. Tetradecanoylphorbol Acetate 13-16 protein kinase C alpha Homo sapiens 76-84 26101063-0 2015 Fisetin regulates TPA-induced breast cell invasion by suppressing matrix metalloproteinase-9 activation via the PKC/ROS/MAPK pathways. Tetradecanoylphorbol Acetate 18-21 protein kinase C alpha Homo sapiens 112-115 26096873-7 2015 Using these parameters, we present an example of sequential fluorescence and bioluminescence microscopic observation of signal transduction (translocation of protein kinase C alpha from the cytoplasm to the plasma membrane) coupled with activation of gene expression by nuclear factor of kappa light polypeptide B in individual cells and show that the gene expression response is not completely concordant with upstream signaling following stimulation with phorbol-12-myristate-13-acetate. Tetradecanoylphorbol Acetate 457-488 protein kinase C alpha Homo sapiens 158-180 26222138-10 2015 Taken together, our results suggest that the NRF2 system functions to suppress PMA-stimulated U937 cell differentiation into pro-inflammatory macrophages and provide evidence that the ROS-PKCalpha-ERK-NFkB axis is involved in PMA-facilitated differentiation of NRF2-silenced U937 cells. Tetradecanoylphorbol Acetate 79-82 protein kinase C alpha Homo sapiens 188-196 25514083-5 2015 Silencing or inhibition of PKCalpha and PKCdelta blocked PR phosphorylation and degradation induced by TPA. Tetradecanoylphorbol Acetate 103-106 protein kinase C alpha Homo sapiens 27-35 25514083-6 2015 Both PR isoforms were associated with PKCalpha and reached the maximum association after 5 minutes of TPA addition. Tetradecanoylphorbol Acetate 102-105 protein kinase C alpha Homo sapiens 38-46 25514083-7 2015 These data correlated with immunnofluorescence assays in which nuclear colocalization of PKCalpha with PR increased after TPA treatment. Tetradecanoylphorbol Acetate 122-125 protein kinase C alpha Homo sapiens 89-97 24464434-0 2014 Roles of PKC Isoforms in PMA-Induced Modulation of the hERG Channel (Kv11.1). Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 9-12 25698902-0 2015 Galangin, a novel dietary flavonoid, attenuates metastatic feature via PKC/ERK signaling pathway in TPA-treated liver cancer HepG2 cells. Tetradecanoylphorbol Acetate 100-103 protein kinase C alpha Homo sapiens 71-74 25698902-5 2015 We also observed through a Western blotting assay that galangin strongly inhibited the TPA-induced protein expressions of protein kinase Calpha (PKCalpha), protein kinase Cdelta (PKCdelta), phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), the phospho-inhibitor of kappaBalpha (phospho-IkappaBalpha), c-Fos, c-Jun, and nuclear factor kappa B (NF-kappaB). Tetradecanoylphorbol Acetate 87-90 protein kinase C alpha Homo sapiens 122-154 25698902-7 2015 CONCLUSIONS: The results revealed that galangin effectively inhibited the TPA-induced invasion and migration of HepG2 cells through a protein kinase C/extracellular signal-regulated kinase (PKC/ERK) pathway. Tetradecanoylphorbol Acetate 74-77 protein kinase C alpha Homo sapiens 190-193 24461294-7 2014 Conversely, PKC promoter phorbol 12-myristate 13-acetate (PMA) and JNK inhibitor SP600125 reversed the cleavages of caspase 3 and PARP induced by GA in NCI-H460 cells. Tetradecanoylphorbol Acetate 25-56 protein kinase C alpha Homo sapiens 12-15 24604087-8 2014 These results indicate that decursin-mediated inhibition of TPA-induced MMP-9 expression and cell invasion involves the suppression of the PKCalpha, MAPK and NF-kappaB pathways in MCF-7 cells. Tetradecanoylphorbol Acetate 60-63 protein kinase C alpha Homo sapiens 139-147 24682423-5 2014 Activation of PKC with phorbol 12-myristate 13-acetate (PMA) resulted in a strong reduction of Kv1.5/Kvbeta1.2 current. Tetradecanoylphorbol Acetate 23-54 protein kinase C alpha Homo sapiens 14-17 24682423-5 2014 Activation of PKC with phorbol 12-myristate 13-acetate (PMA) resulted in a strong reduction of Kv1.5/Kvbeta1.2 current. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 14-17 24138399-5 2014 A total of 300 heterocyclic compounds with 70% similarity to phorbol 12-myristate 13-acetate (PMA) were selected, and virtual docking was performed with PKC-alpha as target. Tetradecanoylphorbol Acetate 94-97 protein kinase C alpha Homo sapiens 153-162 24138399-8 2014 In addition, as these compounds showed better binding than PMA, more interaction with PKC residues (hydrogen bonding and hydrophobic), and the top five hit molecules was potent enough to abolish carcinogenic effects of PMA. Tetradecanoylphorbol Acetate 59-62 protein kinase C alpha Homo sapiens 86-89 24604087-0 2014 Decursin prevents TPA-induced invasion through suppression of PKCalpha/p38/NF-kappaB-dependent MMP-9 expression in MCF-7 human breast carcinoma cells. Tetradecanoylphorbol Acetate 18-21 protein kinase C alpha Homo sapiens 62-70 24604087-7 2014 Furthermore, decursin repressed the TPA-induced phosphorylation of p38 MAPK and inhibited TPA-induced translocation of PKCalpha from the cytosol to the membrane, but did not affect the translocation of PKCdelta. Tetradecanoylphorbol Acetate 90-93 protein kinase C alpha Homo sapiens 119-127 24461294-7 2014 Conversely, PKC promoter phorbol 12-myristate 13-acetate (PMA) and JNK inhibitor SP600125 reversed the cleavages of caspase 3 and PARP induced by GA in NCI-H460 cells. Tetradecanoylphorbol Acetate 58-61 protein kinase C alpha Homo sapiens 12-15 24239722-1 2014 The role of protein kinase C (PKC) isozymes in phorbol myristate acetate (PMA)-induced sphingosine 1-phosphate (S1P) receptor 1 (S1P1) phosphorylation was studied. Tetradecanoylphorbol Acetate 47-72 protein kinase C alpha Homo sapiens 30-33 24239722-1 2014 The role of protein kinase C (PKC) isozymes in phorbol myristate acetate (PMA)-induced sphingosine 1-phosphate (S1P) receptor 1 (S1P1) phosphorylation was studied. Tetradecanoylphorbol Acetate 74-77 protein kinase C alpha Homo sapiens 30-33 24239722-7 2014 Additionally, expression of dominant-negative mutants of PKC alpha or beta and knockdown of these isozymes using short hairpin RNA, markedly attenuated PMA-induced S1P1 phosphorylation. Tetradecanoylphorbol Acetate 152-155 protein kinase C alpha Homo sapiens 57-66 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 82-107 protein kinase C alpha Homo sapiens 33-36 24447339-2 2014 Phorbol 12-myristate 13-acetate (PMA), a well-known PKC activator, increases the cytotoxicity of several anticancer drugs. Tetradecanoylphorbol Acetate 0-31 protein kinase C alpha Homo sapiens 52-55 24447339-2 2014 Phorbol 12-myristate 13-acetate (PMA), a well-known PKC activator, increases the cytotoxicity of several anticancer drugs. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 52-55 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 277-280 protein kinase C alpha Homo sapiens 167-175 24672638-6 2014 Western blot analysis documented that resveratrol in concentrations of 10 and 100 muM significantly decreased PMA-induced phosphorylation of PKC alpha/beta II. Tetradecanoylphorbol Acetate 110-113 protein kinase C alpha Homo sapiens 141-158 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 82-107 protein kinase C alpha Homo sapiens 73-76 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 82-107 protein kinase C alpha Homo sapiens 167-175 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 82-107 protein kinase C alpha Homo sapiens 73-76 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 82-107 protein kinase C alpha Homo sapiens 167-175 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 33-36 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 73-76 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 167-175 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 73-76 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 167-175 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 277-280 protein kinase C alpha Homo sapiens 33-36 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 277-280 protein kinase C alpha Homo sapiens 136-144 24260363-4 2013 Here, we showed that interfering PKC expression by chronic activation of PKC with phorbol myristate acetate (PMA) or shRNA targeting at PKCalpha lowered the levels of PKCalpha in cytosol, peripheral membrane and integral membrane pools, while short-term activation of PKC with PMA induced accumulation of PKCalpha in the membrane pool accompanied by a dramatic decrease in the cytosol fraction. Tetradecanoylphorbol Acetate 277-280 protein kinase C alpha Homo sapiens 167-175 23937324-6 2013 Moreover, using a yeast-based assay previously developed for the screening of PKC inhibitors, it was also shown that, like the known PKC inhibitor NPC 15437, ceramide reduced the PMA-induced growth inhibition, supporting an inhibitory effect of ceramide on PKCdelta. Tetradecanoylphorbol Acetate 179-182 protein kinase C alpha Homo sapiens 78-81 23804203-5 2013 In contrast, activation of PKC with phorbol 12-myristate 13-acetate mimicked the inhibitory effect of REV on K(v)2.2 by modifying the activation or inactivation properties of Kv2.2 channels and eliminated any further inhibition by REV. Tetradecanoylphorbol Acetate 36-67 protein kinase C alpha Homo sapiens 27-30 23937324-6 2013 Moreover, using a yeast-based assay previously developed for the screening of PKC inhibitors, it was also shown that, like the known PKC inhibitor NPC 15437, ceramide reduced the PMA-induced growth inhibition, supporting an inhibitory effect of ceramide on PKCdelta. Tetradecanoylphorbol Acetate 179-182 protein kinase C alpha Homo sapiens 133-136 23430963-4 2013 We observed that, in human neutrophils, calcium ionophore induced histone deimination, whereas phorbol myristate acetate (PMA), an activator of protein kinase C (PKC), suppressed ionophore-induced deimination. Tetradecanoylphorbol Acetate 95-120 protein kinase C alpha Homo sapiens 162-165 23536578-8 2013 In Nanog-expressing human embryonal carcinoma cell lines, NT2/D1 and NCCIT, Nanog expression was suppressed by exposure to PKC activator Phorbol-12-myristate-13-acetate (PMA). Tetradecanoylphorbol Acetate 137-168 protein kinase C alpha Homo sapiens 123-126 23536578-8 2013 In Nanog-expressing human embryonal carcinoma cell lines, NT2/D1 and NCCIT, Nanog expression was suppressed by exposure to PKC activator Phorbol-12-myristate-13-acetate (PMA). Tetradecanoylphorbol Acetate 170-173 protein kinase C alpha Homo sapiens 123-126 23114726-0 2013 Suppression of 12-O-tetradecanoylphorbol-13-acetate-induced MCF-7 breast adenocarcinoma cells invasion/migration by alpha-tomatine through activating PKCalpha/ERK/NF-kappaB-dependent MMP-2/MMP-9 expressions. Tetradecanoylphorbol Acetate 15-51 protein kinase C alpha Homo sapiens 150-158 23114726-4 2013 Data also showed alpha-tomatine could inhibit the activation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and protein kinase C-alpha (PKCalpha) involved in the downregulation of the enzyme activities and messenger RNA levels of matrix metalloproteinase-2/9 (MMP-2/MMP-9) induced by TPA. Tetradecanoylphorbol Acetate 295-298 protein kinase C alpha Homo sapiens 147-155 23114726-6 2013 In addition, TPA-induced translocation of PKC-alpha from cytosol to membranes, and suppression of TPA elicited the expression of PKC-alpha by adding the PKC-alpha inhibitors, GF-109203X and Go-6983. Tetradecanoylphorbol Acetate 13-16 protein kinase C alpha Homo sapiens 42-51 23114726-6 2013 In addition, TPA-induced translocation of PKC-alpha from cytosol to membranes, and suppression of TPA elicited the expression of PKC-alpha by adding the PKC-alpha inhibitors, GF-109203X and Go-6983. Tetradecanoylphorbol Acetate 13-16 protein kinase C alpha Homo sapiens 129-138 23114726-6 2013 In addition, TPA-induced translocation of PKC-alpha from cytosol to membranes, and suppression of TPA elicited the expression of PKC-alpha by adding the PKC-alpha inhibitors, GF-109203X and Go-6983. Tetradecanoylphorbol Acetate 13-16 protein kinase C alpha Homo sapiens 129-138 23114726-6 2013 In addition, TPA-induced translocation of PKC-alpha from cytosol to membranes, and suppression of TPA elicited the expression of PKC-alpha by adding the PKC-alpha inhibitors, GF-109203X and Go-6983. Tetradecanoylphorbol Acetate 98-101 protein kinase C alpha Homo sapiens 129-138 23114726-6 2013 In addition, TPA-induced translocation of PKC-alpha from cytosol to membranes, and suppression of TPA elicited the expression of PKC-alpha by adding the PKC-alpha inhibitors, GF-109203X and Go-6983. Tetradecanoylphorbol Acetate 98-101 protein kinase C alpha Homo sapiens 129-138 23430963-4 2013 We observed that, in human neutrophils, calcium ionophore induced histone deimination, whereas phorbol myristate acetate (PMA), an activator of protein kinase C (PKC), suppressed ionophore-induced deimination. Tetradecanoylphorbol Acetate 122-125 protein kinase C alpha Homo sapiens 162-165 23430963-6 2013 In addition, a peptide inhibitor of PKCalpha superinduced ionophore activation of PAD4, thus identifying PKCalpha as the PMA-induced inhibitor of PAD4. Tetradecanoylphorbol Acetate 121-124 protein kinase C alpha Homo sapiens 36-44 23430963-6 2013 In addition, a peptide inhibitor of PKCalpha superinduced ionophore activation of PAD4, thus identifying PKCalpha as the PMA-induced inhibitor of PAD4. Tetradecanoylphorbol Acetate 121-124 protein kinase C alpha Homo sapiens 105-113 21705328-0 2011 Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively. Tetradecanoylphorbol Acetate 43-79 protein kinase C alpha Homo sapiens 35-38 22583821-2 2012 CNP mRNA is up-regulated in human vascular smooth muscle cells (SMC) by PDGF-BB via a protein kinase C (PKC)-dependent pathways, and by general PKC activation with phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 164-189 protein kinase C alpha Homo sapiens 144-147 22583821-2 2012 CNP mRNA is up-regulated in human vascular smooth muscle cells (SMC) by PDGF-BB via a protein kinase C (PKC)-dependent pathways, and by general PKC activation with phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 191-194 protein kinase C alpha Homo sapiens 144-147 22583821-10 2012 A 8-10-fold greater PMA-induced increase in CNP transcript in SMC than in HAEC suggests that smooth muscle cells could be selectively targeted for CNP up-regulation by PKC-alpha- and PKC-delta-activators. Tetradecanoylphorbol Acetate 20-23 protein kinase C alpha Homo sapiens 168-177 22299029-1 2012 We have previously shown that TPA activates HTLV-1 LTR in Jurkat T-cells by inducing the binding of Sp1-p53 complex to the Sp1 site residing within the Ets responsive region 1 (ERR-1) of the LTR and that this activation is inhibited by PKCalpha and PKCepsilon. Tetradecanoylphorbol Acetate 30-33 protein kinase C alpha Homo sapiens 236-244 22160590-8 2011 All such changes after TPA treatment were prevented by inhibitors of panPKC and PKCalpha. Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 69-88 21842414-9 2011 Taken together, ROS mediated cross talk of PKC and integrin for migration of HepG2 induced by TPA. Tetradecanoylphorbol Acetate 94-97 protein kinase C alpha Homo sapiens 43-46 22921746-0 2012 Curcumin suppresses the TPA-induced invasion through inhibition of PKCalpha-dependent MMP-expression in MCF-7 human breast cancer cells. Tetradecanoylphorbol Acetate 24-27 protein kinase C alpha Homo sapiens 67-75 22921746-6 2012 Also, curcumin strongly repressed the TPA-induced phosphorylation of p38 and JNK and inhibited TPA-induced translocation of PKCalpha from the cytosol to the membrane, but did not affect the translocation of PKCdelta. Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 124-132 22921746-7 2012 These results indicate that curcumin-mediated inhibition of TPA-induced MMP-9 expression and cell invasion involves the suppression of the PKCalpha, MAPK and NF-kappaB/AP-1 pathway in MCF-7 cells. Tetradecanoylphorbol Acetate 60-63 protein kinase C alpha Homo sapiens 139-147 22892130-5 2012 Several PKC activators, including phorbol 12,13-dibutyrate, 12-O-tetradecanoylphorbol-13-acetate and indolactam V caused upregulation of PKCeta, whereas the general PKC inhibitor Go 6983, but not the conventional PKC inhibitor Go 6976 led to the downregulation of PKCeta. Tetradecanoylphorbol Acetate 60-96 protein kinase C alpha Homo sapiens 8-11 22892130-5 2012 Several PKC activators, including phorbol 12,13-dibutyrate, 12-O-tetradecanoylphorbol-13-acetate and indolactam V caused upregulation of PKCeta, whereas the general PKC inhibitor Go 6983, but not the conventional PKC inhibitor Go 6976 led to the downregulation of PKCeta. Tetradecanoylphorbol Acetate 60-96 protein kinase C alpha Homo sapiens 137-140 22892130-5 2012 Several PKC activators, including phorbol 12,13-dibutyrate, 12-O-tetradecanoylphorbol-13-acetate and indolactam V caused upregulation of PKCeta, whereas the general PKC inhibitor Go 6983, but not the conventional PKC inhibitor Go 6976 led to the downregulation of PKCeta. Tetradecanoylphorbol Acetate 60-96 protein kinase C alpha Homo sapiens 137-140 22381172-0 2012 Berberine suppresses the TPA-induced MMP-1 and MMP-9 expressions through the inhibition of PKC-alpha in breast cancer cells. Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 91-100 22381172-11 2012 In addition, the TPA-induced MMP-1 and MMP-9 expressions were completely decreased by Go6983 and PKC-alpha siRNA, respectively. Tetradecanoylphorbol Acetate 17-20 protein kinase C alpha Homo sapiens 97-106 22381172-12 2012 TPA-induced PKC-alpha phosphorylation was dose-dependently decreased by BBR treatment. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 12-21 22381172-13 2012 CONCLUSION: The TPA-induced PKC-alpha phosphorylation is suppressed and then the MMP-1 and MMP-9 expressions are also inhibited by berberine. Tetradecanoylphorbol Acetate 16-19 protein kinase C alpha Homo sapiens 28-37 21923556-5 2012 Treatment with phorbol 12-myristate 13-acetate (PMA) for 30 min (short-term) activated Erk1/2, whereas 12 h (long-term) PMA treatment abrogated PKCalpha, reduced Erk1/2 activation and significantly increased cell death under OGD. Tetradecanoylphorbol Acetate 120-123 protein kinase C alpha Homo sapiens 144-152 22988493-5 2012 In contrast to this observation, but in keeping with literature, PKC activation by phorbol-12-myristate-13-acetate (PMA) also led to the expression of senescence markers. Tetradecanoylphorbol Acetate 83-114 protein kinase C alpha Homo sapiens 65-68 22988493-5 2012 In contrast to this observation, but in keeping with literature, PKC activation by phorbol-12-myristate-13-acetate (PMA) also led to the expression of senescence markers. Tetradecanoylphorbol Acetate 116-119 protein kinase C alpha Homo sapiens 65-68 22988493-6 2012 We explain this antithesis by demonstrating that PMA-treated cells show reduction in the activity of PKC alpha, thereby simulating inhibition. Tetradecanoylphorbol Acetate 49-52 protein kinase C alpha Homo sapiens 101-110 22299029-0 2012 Differential role of PKC-induced c-Jun in HTLV-1 LTR activation by 12-O-tetradecanoylphorbol-13-acetate in different human T-cell lines. Tetradecanoylphorbol Acetate 67-103 protein kinase C alpha Homo sapiens 21-24 22001118-7 2011 While the PKC agonist, PMA, did not affect GR internalization when tested alone, it increased glucagon-mediated GR internalization by 25-40% in GR-expressing HEK-293 cells (HEK-GR cells). Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 10-13 21842414-3 2011 Using human hepatoma HepG2 as a model, we have found reactive oxygen species (ROS) may cooperate with protein kinase C (PKC) for sustained ERK phosphorylation and migration of HepG2 induced by 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 193-230 protein kinase C alpha Homo sapiens 120-123 21842414-3 2011 Using human hepatoma HepG2 as a model, we have found reactive oxygen species (ROS) may cooperate with protein kinase C (PKC) for sustained ERK phosphorylation and migration of HepG2 induced by 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 232-235 protein kinase C alpha Homo sapiens 120-123 21842414-5 2011 Various antagonists of integrin signaling prevented TPA-induced activation of ERK and PKC, ROS generation and migration of HepG2. Tetradecanoylphorbol Acetate 52-55 protein kinase C alpha Homo sapiens 86-89 21903576-5 2011 SSeCKS-null mouse embryo fibroblasts displayed increased relative basal and phorbol ester (phorbol 12-myristate 13-acetate)-induced PKC activity but were defective in phorbol 12-myristate 13-acetate-induced actin cytoskeletal reorganization and cell shape change; these responses could be rescued by the forced expression of full-length SSeCKS but not by an SSeCKS variant deleted of its PKC-binding domains. Tetradecanoylphorbol Acetate 91-122 protein kinase C alpha Homo sapiens 132-135 21624785-7 2011 Because we had previously shown that PMA-mediated augmentation of I(NMDA) of NMDARs expressed in these cells is by activation of PKCalpha, we assessed the effect of ethanol (1, 10, 50, and 100 mM) on PKCalpha activity. Tetradecanoylphorbol Acetate 37-40 protein kinase C alpha Homo sapiens 129-137 21624785-7 2011 Because we had previously shown that PMA-mediated augmentation of I(NMDA) of NMDARs expressed in these cells is by activation of PKCalpha, we assessed the effect of ethanol (1, 10, 50, and 100 mM) on PKCalpha activity. Tetradecanoylphorbol Acetate 37-40 protein kinase C alpha Homo sapiens 200-208 21624785-9 2011 The data suggest that ethanol disruption of PMA-mediated augmentation of I(NMDA) may be due to a decrease in PKCalpha activity by ethanol. Tetradecanoylphorbol Acetate 44-47 protein kinase C alpha Homo sapiens 109-117 21705328-0 2011 Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively. Tetradecanoylphorbol Acetate 43-79 protein kinase C alpha Homo sapiens 178-187 21705328-0 2011 Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively. Tetradecanoylphorbol Acetate 43-79 protein kinase C alpha Homo sapiens 178-181 21705328-0 2011 Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively. Tetradecanoylphorbol Acetate 81-84 protein kinase C alpha Homo sapiens 35-38 21705328-0 2011 Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively. Tetradecanoylphorbol Acetate 81-84 protein kinase C alpha Homo sapiens 178-187 21705328-0 2011 Dual function of protein kinase C (PKC) in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced manganese superoxide dismutase (MnSOD) expression: activation of CREB and FOXO3a by PKC-alpha phosphorylation and by PKC-mediated inactivation of Akt, respectively. Tetradecanoylphorbol Acetate 81-84 protein kinase C alpha Homo sapiens 178-181 21705328-1 2011 12-O-tetradecanoylphorbol-13-acetate (TPA) has been shown to induce transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA in human lung carcinoma cells, A549, mediated by a protein kinase C (PKC)-dependent activation of cAMP-responsive element-binding protein (CREB)-1/ATF-1-like factors. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 217-220 21705328-1 2011 12-O-tetradecanoylphorbol-13-acetate (TPA) has been shown to induce transcriptional activation of human manganese superoxide dismutase (MnSOD) mRNA in human lung carcinoma cells, A549, mediated by a protein kinase C (PKC)-dependent activation of cAMP-responsive element-binding protein (CREB)-1/ATF-1-like factors. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 217-220 21705328-3 2011 TPA-induced generation of reactive oxygen species (ROS) was blocked by pretreatment of the PKC inhibitor BIM and NADPH oxidase inhibitor DPI. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 91-94 21705328-5 2011 To identify the PKC isozyme involved, we used a sod2 gene response reporter plasmid, pSODLUC-3340-I2E-C, capable of sensing the effect of TNF-alpha and TPA, to monitor the effects of PKC isozyme-specific inhibitors and siRNA-induced knockdown of specific PKC isozyme. Tetradecanoylphorbol Acetate 152-155 protein kinase C alpha Homo sapiens 16-19 21705328-6 2011 Our data indicate that TPA-induced MnSOD expression was independent of p53 and most likely mediated by PKC-alpha-, and -epsilon-dependent signaling pathways. Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 103-112 21705328-8 2011 Together, our results revealed that TPA up-regulates, in part, two PKC-dependent transcriptional pathways to induce MnSOD expression. Tetradecanoylphorbol Acetate 36-39 protein kinase C alpha Homo sapiens 67-70 21375937-2 2011 METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to determine the expressions of protein kinase Calpha (PKCalpha) and multidrug resistance-related genes ABCG2, ABCC1, MDR1, and P-glycoprotein (P-gp) in MCF-7Taxol cells after treatment with chelerythrine and phorbol-12-myristate-13-acetate (PMA). Tetradecanoylphorbol Acetate 302-333 protein kinase C alpha Homo sapiens 125-146 21381080-2 2011 The stomach isoform of Cldn18, Cldn18a2 is regulated via a PKC/MAPK/AP-1-dependent pathway in PKC activator 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated gastric cancer cells. Tetradecanoylphorbol Acetate 108-144 protein kinase C alpha Homo sapiens 59-62 21381080-2 2011 The stomach isoform of Cldn18, Cldn18a2 is regulated via a PKC/MAPK/AP-1-dependent pathway in PKC activator 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated gastric cancer cells. Tetradecanoylphorbol Acetate 146-149 protein kinase C alpha Homo sapiens 59-62 21381080-6 2011 The upregulation of Cldn18 by TPA in human pancreatic cancer cell lines was prevented by inhibitors of PKCdelta, PKCepsilon, and PKCalpha, whereas the upregulation of Cldn18 by TPA in hTERT-HPDE cells was prevented by inhibitors of PKCdelta, PKCtheta, and PKCalpha. Tetradecanoylphorbol Acetate 30-33 protein kinase C alpha Homo sapiens 129-137 21381080-6 2011 The upregulation of Cldn18 by TPA in human pancreatic cancer cell lines was prevented by inhibitors of PKCdelta, PKCepsilon, and PKCalpha, whereas the upregulation of Cldn18 by TPA in hTERT-HPDE cells was prevented by inhibitors of PKCdelta, PKCtheta, and PKCalpha. Tetradecanoylphorbol Acetate 30-33 protein kinase C alpha Homo sapiens 256-264 21354279-7 2011 Furthermore, piperine strongly repressed the PMA-induced phosphorylation of ERK, which are dependent on the PKCalpha pathway. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 108-116 21062642-2 2011 In HEK293 and Jurkat cells, the Ca2(+) release and Ca2(+) uptake stimulated by several different activators were attenuated by activation of PKC with phorbol myristate acetate (PMA) or 1-oleoyl-2-acetyl-sn-glycerol (OAG) and potentiated by PKC inhibition with Go6983 or knockdown of PKCalpha or PKCbeta using shRNA. Tetradecanoylphorbol Acetate 150-175 protein kinase C alpha Homo sapiens 141-144 21062642-2 2011 In HEK293 and Jurkat cells, the Ca2(+) release and Ca2(+) uptake stimulated by several different activators were attenuated by activation of PKC with phorbol myristate acetate (PMA) or 1-oleoyl-2-acetyl-sn-glycerol (OAG) and potentiated by PKC inhibition with Go6983 or knockdown of PKCalpha or PKCbeta using shRNA. Tetradecanoylphorbol Acetate 150-175 protein kinase C alpha Homo sapiens 240-243 21062642-2 2011 In HEK293 and Jurkat cells, the Ca2(+) release and Ca2(+) uptake stimulated by several different activators were attenuated by activation of PKC with phorbol myristate acetate (PMA) or 1-oleoyl-2-acetyl-sn-glycerol (OAG) and potentiated by PKC inhibition with Go6983 or knockdown of PKCalpha or PKCbeta using shRNA. Tetradecanoylphorbol Acetate 150-175 protein kinase C alpha Homo sapiens 283-291 21062642-2 2011 In HEK293 and Jurkat cells, the Ca2(+) release and Ca2(+) uptake stimulated by several different activators were attenuated by activation of PKC with phorbol myristate acetate (PMA) or 1-oleoyl-2-acetyl-sn-glycerol (OAG) and potentiated by PKC inhibition with Go6983 or knockdown of PKCalpha or PKCbeta using shRNA. Tetradecanoylphorbol Acetate 177-180 protein kinase C alpha Homo sapiens 141-144 21062642-2 2011 In HEK293 and Jurkat cells, the Ca2(+) release and Ca2(+) uptake stimulated by several different activators were attenuated by activation of PKC with phorbol myristate acetate (PMA) or 1-oleoyl-2-acetyl-sn-glycerol (OAG) and potentiated by PKC inhibition with Go6983 or knockdown of PKCalpha or PKCbeta using shRNA. Tetradecanoylphorbol Acetate 177-180 protein kinase C alpha Homo sapiens 240-243 21062642-2 2011 In HEK293 and Jurkat cells, the Ca2(+) release and Ca2(+) uptake stimulated by several different activators were attenuated by activation of PKC with phorbol myristate acetate (PMA) or 1-oleoyl-2-acetyl-sn-glycerol (OAG) and potentiated by PKC inhibition with Go6983 or knockdown of PKCalpha or PKCbeta using shRNA. Tetradecanoylphorbol Acetate 177-180 protein kinase C alpha Homo sapiens 283-291 21354279-0 2011 Suppression of phorbol-12-myristate-13-acetate-induced tumor cell invasion by piperine via the inhibition of PKCalpha/ERK1/2-dependent matrix metalloproteinase-9 expression. Tetradecanoylphorbol Acetate 15-46 protein kinase C alpha Homo sapiens 109-117 21375937-2 2011 METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were used to determine the expressions of protein kinase Calpha (PKCalpha) and multidrug resistance-related genes ABCG2, ABCC1, MDR1, and P-glycoprotein (P-gp) in MCF-7Taxol cells after treatment with chelerythrine and phorbol-12-myristate-13-acetate (PMA). Tetradecanoylphorbol Acetate 335-338 protein kinase C alpha Homo sapiens 125-146 21857090-4 2011 Western blot analysis documented that in concentrations of 10 and 100 muM, N-f-5HT isomers significantly decreased PMA-induced phosphorylation of PKC alpha/beta II. Tetradecanoylphorbol Acetate 115-118 protein kinase C alpha Homo sapiens 146-163 20032081-10 2010 RSG only reduced VEGF- and PMA-stimulated PKCalpha membrane translocation. Tetradecanoylphorbol Acetate 27-30 protein kinase C alpha Homo sapiens 42-50 20826143-2 2010 In this work, the effect of the PKC activator phorbol 12-myristate 13-acetate (PMA) on the antilipolytic action of insulin was determined by analyzing lipolysis induced by a beta3-adrenoceptor agonist CL 316243. Tetradecanoylphorbol Acetate 46-77 protein kinase C alpha Homo sapiens 32-35 20826143-2 2010 In this work, the effect of the PKC activator phorbol 12-myristate 13-acetate (PMA) on the antilipolytic action of insulin was determined by analyzing lipolysis induced by a beta3-adrenoceptor agonist CL 316243. Tetradecanoylphorbol Acetate 79-82 protein kinase C alpha Homo sapiens 32-35 20826143-4 2010 The pan-PKC inhibitors GF 109203X and chelerythrine inhibited the PMA effect, but the PKCalpha/beta inhibitors Go 6976 and CGP 53353 did not. Tetradecanoylphorbol Acetate 66-69 protein kinase C alpha Homo sapiens 8-11 20458747-5 2010 Transfection of GBM8401 cells with PKCalpha siRNA specifically reduced PKCalpha protein expression with blocking TPA-induced MMP-9 activation and migration. Tetradecanoylphorbol Acetate 113-116 protein kinase C alpha Homo sapiens 35-43 20458747-5 2010 Transfection of GBM8401 cells with PKCalpha siRNA specifically reduced PKCalpha protein expression with blocking TPA-induced MMP-9 activation and migration. Tetradecanoylphorbol Acetate 113-116 protein kinase C alpha Homo sapiens 71-79 20590612-10 2010 CONCLUSIONS AND IMPLICATIONS: Metformin inhibited PMA-induced invasion and migration of human fibrosarcoma cells via Ca(2+)-dependent PKCalpha/ERK and JNK/AP-1-signalling pathways. Tetradecanoylphorbol Acetate 50-53 protein kinase C alpha Homo sapiens 134-142 20669099-3 2010 MATERIAL AND METHODS: The activation of NF-kappaB by PKC alpha and PKC delta was assessed by Western blotting after the stimulation with Phorbol 12- Myristate 13-Acetate (PMA). Tetradecanoylphorbol Acetate 137-169 protein kinase C alpha Homo sapiens 53-62 20669099-3 2010 MATERIAL AND METHODS: The activation of NF-kappaB by PKC alpha and PKC delta was assessed by Western blotting after the stimulation with Phorbol 12- Myristate 13-Acetate (PMA). Tetradecanoylphorbol Acetate 171-174 protein kinase C alpha Homo sapiens 53-62 20669099-5 2010 RESULTS: PMA induced the phosphorylation of NF-kappaB/p65 by PKC alpha. Tetradecanoylphorbol Acetate 9-12 protein kinase C alpha Homo sapiens 61-70 20152819-8 2010 Furthermore, DHA strongly repressed the PMA-induced phosphorylation of Raf/ERK and JNK, which are dependent on the PKCalpha pathway. Tetradecanoylphorbol Acetate 40-43 protein kinase C alpha Homo sapiens 115-123 20458747-0 2010 12-O-tetradecanoylphorbol-13-acetate-induced invasion/migration of glioblastoma cells through activating PKCalpha/ERK/NF-kappaB-dependent MMP-9 expression. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 105-113 20458747-2 2010 TPA-induced translocation of protein kinase C (PKC)alpha from the cytosol to membranes, and migration of GBM8401 elicited by TPA was suppressed by adding the PKCalpha inhibitors, GF109203X and H7. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 47-56 20458747-2 2010 TPA-induced translocation of protein kinase C (PKC)alpha from the cytosol to membranes, and migration of GBM8401 elicited by TPA was suppressed by adding the PKCalpha inhibitors, GF109203X and H7. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 158-166 20458747-2 2010 TPA-induced translocation of protein kinase C (PKC)alpha from the cytosol to membranes, and migration of GBM8401 elicited by TPA was suppressed by adding the PKCalpha inhibitors, GF109203X and H7. Tetradecanoylphorbol Acetate 125-128 protein kinase C alpha Homo sapiens 158-166 20445555-4 2010 In this study, we use small interfering RNA knockdown to study the role of individual PKC isoforms as regulators of keratinocyte differentiation induced by the potent differentiating stimulus, 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 193-229 protein kinase C alpha Homo sapiens 86-89 20445555-4 2010 In this study, we use small interfering RNA knockdown to study the role of individual PKC isoforms as regulators of keratinocyte differentiation induced by the potent differentiating stimulus, 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 231-234 protein kinase C alpha Homo sapiens 86-89 20673182-10 2010 Furthermore, PMC exhibited obvious inhibitory effects on phorbol 12-myristate 13-acetate (PMA)-induced protein kinase C (PKC)-alpha translocation and phospho-(Ser/Thr) substrate phosphorylation. Tetradecanoylphorbol Acetate 57-88 protein kinase C alpha Homo sapiens 121-131 20673182-10 2010 Furthermore, PMC exhibited obvious inhibitory effects on phorbol 12-myristate 13-acetate (PMA)-induced protein kinase C (PKC)-alpha translocation and phospho-(Ser/Thr) substrate phosphorylation. Tetradecanoylphorbol Acetate 90-93 protein kinase C alpha Homo sapiens 121-131 20444294-15 2010 Using lenti-virus-mediated shRNA to knockdown endogenous PKCalpha expression, we observed that TPA induced growth arrest, elevation of miR-101 and reduction of EZH2, EED and H3K27me3 proteins were all PKCalpha dependent. Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 57-65 20444294-15 2010 Using lenti-virus-mediated shRNA to knockdown endogenous PKCalpha expression, we observed that TPA induced growth arrest, elevation of miR-101 and reduction of EZH2, EED and H3K27me3 proteins were all PKCalpha dependent. Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 201-209 20426528-10 2010 The activation of PKC alpha with phorbol myristate acetate (PMA), a PKC activator, up-regulated cyclin D1 expression and increased the proliferation of passively sensitized HASMCs. Tetradecanoylphorbol Acetate 33-58 protein kinase C alpha Homo sapiens 18-27 20426528-10 2010 The activation of PKC alpha with phorbol myristate acetate (PMA), a PKC activator, up-regulated cyclin D1 expression and increased the proliferation of passively sensitized HASMCs. Tetradecanoylphorbol Acetate 33-58 protein kinase C alpha Homo sapiens 18-21 20426528-10 2010 The activation of PKC alpha with phorbol myristate acetate (PMA), a PKC activator, up-regulated cyclin D1 expression and increased the proliferation of passively sensitized HASMCs. Tetradecanoylphorbol Acetate 60-63 protein kinase C alpha Homo sapiens 18-27 20426528-10 2010 The activation of PKC alpha with phorbol myristate acetate (PMA), a PKC activator, up-regulated cyclin D1 expression and increased the proliferation of passively sensitized HASMCs. Tetradecanoylphorbol Acetate 60-63 protein kinase C alpha Homo sapiens 18-21 19887445-1 2010 Although treatment with the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) is known to protect a subset of cells from induction of apoptosis by death ligands such as Fas ligand and tumor necrosis factor-alpha-related apoptosis-inducing ligand, the mechanism of this protection is unknown. Tetradecanoylphorbol Acetate 61-92 protein kinase C alpha Homo sapiens 46-49 20020096-7 2010 RESULTS: The PKC activator phorbol 12-myristate 13-acetate (PMA) stimulated glucagon secretion from mouse and human islets about fivefold (p < 0.01). Tetradecanoylphorbol Acetate 27-58 protein kinase C alpha Homo sapiens 13-16 20020096-7 2010 RESULTS: The PKC activator phorbol 12-myristate 13-acetate (PMA) stimulated glucagon secretion from mouse and human islets about fivefold (p < 0.01). Tetradecanoylphorbol Acetate 60-63 protein kinase C alpha Homo sapiens 13-16 19887445-1 2010 Although treatment with the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) is known to protect a subset of cells from induction of apoptosis by death ligands such as Fas ligand and tumor necrosis factor-alpha-related apoptosis-inducing ligand, the mechanism of this protection is unknown. Tetradecanoylphorbol Acetate 94-97 protein kinase C alpha Homo sapiens 46-49 19429793-0 2009 Phorbol 12-myristate 13-acetate potentiation of N-methyl-D-aspartate-induced currents in primary cultured cerebellar granule cells is mediated by protein kinase C alpha. Tetradecanoylphorbol Acetate 0-31 protein kinase C alpha Homo sapiens 146-168 19755418-6 2009 Pretreatment of WM1205Lu cells with either a protein-tyrosine phosphatase inhibitor or a protein kinase C (PKC) inhibitor prevented the inhibitory effects of TPA on the level of phosphorylated STAT3. Tetradecanoylphorbol Acetate 158-161 protein kinase C alpha Homo sapiens 107-110 19755418-8 2009 Introduction of the dominant negative mutant of one of these PKC isoforms into WM1205Lu cells inhibited the TPA-induced dephosphorylation of STAT3. Tetradecanoylphorbol Acetate 108-111 protein kinase C alpha Homo sapiens 61-64 19755418-11 2009 Because TPA did not affect c-Src activity, we conclude that the growth inhibitory effect of TPA on melanoma cells is mediated through inactivation of STAT3 by a PKC-activated tyrosine phosphatase(s). Tetradecanoylphorbol Acetate 92-95 protein kinase C alpha Homo sapiens 161-164 20177957-0 2009 Specific subcellular targeting of PKCalpha and PKCepsilon in normal and tumoral lactotroph cells by PMA-mitogenic stimulus. Tetradecanoylphorbol Acetate 100-103 protein kinase C alpha Homo sapiens 34-42 19343040-6 2009 The phosphorylation of this residue is operated by the protein kinase C (PKC), as S193 phosphorylation is markedly increased by treatment with 12-O-tetradecanoylphorbol-13-acetate and decreased by inhibition of PKCalpha and PKCbeta. Tetradecanoylphorbol Acetate 143-179 protein kinase C alpha Homo sapiens 73-76 19343040-6 2009 The phosphorylation of this residue is operated by the protein kinase C (PKC), as S193 phosphorylation is markedly increased by treatment with 12-O-tetradecanoylphorbol-13-acetate and decreased by inhibition of PKCalpha and PKCbeta. Tetradecanoylphorbol Acetate 143-179 protein kinase C alpha Homo sapiens 211-219 20011080-4 2009 To identify the isoform of PKC responsible for the increased progression of the cells through the cell cycle, we monitored the effect of phorbol 12-myristate 13-acetate (PMA) on the subcellular localization of the nine PKC isoforms expressed in RPE cells. Tetradecanoylphorbol Acetate 137-168 protein kinase C alpha Homo sapiens 27-30 20011080-4 2009 To identify the isoform of PKC responsible for the increased progression of the cells through the cell cycle, we monitored the effect of phorbol 12-myristate 13-acetate (PMA) on the subcellular localization of the nine PKC isoforms expressed in RPE cells. Tetradecanoylphorbol Acetate 170-173 protein kinase C alpha Homo sapiens 27-30 20011080-4 2009 To identify the isoform of PKC responsible for the increased progression of the cells through the cell cycle, we monitored the effect of phorbol 12-myristate 13-acetate (PMA) on the subcellular localization of the nine PKC isoforms expressed in RPE cells. Tetradecanoylphorbol Acetate 170-173 protein kinase C alpha Homo sapiens 219-222 20011080-7 2009 Of the nine PKC isoforms that were present in RPE cells, we found PKC(alpha) was both necessary and sufficient to promote cell cycle progression after being stimulated with PMA. Tetradecanoylphorbol Acetate 173-176 protein kinase C alpha Homo sapiens 66-76 19586612-3 2009 Here we show that endosomes and proteasome cooperate in phorbol ester 12-O-tetradecanoyl phorbol acetate (TPA)-induced down-regulation of PKC alpha. Tetradecanoylphorbol Acetate 70-104 protein kinase C alpha Homo sapiens 138-147 19586612-3 2009 Here we show that endosomes and proteasome cooperate in phorbol ester 12-O-tetradecanoyl phorbol acetate (TPA)-induced down-regulation of PKC alpha. Tetradecanoylphorbol Acetate 106-109 protein kinase C alpha Homo sapiens 138-147 19586612-4 2009 We show that following TPA treatment and translocation to the plasma membrane, PKC alpha undergoes multimonoubiquitination prior to its degradation by the proteasome. Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 79-88 19429793-1 2009 We have previously reported that activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) results in potentiation of N-methyl-D-aspartate-induced currents (I(NMDA))of receptors contained in primary cultured cerebellar granule cells (CGCs). Tetradecanoylphorbol Acetate 73-104 protein kinase C alpha Homo sapiens 65-68 19429793-1 2009 We have previously reported that activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) results in potentiation of N-methyl-D-aspartate-induced currents (I(NMDA))of receptors contained in primary cultured cerebellar granule cells (CGCs). Tetradecanoylphorbol Acetate 106-109 protein kinase C alpha Homo sapiens 65-68 19429793-10 2009 Collectively, our data provide strong evidence that PMA-enhanced function of native NMDA receptors expressed in primary cultured CGCs is mediated by activation of PKCalpha. Tetradecanoylphorbol Acetate 52-55 protein kinase C alpha Homo sapiens 163-171 18755856-6 2008 Furthermore, phorbol 12-myristate 13-acetate , a PKC activator, induces the phosphorylation of endogenous FXR in HepG2 cells and PKCalpha phosphorylates in vitro FXR in its DNA-binding domain on S135 and S154. Tetradecanoylphorbol Acetate 13-44 protein kinase C alpha Homo sapiens 49-52 19029835-3 2009 Similarly, KD-PKCalpha blocks the apoptotic response elicited by combination of TPA and radiation, whereas expression of constitutively active PKCalpha is sufficient to sensitize cells to radiation alone, without a need to pre-treat the cells with TPA. Tetradecanoylphorbol Acetate 80-83 protein kinase C alpha Homo sapiens 14-22 19077250-12 2008 TPA induced phosphorylation of the PKC substrate myristoylated alanine-rich C kinase substrate (MARCKS) which was suppressed by the PKC inhibitors. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 35-38 18778746-8 2008 Furthermore, the inhibitory effects of PMA or thymeleatoxin (THX), which is a selective activator of conventional PKC (cPKC), were blocked by the downregulation of all PKCs expressed in C6 cells by long-term incubation with THX, or pretreatment with GF109203X or Go6983, which are broad inhibitors of PKC, or Go6976, a selective inhibitor of cPKC. Tetradecanoylphorbol Acetate 39-42 protein kinase C alpha Homo sapiens 114-117 18755856-6 2008 Furthermore, phorbol 12-myristate 13-acetate , a PKC activator, induces the phosphorylation of endogenous FXR in HepG2 cells and PKCalpha phosphorylates in vitro FXR in its DNA-binding domain on S135 and S154. Tetradecanoylphorbol Acetate 13-44 protein kinase C alpha Homo sapiens 129-137 18372343-4 2008 The present studies revealed that protein kinase C (PKC) alpha/ERK signaling is important for the activation of LHR promoter activity, and the increase of endogenous transcripts induced by phorbol-12-myristate-13-acetate (PMA) in HeLa cells. Tetradecanoylphorbol Acetate 189-220 protein kinase C alpha Homo sapiens 34-62 18778746-8 2008 Furthermore, the inhibitory effects of PMA or thymeleatoxin (THX), which is a selective activator of conventional PKC (cPKC), were blocked by the downregulation of all PKCs expressed in C6 cells by long-term incubation with THX, or pretreatment with GF109203X or Go6983, which are broad inhibitors of PKC, or Go6976, a selective inhibitor of cPKC. Tetradecanoylphorbol Acetate 39-42 protein kinase C alpha Homo sapiens 120-123 18541361-8 2008 PMA stimulated the translocation of protein kinase C (PKC) alpha, betaI and delta isoforms to the cell membrane. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 36-64 18534741-2 2008 In primary pituitary cultures, the activation of protein kinase C (PKC) by PMA for 15 min stimulated lactotroph proliferation; whereas a prolonged activation for 3-8h diminished this proliferative effect. Tetradecanoylphorbol Acetate 75-78 protein kinase C alpha Homo sapiens 67-70 18534741-3 2008 The use of PMA for 15 min-activated PKCepsilon and ERK1/2, whereas incubation with PMA for 3 h induced PKCalpha activation and attenuated the PMA-triggered phosphorylation of ERK1/2. Tetradecanoylphorbol Acetate 83-86 protein kinase C alpha Homo sapiens 103-111 18372343-4 2008 The present studies revealed that protein kinase C (PKC) alpha/ERK signaling is important for the activation of LHR promoter activity, and the increase of endogenous transcripts induced by phorbol-12-myristate-13-acetate (PMA) in HeLa cells. Tetradecanoylphorbol Acetate 222-225 protein kinase C alpha Homo sapiens 34-62 17654516-7 2008 PKC-alpha expression and phosphorylation were almost completely downregulated under combined treatment with TGF-beta + TPA at 24 and 72 h, as shown by immunoblots. Tetradecanoylphorbol Acetate 119-122 protein kinase C alpha Homo sapiens 0-9 18291120-3 2008 Treatment of human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 endothelial cells with phorbol 12-myristate 13-acetate (PMA) or phorbol 12,13-dibutyrate led to a PKC-dependent biphasic expression of the gp91phox homolog Nox4. Tetradecanoylphorbol Acetate 111-142 protein kinase C alpha Homo sapiens 186-189 18056764-6 2008 Phorbol-12-myristate-13-acetate (PMA) enhanced the ability of HUVEC to organize into tubular networks when plated on Matrigel, a phenomenon that could be prevented by PKC inhibitors. Tetradecanoylphorbol Acetate 0-31 protein kinase C alpha Homo sapiens 167-170 18056764-6 2008 Phorbol-12-myristate-13-acetate (PMA) enhanced the ability of HUVEC to organize into tubular networks when plated on Matrigel, a phenomenon that could be prevented by PKC inhibitors. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 167-170 18594782-3 2008 RESULTS: Activation of endothelial protein kinase C (PKC) by either phorbol myristate acetate (PMA) or bryostatin-1 (a potent PKC delta and epsilon activator) completely abolished neutrophil migration mediated by either endothelial TNF-alpha stimulation or LTB4. Tetradecanoylphorbol Acetate 68-93 protein kinase C alpha Homo sapiens 53-56 18594782-3 2008 RESULTS: Activation of endothelial protein kinase C (PKC) by either phorbol myristate acetate (PMA) or bryostatin-1 (a potent PKC delta and epsilon activator) completely abolished neutrophil migration mediated by either endothelial TNF-alpha stimulation or LTB4. Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 53-56 17654516-8 2008 Confocal microscopy demonstrated that TGF-beta-induced nuclear accumulation of PKC-alpha was abolished in the presence of TPA at the same time points. Tetradecanoylphorbol Acetate 122-125 protein kinase C alpha Homo sapiens 79-88 17504762-3 2007 In MCF-7 human breast cancer cells, the action of the PKC activator 4beta-phorbol-12-myristate-13-acetate (PMA) evokes ceramide formation, which in turn prevents PKCalpha/betaII translocation to the pericentrion. Tetradecanoylphorbol Acetate 68-105 protein kinase C alpha Homo sapiens 54-57 17504762-3 2007 In MCF-7 human breast cancer cells, the action of the PKC activator 4beta-phorbol-12-myristate-13-acetate (PMA) evokes ceramide formation, which in turn prevents PKCalpha/betaII translocation to the pericentrion. Tetradecanoylphorbol Acetate 68-105 protein kinase C alpha Homo sapiens 162-177 17504762-3 2007 In MCF-7 human breast cancer cells, the action of the PKC activator 4beta-phorbol-12-myristate-13-acetate (PMA) evokes ceramide formation, which in turn prevents PKCalpha/betaII translocation to the pericentrion. Tetradecanoylphorbol Acetate 107-110 protein kinase C alpha Homo sapiens 54-57 17504762-3 2007 In MCF-7 human breast cancer cells, the action of the PKC activator 4beta-phorbol-12-myristate-13-acetate (PMA) evokes ceramide formation, which in turn prevents PKCalpha/betaII translocation to the pericentrion. Tetradecanoylphorbol Acetate 107-110 protein kinase C alpha Homo sapiens 162-177 17267550-12 2007 Treatment of cells with 100 nM PMA for 24 h, to downregulate PKC, reduced [Ca(2+)](i) transients by 49.9 +/- 5.2% (at 1 mM Ca(2+)) and 40.5 +/- 6.5% (at 2 mM Ca(2+)), compared with controls. Tetradecanoylphorbol Acetate 31-34 protein kinase C alpha Homo sapiens 61-64 17171646-9 2007 Phorbol myristate acetate (PMA, 100 nM) that completely depleted PKC-alpha also enhanced cancer cell proliferation and attenuated VIN-induced cytotoxicity. Tetradecanoylphorbol Acetate 0-25 protein kinase C alpha Homo sapiens 65-74 17171646-9 2007 Phorbol myristate acetate (PMA, 100 nM) that completely depleted PKC-alpha also enhanced cancer cell proliferation and attenuated VIN-induced cytotoxicity. Tetradecanoylphorbol Acetate 27-30 protein kinase C alpha Homo sapiens 65-74 17321112-9 2007 Protein kinase C (PKC) activation by phorbol myristate acetate (PMA) potentiated IL-6 mRNA expression, whereas PKC inhibition by bisindolylmaleimide blocked SPC-induced p42/44 ERK phosphorylation and IL-6 expression. Tetradecanoylphorbol Acetate 37-62 protein kinase C alpha Homo sapiens 18-21 17321112-9 2007 Protein kinase C (PKC) activation by phorbol myristate acetate (PMA) potentiated IL-6 mRNA expression, whereas PKC inhibition by bisindolylmaleimide blocked SPC-induced p42/44 ERK phosphorylation and IL-6 expression. Tetradecanoylphorbol Acetate 64-67 protein kinase C alpha Homo sapiens 18-21 17207890-5 2007 TNF-alpha stimulated expression of both chemokines, while the PKCalpha/beta activator 12-O-tetradecanoyl-phorbol-13-acetate (TPA) induced only expression of IL-8 and inhibited TNF-alpha-induced RANTES expression. Tetradecanoylphorbol Acetate 86-123 protein kinase C alpha Homo sapiens 62-75 17207890-5 2007 TNF-alpha stimulated expression of both chemokines, while the PKCalpha/beta activator 12-O-tetradecanoyl-phorbol-13-acetate (TPA) induced only expression of IL-8 and inhibited TNF-alpha-induced RANTES expression. Tetradecanoylphorbol Acetate 125-128 protein kinase C alpha Homo sapiens 62-75 17207890-6 2007 The PKCalpha/beta inhibitor Go 6976 increased TNF-alpha-induced RANTES production and prevented its down-regulation by TPA. Tetradecanoylphorbol Acetate 119-122 protein kinase C alpha Homo sapiens 4-12 17207890-12 2007 Immunoblotting experiments showed that TPA was more potent than TNF-alpha to induce in a PKCalpha/beta dependent manner the p44/p42 mitogen-activated protein kinases (MAPK) signaling cascade which controls AP-1 activity. Tetradecanoylphorbol Acetate 39-42 protein kinase C alpha Homo sapiens 89-102 17430640-5 2007 Furthermore, ergolide-mediated protein kinase Calpha (PKCalpha) inhibition is involved in reduction of NF-kappaB inhibition, as demonstrated by the observation that dominant negative PKCalpha, but not p44/42 MAPK and p38 MAPK, inhibits TPA-stimulated reporter gene expression. Tetradecanoylphorbol Acetate 236-239 protein kinase C alpha Homo sapiens 54-62 17334233-0 2007 PMA-induced up-regulation of MMP-9 is regulated by a PKCalpha-NF-kappaB cascade in human lung epithelial cells. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 53-61 17334233-3 2007 In this study, we show that phorbol myristate acetate (PMA) induces MMP-9 expression via a protein kinase Calpha (PKCalpha)-dependent signaling cascade in BEAS-2B human lung epithelial cells. Tetradecanoylphorbol Acetate 28-53 protein kinase C alpha Homo sapiens 114-122 17334233-3 2007 In this study, we show that phorbol myristate acetate (PMA) induces MMP-9 expression via a protein kinase Calpha (PKCalpha)-dependent signaling cascade in BEAS-2B human lung epithelial cells. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 114-122 17334233-4 2007 Pretreatment with either GF109203X, a general PKC inhibitor, or Go6976, a PKCalpha/beta isozyme inhibitor, inhibited PMA-induced activation of the MMP-9 promoter, as did transient transfection with PKCalpha antisense oligonuclotides. Tetradecanoylphorbol Acetate 117-120 protein kinase C alpha Homo sapiens 46-49 17334233-4 2007 Pretreatment with either GF109203X, a general PKC inhibitor, or Go6976, a PKCalpha/beta isozyme inhibitor, inhibited PMA-induced activation of the MMP-9 promoter, as did transient transfection with PKCalpha antisense oligonuclotides. Tetradecanoylphorbol Acetate 117-120 protein kinase C alpha Homo sapiens 74-82 17334233-4 2007 Pretreatment with either GF109203X, a general PKC inhibitor, or Go6976, a PKCalpha/beta isozyme inhibitor, inhibited PMA-induced activation of the MMP-9 promoter, as did transient transfection with PKCalpha antisense oligonuclotides. Tetradecanoylphorbol Acetate 117-120 protein kinase C alpha Homo sapiens 198-206 17325208-5 2007 Activation of PPARgamma1 wild type, but not an agonist-binding mutant of PPARgamma1, attenuated PMA-mediated PKCalpha cytosol to membrane translocation. Tetradecanoylphorbol Acetate 96-99 protein kinase C alpha Homo sapiens 109-117 17013757-7 2006 In addition, PKC inhibitor GF-109203X treatment blocks TPA-induced ERKs and JNKs protein phosphorylation, which indicates that activation of PKC locates at upstream of MAPKs activation in TPA-treated HL-60 cells. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 13-16 17355198-4 2007 The algorithm successfully quantified phorbol 12-myristate 13-acetate (PMA)-induced plasma membrane localization of PKCalpha in HeLa cells (Z" of 0.88). Tetradecanoylphorbol Acetate 38-69 protein kinase C alpha Homo sapiens 116-124 17355198-4 2007 The algorithm successfully quantified phorbol 12-myristate 13-acetate (PMA)-induced plasma membrane localization of PKCalpha in HeLa cells (Z" of 0.88). Tetradecanoylphorbol Acetate 71-74 protein kinase C alpha Homo sapiens 116-124 17091491-3 2007 The PKC activator, PMA, selectively increased the number of astrocytes, whereas it decreased the generation of neurons and oligodendrocytes. Tetradecanoylphorbol Acetate 19-22 protein kinase C alpha Homo sapiens 4-7 17200207-5 2007 In a transmembrane invasion assay, phorbol-12-myristate-13-acetate (100 nmol/L) increased the number of invaded HP75 cells, a process that was attenuated by PKC inhibitors, MMP-9 antibody, PKC-alpha siRNA, or PKC-delta siRNA. Tetradecanoylphorbol Acetate 35-66 protein kinase C alpha Homo sapiens 157-160 17200207-5 2007 In a transmembrane invasion assay, phorbol-12-myristate-13-acetate (100 nmol/L) increased the number of invaded HP75 cells, a process that was attenuated by PKC inhibitors, MMP-9 antibody, PKC-alpha siRNA, or PKC-delta siRNA. Tetradecanoylphorbol Acetate 35-66 protein kinase C alpha Homo sapiens 189-198 17170089-5 2006 PKC downregulation, obtained by long-term treatment with phorbol 12-myristate 13-acetate (PMA), resulted in promoter stimulation at similar levels in sub-confluent cells. Tetradecanoylphorbol Acetate 57-88 protein kinase C alpha Homo sapiens 0-3 17170089-5 2006 PKC downregulation, obtained by long-term treatment with phorbol 12-myristate 13-acetate (PMA), resulted in promoter stimulation at similar levels in sub-confluent cells. Tetradecanoylphorbol Acetate 90-93 protein kinase C alpha Homo sapiens 0-3 17013757-7 2006 In addition, PKC inhibitor GF-109203X treatment blocks TPA-induced ERKs and JNKs protein phosphorylation, which indicates that activation of PKC locates at upstream of MAPKs activation in TPA-treated HL-60 cells. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 141-144 17013757-7 2006 In addition, PKC inhibitor GF-109203X treatment blocks TPA-induced ERKs and JNKs protein phosphorylation, which indicates that activation of PKC locates at upstream of MAPKs activation in TPA-treated HL-60 cells. Tetradecanoylphorbol Acetate 188-191 protein kinase C alpha Homo sapiens 13-16 17013757-7 2006 In addition, PKC inhibitor GF-109203X treatment blocks TPA-induced ERKs and JNKs protein phosphorylation, which indicates that activation of PKC locates at upstream of MAPKs activation in TPA-treated HL-60 cells. Tetradecanoylphorbol Acetate 188-191 protein kinase C alpha Homo sapiens 141-144 17013757-10 2006 This suggests that activation of PKC and JNKs participate in TPA"s prevention of BE-induced apoptosis via suppressing mitochondrial dysfunction in HL-60 cells. Tetradecanoylphorbol Acetate 61-64 protein kinase C alpha Homo sapiens 33-36 16890208-7 2006 RLIP76-/- MEFs were resistant to PKCalpha-depletion mediated growth inhibition, as well as to the PKCalpha-dependent mitogen, phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 126-157 protein kinase C alpha Homo sapiens 98-106 16916948-9 2006 The desensitizing effect of CDCA was bile acid-specific and was significantly reduced in the presence of PKC inhibitors and after PKC down-regulation by phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 153-184 protein kinase C alpha Homo sapiens 130-133 16979556-6 2006 Phorbol myristate acetate (PMA) activated alphaIIbbeta3 only after the increased expression of both recombinant protein kinase Calpha (PKCalpha) and talin to levels approximating those in platelets. Tetradecanoylphorbol Acetate 0-25 protein kinase C alpha Homo sapiens 135-143 16979556-6 2006 Phorbol myristate acetate (PMA) activated alphaIIbbeta3 only after the increased expression of both recombinant protein kinase Calpha (PKCalpha) and talin to levels approximating those in platelets. Tetradecanoylphorbol Acetate 27-30 protein kinase C alpha Homo sapiens 135-143 16571380-11 2006 Interestingly, only depletion of PKC-alpha leads to a complete loss of TPA- and histamine-triggered SK-1 induction and cell migration. Tetradecanoylphorbol Acetate 71-74 protein kinase C alpha Homo sapiens 33-42 16710050-8 2006 CDCA at concentrations less than 50 microM enhanced the PKCalpha activation induced by PMA, whereas greater CDCA concentrations reduced the PMA-induced PKCalpha activation. Tetradecanoylphorbol Acetate 87-90 protein kinase C alpha Homo sapiens 56-64 16574739-7 2006 By comparing the pharmacological characteristics of phorbol 12-myristate 13-acetate-stimulated Ser24 phosphorylation with phosphorylation at two other sites previously linked to PKC activity (Ser307 and Ser612), we show that PKCalpha is likely to be directly involved in Ser24 phosphorylation, but indirectly involved in Ser307 and Ser612 phosphorylation. Tetradecanoylphorbol Acetate 52-83 protein kinase C alpha Homo sapiens 225-233 16635257-3 2006 To investigate possible interactions between these two pathways before they converge on Raf activation, we evaluated whether phorbol ester (12-O-tetradecanoyl-phorbol-13-acetate, TPA)-dependent PKC activation required Ras for regulation of TH expression in IMR-32 cells. Tetradecanoylphorbol Acetate 140-177 protein kinase C alpha Homo sapiens 194-197 16635257-3 2006 To investigate possible interactions between these two pathways before they converge on Raf activation, we evaluated whether phorbol ester (12-O-tetradecanoyl-phorbol-13-acetate, TPA)-dependent PKC activation required Ras for regulation of TH expression in IMR-32 cells. Tetradecanoylphorbol Acetate 179-182 protein kinase C alpha Homo sapiens 194-197 16635257-4 2006 We found that long-term treatment with TPA, which induces down-regulation of PKC-alpha, led to induction of both protein and message levels of TH by autocrine factors. Tetradecanoylphorbol Acetate 39-42 protein kinase C alpha Homo sapiens 77-86 16184549-1 2006 Phorbol 12-myristate 13-acetate (PMA)-induced apoptosis of androgen sensitive LNCaP human prostate cancer cells is a well known phenomenon that involves prolonged translocation of multiple protein kinase C (PKC) isozymes to nonnuclear membranes. Tetradecanoylphorbol Acetate 0-31 protein kinase C alpha Homo sapiens 207-210 16184549-1 2006 Phorbol 12-myristate 13-acetate (PMA)-induced apoptosis of androgen sensitive LNCaP human prostate cancer cells is a well known phenomenon that involves prolonged translocation of multiple protein kinase C (PKC) isozymes to nonnuclear membranes. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 207-210 16184549-2 2006 We have shown recently that PMA-induced death of C4-2 cells, androgen hypersensitive derivatives of LNCaP cells, requires both PKCdelta and a redundant pathway that includes PKCs alpha and epsilon. Tetradecanoylphorbol Acetate 28-31 protein kinase C alpha Homo sapiens 174-196 16184549-5 2006 Moreover, overexpression of very high amounts of PKCepsilon sensitized LNCaP cells to induction of apoptosis by bryostatin 1, a non tumor-promoting activator and down-regulator of PKC isozymes that blocks PMA-induced apoptosis of parental LNCaP cells, mimicked our previous results with overexpression of PKCalpha in LNCaP cells. Tetradecanoylphorbol Acetate 205-208 protein kinase C alpha Homo sapiens 49-52 17013757-5 2006 Interestingly, the apoptotic events such as DNA ladders formation and activation of the caspase 3 cascade were significantly blocked by TPA addition in the presence of membrane translocation of PKCalpha, and TPA-induced protection was reduced by adding the PKC inhibitors, GF-109203X and staurosporin. Tetradecanoylphorbol Acetate 136-139 protein kinase C alpha Homo sapiens 194-202 17013757-5 2006 Interestingly, the apoptotic events such as DNA ladders formation and activation of the caspase 3 cascade were significantly blocked by TPA addition in the presence of membrane translocation of PKCalpha, and TPA-induced protection was reduced by adding the PKC inhibitors, GF-109203X and staurosporin. Tetradecanoylphorbol Acetate 136-139 protein kinase C alpha Homo sapiens 194-197 17013757-5 2006 Interestingly, the apoptotic events such as DNA ladders formation and activation of the caspase 3 cascade were significantly blocked by TPA addition in the presence of membrane translocation of PKCalpha, and TPA-induced protection was reduced by adding the PKC inhibitors, GF-109203X and staurosporin. Tetradecanoylphorbol Acetate 208-211 protein kinase C alpha Homo sapiens 194-202 17013757-5 2006 Interestingly, the apoptotic events such as DNA ladders formation and activation of the caspase 3 cascade were significantly blocked by TPA addition in the presence of membrane translocation of PKCalpha, and TPA-induced protection was reduced by adding the PKC inhibitors, GF-109203X and staurosporin. Tetradecanoylphorbol Acetate 208-211 protein kinase C alpha Homo sapiens 194-197 16574993-8 2006 PMA-induced transcellular ISC correlated with PKC-alpha membrane association, whereas low doses of both agents inhibited transcellular and apical membrane ISC-cAMP, increased PKC-beta1, decreased PKC-beta2 membrane association, and caused reciprocal changes in isoform mass. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 46-55 16169661-0 2006 Protein kinase C alpha trigger Ras and Raf-independent MEK/ERK activation for TPA-induced growth inhibition of human hepatoma cell HepG2. Tetradecanoylphorbol Acetate 78-81 protein kinase C alpha Homo sapiens 0-22 16169661-1 2006 The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is a well-known activator of both protein kinase C (PKC) and mitogen activated protein kinase (MAPK) signal cascade triggering a lot of effects in many non-tumor and tumor cells. Tetradecanoylphorbol Acetate 19-55 protein kinase C alpha Homo sapiens 114-117 16169661-1 2006 The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is a well-known activator of both protein kinase C (PKC) and mitogen activated protein kinase (MAPK) signal cascade triggering a lot of effects in many non-tumor and tumor cells. Tetradecanoylphorbol Acetate 57-60 protein kinase C alpha Homo sapiens 114-117 16169661-2 2006 We have reported activation of PKCalpha isozyme was specifically required for TPA-induced ERK (MAPK) signaling that mediated gene expressions of the CDK inhibitors p15(INK4b) and p16 (INK4a) leading to growth inhibition of hepatoma cell HepG2. Tetradecanoylphorbol Acetate 78-81 protein kinase C alpha Homo sapiens 31-39 16169661-14 2006 Taken together, we conclude that PKCalpha may activate MEK, independently of Raf and Ras, to trigger sustained ERK (MAPK) signaling and cell cycle arrest of HepG2 induced by TPA. Tetradecanoylphorbol Acetate 174-177 protein kinase C alpha Homo sapiens 33-41 15985361-6 2005 Nevertheless, PMA stimulated translocation of PKC-alpha, -betaI, -betaII, and -gamma, but only anti-PKC-gamma co-immunoprecipitated the receptors. Tetradecanoylphorbol Acetate 14-17 protein kinase C alpha Homo sapiens 46-55 16374540-2 2006 Safingol inhibited the translocation of PKC following treatment with 12-o-tetradecanoylphorbol 13-acetate (TPA) in PKC alpha-EGFP-transfected cells, but not in PKC beta-EGFP- transfected cells, indicating selective inhibition for PKC alpha in oral SCC cells. Tetradecanoylphorbol Acetate 69-105 protein kinase C alpha Homo sapiens 40-43 16374540-2 2006 Safingol inhibited the translocation of PKC following treatment with 12-o-tetradecanoylphorbol 13-acetate (TPA) in PKC alpha-EGFP-transfected cells, but not in PKC beta-EGFP- transfected cells, indicating selective inhibition for PKC alpha in oral SCC cells. Tetradecanoylphorbol Acetate 69-105 protein kinase C alpha Homo sapiens 115-124 16374540-2 2006 Safingol inhibited the translocation of PKC following treatment with 12-o-tetradecanoylphorbol 13-acetate (TPA) in PKC alpha-EGFP-transfected cells, but not in PKC beta-EGFP- transfected cells, indicating selective inhibition for PKC alpha in oral SCC cells. Tetradecanoylphorbol Acetate 107-110 protein kinase C alpha Homo sapiens 40-43 16374540-2 2006 Safingol inhibited the translocation of PKC following treatment with 12-o-tetradecanoylphorbol 13-acetate (TPA) in PKC alpha-EGFP-transfected cells, but not in PKC beta-EGFP- transfected cells, indicating selective inhibition for PKC alpha in oral SCC cells. Tetradecanoylphorbol Acetate 107-110 protein kinase C alpha Homo sapiens 115-124 16305951-2 2005 METHODS: KBV200 cells were preincubated with PKC activator phorbol-12-myristate-13-acetate (PMA, 200 nmol/L) and PKC activity was assayed by measurement of peptide substrate (32)P incorporation from [gamma-(32)P]ATP, with the cells without PMA preincubation serving as the control. Tetradecanoylphorbol Acetate 59-90 protein kinase C alpha Homo sapiens 45-48 16305951-4 2005 RESULTS: PMA preincubation of the cells significantly enhanced the activity of the total PKC and the membrane fraction, but lowered the PKC activity of the cytosol fraction, as compared with the cells without PMA treatment (P<0.01). Tetradecanoylphorbol Acetate 9-12 protein kinase C alpha Homo sapiens 89-92 16305951-4 2005 RESULTS: PMA preincubation of the cells significantly enhanced the activity of the total PKC and the membrane fraction, but lowered the PKC activity of the cytosol fraction, as compared with the cells without PMA treatment (P<0.01). Tetradecanoylphorbol Acetate 9-12 protein kinase C alpha Homo sapiens 136-139 16117614-5 2005 To explain the apoptotic effects of SNL glycoprotein, we investigated its effects on 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated protein kinase C (PKC) alpha activity and DNA-binding activity of nuclear factor (NF) kappaB in HT-29 cells, using western blot analysis and electrophoretic mobility shift assays. Tetradecanoylphorbol Acetate 85-121 protein kinase C alpha Homo sapiens 157-160 16055435-3 2005 Activation of PKC with phorbol 12-myristate 13-acetate (PMA) in early G1 phase impaired progression of lung adenocarcinoma cells into S phase, an effect that was completely abolished by specific depletion of PKCdelta, but not PKCalpha. Tetradecanoylphorbol Acetate 23-54 protein kinase C alpha Homo sapiens 14-17 16055435-3 2005 Activation of PKC with phorbol 12-myristate 13-acetate (PMA) in early G1 phase impaired progression of lung adenocarcinoma cells into S phase, an effect that was completely abolished by specific depletion of PKCdelta, but not PKCalpha. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 14-17 16055435-3 2005 Activation of PKC with phorbol 12-myristate 13-acetate (PMA) in early G1 phase impaired progression of lung adenocarcinoma cells into S phase, an effect that was completely abolished by specific depletion of PKCdelta, but not PKCalpha. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 226-234 16122920-6 2005 Both DCA and phorbol myristate acetate (PMA) but not UDCA caused translocation of endogenous PKC alpha, epsilon and delta and transfected PKC beta1-, epsilon- and delta-EGFP from cytosol to plasma membrane, reflecting isoenzyme activation. Tetradecanoylphorbol Acetate 13-38 protein kinase C alpha Homo sapiens 93-121 16122920-6 2005 Both DCA and phorbol myristate acetate (PMA) but not UDCA caused translocation of endogenous PKC alpha, epsilon and delta and transfected PKC beta1-, epsilon- and delta-EGFP from cytosol to plasma membrane, reflecting isoenzyme activation. Tetradecanoylphorbol Acetate 40-43 protein kinase C alpha Homo sapiens 93-121 15764646-8 2005 Pretreatment with PKC inhibitor Go-6983 (concentrations selective for classic PKC), PMA-induced depletion of PKCalpha, and transfection of antisense PKCalpha oligonucleotide each prevented 40-50% of the LPC-induced resistance decrease. Tetradecanoylphorbol Acetate 84-87 protein kinase C alpha Homo sapiens 109-117 16117614-5 2005 To explain the apoptotic effects of SNL glycoprotein, we investigated its effects on 12-O-tetradecanoylphorbol 13-acetate (TPA)-stimulated protein kinase C (PKC) alpha activity and DNA-binding activity of nuclear factor (NF) kappaB in HT-29 cells, using western blot analysis and electrophoretic mobility shift assays. Tetradecanoylphorbol Acetate 123-126 protein kinase C alpha Homo sapiens 157-160 16117614-6 2005 Results from these experiments showed that SNL glycoprotein has remarkable inhibitory effects on the activities of TPA (100 nM)-stimulated PKCalpha and NF-kappaB in HT-29 cells. Tetradecanoylphorbol Acetate 115-118 protein kinase C alpha Homo sapiens 139-147 16117614-7 2005 They also substantiated that PKCalpha is a part of the TPA-activated upstream signal pathway of NF-kappaB, since NF-kappaB activity was inhibited by staurosporine (a PKC inhibitor) and pyrrolidine dithiocarbamate (an NF-kappaB inhibitor) in a western blot analysis. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 29-37 16117614-7 2005 They also substantiated that PKCalpha is a part of the TPA-activated upstream signal pathway of NF-kappaB, since NF-kappaB activity was inhibited by staurosporine (a PKC inhibitor) and pyrrolidine dithiocarbamate (an NF-kappaB inhibitor) in a western blot analysis. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 29-32 15897236-9 2005 Pharmacologic PKCalpha "knockdown" abrogated TPA-induced Erk1/2 activation without affecting the EGF/EGFR-induced response, indicating that PKCalpha was required for EGFR transactivation but dispensable for signaling of ligand-activated EGFR to Erk1/2 activation. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 14-22 15897236-6 2005 The PKC-selective inhibitors GF109203X and Go6983 each blocked TPA-induced EGFR transactivation, indicating a requirement for PKC. Tetradecanoylphorbol Acetate 63-66 protein kinase C alpha Homo sapiens 4-7 15823586-0 2005 PKCalpha is involved in phorbol ester TPA-mediated stabilization of p14ARF. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 0-8 15823586-6 2005 We further investigated which isoforms of PKC were involved in TPA-mediated p14(ARF) stabilization using short-interference RNA. Tetradecanoylphorbol Acetate 63-66 protein kinase C alpha Homo sapiens 42-45 15823586-7 2005 Knockdown of PKCalpha, but not PKCdelta, attenuated TPA-mediated p14(ARF) stabilization. Tetradecanoylphorbol Acetate 52-55 protein kinase C alpha Homo sapiens 13-21 15823586-8 2005 These findings suggest that PKCalpha is involved in TPA-mediated stabilization of p14(ARF) protein, and this effect of TPA was not affected by the Ras/MAPK pathway or p53 status. Tetradecanoylphorbol Acetate 52-55 protein kinase C alpha Homo sapiens 28-36 15897236-6 2005 The PKC-selective inhibitors GF109203X and Go6983 each blocked TPA-induced EGFR transactivation, indicating a requirement for PKC. Tetradecanoylphorbol Acetate 63-66 protein kinase C alpha Homo sapiens 126-129 15897236-9 2005 Pharmacologic PKCalpha "knockdown" abrogated TPA-induced Erk1/2 activation without affecting the EGF/EGFR-induced response, indicating that PKCalpha was required for EGFR transactivation but dispensable for signaling of ligand-activated EGFR to Erk1/2 activation. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 140-148 15897236-10 2005 We corroborated this by showing that Go6976, which is a PKCalpha-selective inhibitor in PC-3 cells, likewise abolished TPA-induced Erk1/2 activation and did not inhibit EGF/EGFR-induced Erk1/2 activation. Tetradecanoylphorbol Acetate 119-122 protein kinase C alpha Homo sapiens 56-64 15623535-2 2005 Recently, we have shown that PKC isoforms-alpha and -delta, as well as the Rho/Rho kinase (ROK) pathway, play a role in phorbol 12-myristate 13-acetate (PMA)-mediated secretion of the gut peptide neurotensin (NT) in the BON human endocrine cell line. Tetradecanoylphorbol Acetate 120-151 protein kinase C alpha Homo sapiens 29-58 15627650-4 2005 The two fatty acids inhibited the phorbol 12-myristate 13-acetate (PMA)-induced plasma membrane translocation of protein kinase C (PKC)-alpha and -epsilon. Tetradecanoylphorbol Acetate 34-65 protein kinase C alpha Homo sapiens 113-141 15627650-4 2005 The two fatty acids inhibited the phorbol 12-myristate 13-acetate (PMA)-induced plasma membrane translocation of protein kinase C (PKC)-alpha and -epsilon. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 113-141 15623535-2 2005 Recently, we have shown that PKC isoforms-alpha and -delta, as well as the Rho/Rho kinase (ROK) pathway, play a role in phorbol 12-myristate 13-acetate (PMA)-mediated secretion of the gut peptide neurotensin (NT) in the BON human endocrine cell line. Tetradecanoylphorbol Acetate 153-156 protein kinase C alpha Homo sapiens 29-58 15668705-9 2005 Also, the phorbol ester PMA could no longer induce PKCalpha translocation in irradiated cells. Tetradecanoylphorbol Acetate 24-27 protein kinase C alpha Homo sapiens 51-59 15721870-6 2005 Protein kinase C (PKC) has been reported to phosphorylate this residue, and the increase in the phosphorylation of Thr(495) induced by phorbol 12-myristate 13-acetate was attenuated in cells pretreated with ox-LDL. Tetradecanoylphorbol Acetate 135-166 protein kinase C alpha Homo sapiens 18-21 15611126-6 2005 Knockdown of PKCepsilon alone had no effect, but simultaneous knockdown of both PKCalpha and PKCepsilon in C4-2 cells that continued to express normal levels of PKCdelta inhibited PMA-induced apoptosis. Tetradecanoylphorbol Acetate 180-183 protein kinase C alpha Homo sapiens 80-88 15572354-5 2005 Prolonged treatment of cells with 12-O-tetradecanoylphorbol-13-acetate effectively down-regulated immunoreactive PKC-alpha but had little effect on the expression of PKC-epsilon. Tetradecanoylphorbol Acetate 34-70 protein kinase C alpha Homo sapiens 113-122 15661932-1 2005 Protein kinase C (PKC) isoforms are major regulators of cutaneous homeostasis and mediate inflammation in response to 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 118-154 protein kinase C alpha Homo sapiens 18-21 15639488-9 2005 This effect was reversed by the PKC inhibitor Ro-318220 and mimicked by the PKC activator phorbol-12 myristate 13-acetate. Tetradecanoylphorbol Acetate 90-121 protein kinase C alpha Homo sapiens 32-35 15639488-9 2005 This effect was reversed by the PKC inhibitor Ro-318220 and mimicked by the PKC activator phorbol-12 myristate 13-acetate. Tetradecanoylphorbol Acetate 90-121 protein kinase C alpha Homo sapiens 76-79 15661932-1 2005 Protein kinase C (PKC) isoforms are major regulators of cutaneous homeostasis and mediate inflammation in response to 12-O-tetradecanoylphorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 156-159 protein kinase C alpha Homo sapiens 18-21 15917995-0 2005 Activation of protein kinase C alpha is required for TPA-triggered ERK (MAPK) signaling and growth inhibition of human hepatoma cell HepG2. Tetradecanoylphorbol Acetate 53-56 protein kinase C alpha Homo sapiens 14-36 15917995-4 2005 In HepG2 cells only one of the cPKC isozymes, PKCalpha, but not cPKCbetaII, nPKCepsilon or aPKCzeta was activated by TPA as demonstrated by its membrane translocation within 10-30 min and down-regulation at 24 h after TPA treatment. Tetradecanoylphorbol Acetate 117-120 protein kinase C alpha Homo sapiens 46-54 15917995-4 2005 In HepG2 cells only one of the cPKC isozymes, PKCalpha, but not cPKCbetaII, nPKCepsilon or aPKCzeta was activated by TPA as demonstrated by its membrane translocation within 10-30 min and down-regulation at 24 h after TPA treatment. Tetradecanoylphorbol Acetate 218-221 protein kinase C alpha Homo sapiens 46-54 15917995-5 2005 Pretreatment of 0.2-2.0 microM Bisindolylmaleimides, an inhibitor of PKC, attenuated the TPA-induced phosphorylation of ERK, gene expressions of p15(INK4b) and p16(INK4a), and growth inhibition of HepG2 cell in a dose-dependent manner. Tetradecanoylphorbol Acetate 89-92 protein kinase C alpha Homo sapiens 69-72 15917995-7 2005 Taken together, we concluded that PKCalpha is specifically required for TPA-induced ERK(MAPK) signaling to trigger gene expressions of p15(INK4b) and p16(INK4a) leading to HepG2 growth inhibition. Tetradecanoylphorbol Acetate 72-75 protein kinase C alpha Homo sapiens 34-42 15542774-6 2004 Activation of PKC by phorbol ester (phorbol 12-myristate 13-acetate) enhanced EGF action on ERK1/2 phosphorylation without significantly altering p53 phosphorylation by resveratrol. Tetradecanoylphorbol Acetate 36-67 protein kinase C alpha Homo sapiens 14-17 15475174-6 2004 However, pre-incubation with the PKC inhibitor GF109203X or PKC down-regulation by the phorbol ester PMA, had minimal or no effect on PBDE-99 or Aroclor 1254-induced cytotoxicity. Tetradecanoylphorbol Acetate 101-104 protein kinase C alpha Homo sapiens 60-63 15504748-1 2004 The mechanism of inhibition of eosinophil degranulation by protein kinase C (PKC) was investigated in complement C5a (C5a)-stimulated degranulation of highly purified human eosinophils using the specific PKC activator - phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 220-251 protein kinase C alpha Homo sapiens 77-80 15504748-1 2004 The mechanism of inhibition of eosinophil degranulation by protein kinase C (PKC) was investigated in complement C5a (C5a)-stimulated degranulation of highly purified human eosinophils using the specific PKC activator - phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 253-256 protein kinase C alpha Homo sapiens 77-80 15504748-3 2004 The inhibition by PMA, but not histamine, was significantly reversed by the specific, but isoform nonselective, PKC inhibitor Ro 31-8220 (1 microM). Tetradecanoylphorbol Acetate 18-21 protein kinase C alpha Homo sapiens 112-115 15504748-6 2004 The cAMP production by PMA, but not histamine, was significantly reversed by Ro 31-8220 (1 microM) and the selective inhibitor of the novel PKCdelta, rottlerin (1-3 microM), but not the selective inhibitor of the classical PKC isoforms, Go 6976 (0.01-0.1 microM). Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 140-143 15488737-3 2004 In addition, we showed that this induction is mediated by the PKC pathway: in the presence of Ro 31-8220, an inhibitor of all PKC isozymes, or after 48 h of PMA treatment, Tat protein becomes unable to stimulate IL-10 production. Tetradecanoylphorbol Acetate 157-160 protein kinase C alpha Homo sapiens 62-65 15488737-3 2004 In addition, we showed that this induction is mediated by the PKC pathway: in the presence of Ro 31-8220, an inhibitor of all PKC isozymes, or after 48 h of PMA treatment, Tat protein becomes unable to stimulate IL-10 production. Tetradecanoylphorbol Acetate 157-160 protein kinase C alpha Homo sapiens 126-129 14981539-3 2004 Here, we found that the PKC activators, phorbol 12-myristate 13-acetate (PMA) and bryostatin I, induced TRAF1 mRNA expression; pretreatment with actinomycin D blocked PMA-mediated TRAF1 expression suggesting induction at the transcriptional level. Tetradecanoylphorbol Acetate 40-71 protein kinase C alpha Homo sapiens 24-27 15298668-6 2004 Our results show that melatonin increased CaM phosphorylation by PKC alpha with an EC(50) of 10(-8) m in the presence of the phorbol ester, phorbol-12-myristate-13-acetate (PMA) in the in vitro reconstituted enzyme system. Tetradecanoylphorbol Acetate 140-171 protein kinase C alpha Homo sapiens 65-74 15298668-6 2004 Our results show that melatonin increased CaM phosphorylation by PKC alpha with an EC(50) of 10(-8) m in the presence of the phorbol ester, phorbol-12-myristate-13-acetate (PMA) in the in vitro reconstituted enzyme system. Tetradecanoylphorbol Acetate 173-176 protein kinase C alpha Homo sapiens 65-74 15252133-6 2004 Activation of PKC in melanocytes increased the level of PKC-beta co-immunoprecipitated with RACK-I, while the level of melanosome-associated RACK-I decreased when melanocytes were treated chronically with the 12-0-tetradecanoyl-phorbol 13-Acetate (TPA), a condition known to deplete PKC and reduce tyrosinase activity. Tetradecanoylphorbol Acetate 248-251 protein kinase C alpha Homo sapiens 14-17 14739659-6 2004 The effects of resveratrol on TPA-induced PKC isozyme activation were defined by monitoring PKC isozyme translocation and autophosphorylation. Tetradecanoylphorbol Acetate 30-33 protein kinase C alpha Homo sapiens 42-45 14739659-6 2004 The effects of resveratrol on TPA-induced PKC isozyme activation were defined by monitoring PKC isozyme translocation and autophosphorylation. Tetradecanoylphorbol Acetate 30-33 protein kinase C alpha Homo sapiens 92-95 14739659-7 2004 Under conditions where resveratrol suppressed TPA-induced Erk1/2 activation, the phytochemical produced isozyme-selective interference with TPA-induced translocation of cytosolic PKCalpha to the membrane/cytoskeleton and selectively diminished the amount of autophosphorylated PKCalpha in the membrane/cytoskeleton of the TPA-treated cells. Tetradecanoylphorbol Acetate 140-143 protein kinase C alpha Homo sapiens 179-187 14739659-7 2004 Under conditions where resveratrol suppressed TPA-induced Erk1/2 activation, the phytochemical produced isozyme-selective interference with TPA-induced translocation of cytosolic PKCalpha to the membrane/cytoskeleton and selectively diminished the amount of autophosphorylated PKCalpha in the membrane/cytoskeleton of the TPA-treated cells. Tetradecanoylphorbol Acetate 140-143 protein kinase C alpha Homo sapiens 277-285 14739659-7 2004 Under conditions where resveratrol suppressed TPA-induced Erk1/2 activation, the phytochemical produced isozyme-selective interference with TPA-induced translocation of cytosolic PKCalpha to the membrane/cytoskeleton and selectively diminished the amount of autophosphorylated PKCalpha in the membrane/cytoskeleton of the TPA-treated cells. Tetradecanoylphorbol Acetate 140-143 protein kinase C alpha Homo sapiens 179-187 14739659-7 2004 Under conditions where resveratrol suppressed TPA-induced Erk1/2 activation, the phytochemical produced isozyme-selective interference with TPA-induced translocation of cytosolic PKCalpha to the membrane/cytoskeleton and selectively diminished the amount of autophosphorylated PKCalpha in the membrane/cytoskeleton of the TPA-treated cells. Tetradecanoylphorbol Acetate 140-143 protein kinase C alpha Homo sapiens 277-285 15314167-2 2004 Immunofluorescence analysis demonstrated that activation of PKCalpha by phorbol 12-myristate 13-acetate (PMA), or ectopic expression of constitutively activated PKCalpha, directs AFAP-110 to colocalize with and bind to the c-Src SH3 domain, resulting in activation of the tyrosine kinase. Tetradecanoylphorbol Acetate 72-103 protein kinase C alpha Homo sapiens 60-68 15314167-2 2004 Immunofluorescence analysis demonstrated that activation of PKCalpha by phorbol 12-myristate 13-acetate (PMA), or ectopic expression of constitutively activated PKCalpha, directs AFAP-110 to colocalize with and bind to the c-Src SH3 domain, resulting in activation of the tyrosine kinase. Tetradecanoylphorbol Acetate 105-108 protein kinase C alpha Homo sapiens 60-68 14695118-7 2004 An activator of PKC-alpha, phorbol 12-myristate 13-acetate, abrogated the activation of l-arginine transport in PAEC treated with PTX. Tetradecanoylphorbol Acetate 27-58 protein kinase C alpha Homo sapiens 16-25 14695118-8 2004 Incubation of PTX-treated PAEC with phorbol 12-myristate 13-acetate in combination with an inhibitor of PKC-alpha (Go 6976) restored the activating effects of PTX on l-arginine uptake, suggesting PTX-induced activation of l-arginine transport is mediated through downregulation of PKC-alpha. Tetradecanoylphorbol Acetate 36-67 protein kinase C alpha Homo sapiens 281-290 14709334-7 2004 Subcellular localization studies demonstrated that PMA induced translocation of PKC-alpha, -betaII, and -epsilon isoforms, but not PKC-delta, from the cytosol to the membrane. Tetradecanoylphorbol Acetate 51-54 protein kinase C alpha Homo sapiens 80-89 14981539-3 2004 Here, we found that the PKC activators, phorbol 12-myristate 13-acetate (PMA) and bryostatin I, induced TRAF1 mRNA expression; pretreatment with actinomycin D blocked PMA-mediated TRAF1 expression suggesting induction at the transcriptional level. Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 24-27 14729403-8 2004 Pre-incubation with the PKC activator, phorbol 12-myristate 13-acetate, resulted in an additive effect on membrane translocation of PKCalpha. Tetradecanoylphorbol Acetate 39-70 protein kinase C alpha Homo sapiens 24-27 14978237-2 2004 The Tyr701 phosphorylation of signal transducer and activator of transcription 1 (STAT1) induced by interferon-gamma (IFN-gamma) and 12-O-tetradecanoylphorbol 13-acetate (TPA) was inhibited by the protein kinase C (PKC) inhibitor staurosporine, the tyrosine kinase inhibitor herbimycin, or the Src kinase inhibitor PP2. Tetradecanoylphorbol Acetate 171-174 protein kinase C alpha Homo sapiens 215-218 14978237-3 2004 An association between c-Src and STAT1 was increased by IFN-gamma and TPA, indicating the direct phosphorylation of STAT1 by PKC-dependent c-Src activation. Tetradecanoylphorbol Acetate 70-73 protein kinase C alpha Homo sapiens 125-128 14602083-7 2004 The requirement of PKC alpha in LPS-dependent TNFalpha induction was verified in PKC alpha-downregulated microglia which could be induced by phorbol-12-myristate-13-acetate pretreatment. Tetradecanoylphorbol Acetate 141-172 protein kinase C alpha Homo sapiens 19-28 14602083-7 2004 The requirement of PKC alpha in LPS-dependent TNFalpha induction was verified in PKC alpha-downregulated microglia which could be induced by phorbol-12-myristate-13-acetate pretreatment. Tetradecanoylphorbol Acetate 141-172 protein kinase C alpha Homo sapiens 81-90 14729403-8 2004 Pre-incubation with the PKC activator, phorbol 12-myristate 13-acetate, resulted in an additive effect on membrane translocation of PKCalpha. Tetradecanoylphorbol Acetate 39-70 protein kinase C alpha Homo sapiens 132-140 14981400-9 2004 Exposure to TPA for 5 and 30 minutes induced translocation of PKC alpha and PKC delta, respectively. Tetradecanoylphorbol Acetate 12-15 protein kinase C alpha Homo sapiens 62-71 12878187-2 2003 Here, we demonstrate that PKC activation via phorbol 12-myristate 13-acetate (PMA) treatment of MDA-MB-231 cells inhibits EGF-induced cell spreading, the initial event of motility and chemotaxis. Tetradecanoylphorbol Acetate 45-76 protein kinase C alpha Homo sapiens 26-29 14635193-5 2003 MAPK activation is negated by an inhibitor to PKCalpha, but not PKCdelta inhibitors, in cells subjected to EMF exposure or TPA treatment. Tetradecanoylphorbol Acetate 123-126 protein kinase C alpha Homo sapiens 46-54 14714562-5 2003 Phorbol 12-myristate 13-acetate (PMA), an activator of PKC, inhibited proliferation, elevated intracellular calcium concentration, decreased the expression of K10, and increased the expressions of INV, FIL, and TG. Tetradecanoylphorbol Acetate 0-31 protein kinase C alpha Homo sapiens 55-58 14714562-5 2003 Phorbol 12-myristate 13-acetate (PMA), an activator of PKC, inhibited proliferation, elevated intracellular calcium concentration, decreased the expression of K10, and increased the expressions of INV, FIL, and TG. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 55-58 14596936-2 2003 12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced PLD1 activation was suppressed by the introduction of PKCdelta as well as its kinase-negative mutant in MeWo cells, which contain PKCalpha but lack PKCbeta. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 181-189 14596936-2 2003 12-O-Tetradecanoylphorbol-13-acetate (TPA)-induced PLD1 activation was suppressed by the introduction of PKCdelta as well as its kinase-negative mutant in MeWo cells, which contain PKCalpha but lack PKCbeta. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 181-189 14596936-4 2003 In MeWo cells introduced by PKCalpha and PLD1, the association of these proteins was observed, which was enhanced by the TPA treatment. Tetradecanoylphorbol Acetate 121-124 protein kinase C alpha Homo sapiens 28-36 14596936-5 2003 In cells overexpressing PKCdelta in addition to PKCalpha and PLD1, TPA treatment increased the association of PKCdelta and PLD1, while it attenuated the association of PKCalpha and PLD1. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 48-56 14596936-5 2003 In cells overexpressing PKCdelta in addition to PKCalpha and PLD1, TPA treatment increased the association of PKCdelta and PLD1, while it attenuated the association of PKCalpha and PLD1. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 168-176 14596936-6 2003 These results indicate that PKCdelta inhibits TPA-induced PLD1 activation mediated by PKCalpha through the association with PLD1. Tetradecanoylphorbol Acetate 46-49 protein kinase C alpha Homo sapiens 86-94 14563411-6 2003 In addition, evidence is provided that TPA requires only one of the two C1 subdomains to trigger translocation to the plasma membrane.In summary, our data provide evidence that ceramide either directly or indirectly interacts with the Ca(2+)-dependent lipid binding C2 domain of PKCalpha and thereby induces translocation of the enzyme to the Golgi compartment. Tetradecanoylphorbol Acetate 39-42 protein kinase C alpha Homo sapiens 279-287 14717982-9 2004 We have also demonstrated that the ribavirin-treated CMK cells express PKC-alpha, -beta, -delta and -theta, and suggested that PKC-alpha and/or -beta appear to be responsible for PMA-induced activation of alpha IIb beta 3 in CMK cells. Tetradecanoylphorbol Acetate 179-182 protein kinase C alpha Homo sapiens 71-80 14728848-14 2003 Meanwhile expression level of PKCalpha was decreased with the co-treatment of TPA or TAM and FSH comparing with treatment with FSH only. Tetradecanoylphorbol Acetate 78-81 protein kinase C alpha Homo sapiens 30-38 12890670-8 2003 Furthermore, activation of PKC alpha by phorbol 12-myristate 13-acetate inhibited the activity of wild-type DGK zeta, but not DGK zeta S/D, in human embryonic kidney 293 cells. Tetradecanoylphorbol Acetate 40-71 protein kinase C alpha Homo sapiens 27-36 12878187-2 2003 Here, we demonstrate that PKC activation via phorbol 12-myristate 13-acetate (PMA) treatment of MDA-MB-231 cells inhibits EGF-induced cell spreading, the initial event of motility and chemotaxis. Tetradecanoylphorbol Acetate 78-81 protein kinase C alpha Homo sapiens 26-29 12734388-3 2003 Direct activation of PKC by treatment with the phorbol ester phorbol 12-myristate 13-acetate (PMA) or 1,2-dioctanoyl-sn-glycerol (DOG) desensitized CRF1 receptors in Y79 cells, reducing the maximum for CRF- (but not forskolin)-stimulated cAMP accumulation by 56.3 +/- 1.2% and 40.4 +/- 2.1%, respectively (p < 0.001). Tetradecanoylphorbol Acetate 61-92 protein kinase C alpha Homo sapiens 21-24 12734388-3 2003 Direct activation of PKC by treatment with the phorbol ester phorbol 12-myristate 13-acetate (PMA) or 1,2-dioctanoyl-sn-glycerol (DOG) desensitized CRF1 receptors in Y79 cells, reducing the maximum for CRF- (but not forskolin)-stimulated cAMP accumulation by 56.3 +/- 1.2% and 40.4 +/- 2.1%, respectively (p < 0.001). Tetradecanoylphorbol Acetate 94-97 protein kinase C alpha Homo sapiens 21-24 12734388-6 2003 When alpha and beta isoforms of PKC were down-regulated 80 to 90% by a 48-h PMA exposure, PMA-induced CRF1 receptor desensitization was abolished. Tetradecanoylphorbol Acetate 76-79 protein kinase C alpha Homo sapiens 32-35 12694376-5 2003 Both wound-healing and Boyden migration assays showed that TPA treatment promoted neuronal migration of GT1 cells; however, cotreatment of TPA with safingol or rottlerin (a PKC delta-selective inhibitor) clearly blocked this TPA effect, indicating that both PKC alpha and PKC delta may be positive regulators of neuronal migration. Tetradecanoylphorbol Acetate 139-142 protein kinase C alpha Homo sapiens 258-267 12843260-5 2003 In C6 glioma cells, activation of PKC with phorbol 12-myristate 13-acetate (PMA) induced formation of EAAC1-PKCalpha complexes but did not induce formation of complexes with PKCdelta, a PKC not thought to regulate EAAC1. Tetradecanoylphorbol Acetate 43-74 protein kinase C alpha Homo sapiens 34-37 12843260-5 2003 In C6 glioma cells, activation of PKC with phorbol 12-myristate 13-acetate (PMA) induced formation of EAAC1-PKCalpha complexes but did not induce formation of complexes with PKCdelta, a PKC not thought to regulate EAAC1. Tetradecanoylphorbol Acetate 43-74 protein kinase C alpha Homo sapiens 108-116 12843260-5 2003 In C6 glioma cells, activation of PKC with phorbol 12-myristate 13-acetate (PMA) induced formation of EAAC1-PKCalpha complexes but did not induce formation of complexes with PKCdelta, a PKC not thought to regulate EAAC1. Tetradecanoylphorbol Acetate 43-74 protein kinase C alpha Homo sapiens 108-111 12843260-5 2003 In C6 glioma cells, activation of PKC with phorbol 12-myristate 13-acetate (PMA) induced formation of EAAC1-PKCalpha complexes but did not induce formation of complexes with PKCdelta, a PKC not thought to regulate EAAC1. Tetradecanoylphorbol Acetate 76-79 protein kinase C alpha Homo sapiens 34-37 12843260-5 2003 In C6 glioma cells, activation of PKC with phorbol 12-myristate 13-acetate (PMA) induced formation of EAAC1-PKCalpha complexes but did not induce formation of complexes with PKCdelta, a PKC not thought to regulate EAAC1. Tetradecanoylphorbol Acetate 76-79 protein kinase C alpha Homo sapiens 108-116 12843260-5 2003 In C6 glioma cells, activation of PKC with phorbol 12-myristate 13-acetate (PMA) induced formation of EAAC1-PKCalpha complexes but did not induce formation of complexes with PKCdelta, a PKC not thought to regulate EAAC1. Tetradecanoylphorbol Acetate 76-79 protein kinase C alpha Homo sapiens 108-111 12694376-4 2003 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a PKC activator, markedly promoted lamellipodia formation, while safingol (a PKC alpha-selective inhibitor) blocked the TPA-induced lamellipodial actin structure. Tetradecanoylphorbol Acetate 15-51 protein kinase C alpha Homo sapiens 61-64 12562561-2 2003 An activator of classical and novel isoforms of PKC, phorbol 12-myristate-13-acetate (PMA; 100 nM), inhibited CAT-1-mediated l-arginine transport in PAEC after a 1-h treatment and activated l-arginine uptake after an 18-h treatment of cells. Tetradecanoylphorbol Acetate 53-84 protein kinase C alpha Homo sapiens 48-51 12562561-2 2003 An activator of classical and novel isoforms of PKC, phorbol 12-myristate-13-acetate (PMA; 100 nM), inhibited CAT-1-mediated l-arginine transport in PAEC after a 1-h treatment and activated l-arginine uptake after an 18-h treatment of cells. Tetradecanoylphorbol Acetate 86-89 protein kinase C alpha Homo sapiens 48-51 12562561-4 2003 The inhibitory effect of PMA on l-arginine transport was accompanied by a translocation of PKCalpha (a classical PKC isoform) from the cytosol to the membrane fraction, whereas the activating effect of PMA on l-arginine transport was accompanied by full depletion of the expression of PKCalpha in PAEC. Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 91-99 12562561-4 2003 The inhibitory effect of PMA on l-arginine transport was accompanied by a translocation of PKCalpha (a classical PKC isoform) from the cytosol to the membrane fraction, whereas the activating effect of PMA on l-arginine transport was accompanied by full depletion of the expression of PKCalpha in PAEC. Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 91-94 12562561-4 2003 The inhibitory effect of PMA on l-arginine transport was accompanied by a translocation of PKCalpha (a classical PKC isoform) from the cytosol to the membrane fraction, whereas the activating effect of PMA on l-arginine transport was accompanied by full depletion of the expression of PKCalpha in PAEC. Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 285-293 12562561-4 2003 The inhibitory effect of PMA on l-arginine transport was accompanied by a translocation of PKCalpha (a classical PKC isoform) from the cytosol to the membrane fraction, whereas the activating effect of PMA on l-arginine transport was accompanied by full depletion of the expression of PKCalpha in PAEC. Tetradecanoylphorbol Acetate 202-205 protein kinase C alpha Homo sapiens 285-293 12707358-2 2003 A protein kinase C (PKC) inhibitor (staurosporine), tyrosine kinase inhibitors (genistein and herbimycin A), or a Src kinase inhibitor (PP2) attenuated TNF-alpha- or 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced COX-2 promoter activity. Tetradecanoylphorbol Acetate 166-202 protein kinase C alpha Homo sapiens 20-23 12694376-4 2003 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a PKC activator, markedly promoted lamellipodia formation, while safingol (a PKC alpha-selective inhibitor) blocked the TPA-induced lamellipodial actin structure. Tetradecanoylphorbol Acetate 53-56 protein kinase C alpha Homo sapiens 61-64 12694376-4 2003 Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), a PKC activator, markedly promoted lamellipodia formation, while safingol (a PKC alpha-selective inhibitor) blocked the TPA-induced lamellipodial actin structure. Tetradecanoylphorbol Acetate 179-182 protein kinase C alpha Homo sapiens 136-145 12694376-5 2003 Both wound-healing and Boyden migration assays showed that TPA treatment promoted neuronal migration of GT1 cells; however, cotreatment of TPA with safingol or rottlerin (a PKC delta-selective inhibitor) clearly blocked this TPA effect, indicating that both PKC alpha and PKC delta may be positive regulators of neuronal migration. Tetradecanoylphorbol Acetate 59-62 protein kinase C alpha Homo sapiens 258-267 12694376-5 2003 Both wound-healing and Boyden migration assays showed that TPA treatment promoted neuronal migration of GT1 cells; however, cotreatment of TPA with safingol or rottlerin (a PKC delta-selective inhibitor) clearly blocked this TPA effect, indicating that both PKC alpha and PKC delta may be positive regulators of neuronal migration. Tetradecanoylphorbol Acetate 139-142 protein kinase C alpha Homo sapiens 258-267 12694376-7 2003 Among the PKC downstream signal molecules, p130Cas, a mediator of cell migration, and its kinase, focal adhesion kinase (FAK), increased following TPA treatment; phosphorylation of p130Cas was induced in a PKC alpha-dependent manner. Tetradecanoylphorbol Acetate 147-150 protein kinase C alpha Homo sapiens 10-13 12694376-7 2003 Among the PKC downstream signal molecules, p130Cas, a mediator of cell migration, and its kinase, focal adhesion kinase (FAK), increased following TPA treatment; phosphorylation of p130Cas was induced in a PKC alpha-dependent manner. Tetradecanoylphorbol Acetate 147-150 protein kinase C alpha Homo sapiens 206-215 12693944-4 2003 The osteoblast-like cell line MG-63 was pretreated with calphostin C, a PKC inhibitor, or phorbol 12-myristate 13-acetate (PMA) for an extended period, a condition which causes PKC downregulation, and subsequently with AA. Tetradecanoylphorbol Acetate 90-121 protein kinase C alpha Homo sapiens 177-180 12693944-4 2003 The osteoblast-like cell line MG-63 was pretreated with calphostin C, a PKC inhibitor, or phorbol 12-myristate 13-acetate (PMA) for an extended period, a condition which causes PKC downregulation, and subsequently with AA. Tetradecanoylphorbol Acetate 123-126 protein kinase C alpha Homo sapiens 177-180 12454035-8 2002 The PKC inhibitor GF109203X inhibited PMA-induced, but not basal or EGF-induced, phosphorylation of ERK, whereas the EGF receptor inhibitor tyrphostin AG1478 blocked basal and EGF-, but not PMA-, induced phosphorylation of ERK. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 4-7 12813560-9 2003 We used the PKC activator TPA (12-O-tetradecanoyl phorbol 13-acetate) and the PKC inhibitor Calphostin C (Cal C). Tetradecanoylphorbol Acetate 26-29 protein kinase C alpha Homo sapiens 12-15 12813560-13 2003 We speculated that the reason for changes after TPA treatment was the interactions with activated PKC alpha, which provoked syndecan-4/PKC alpha complex translocation to integrins. Tetradecanoylphorbol Acetate 48-51 protein kinase C alpha Homo sapiens 98-107 12813560-13 2003 We speculated that the reason for changes after TPA treatment was the interactions with activated PKC alpha, which provoked syndecan-4/PKC alpha complex translocation to integrins. Tetradecanoylphorbol Acetate 48-51 protein kinase C alpha Homo sapiens 135-144 12183077-3 2002 We found that the specific PKC inhibitor GF109203 suppressed the morphological change and the alpha-naphthyl acetate esterase activity induced in ML-1 cells by treatment with KH1060 plus TPA. Tetradecanoylphorbol Acetate 187-190 protein kinase C alpha Homo sapiens 27-30 12183077-5 2002 ML-1 cells treated with KH1060 alone increased translocation of PKC theta, whereas cells treated with TPA alone increased translocation of PKC alpha and PKC epsilon. Tetradecanoylphorbol Acetate 102-105 protein kinase C alpha Homo sapiens 139-148 12472895-2 2002 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced neurite outgrowth and growth cone formation, effects that were blocked by GF 109203X (a PKC inhibitor), safingolTM(a PKCalpha-selective inhibitor), but not by rottlerinTM (a PKCdelta-selective inhibitor), indicating that PKCalpha may be selectively involved in neurite outgrowth and cytoskeletal changes of filamentous actin and beta-tubulin. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 139-142 12472895-2 2002 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced neurite outgrowth and growth cone formation, effects that were blocked by GF 109203X (a PKC inhibitor), safingolTM(a PKCalpha-selective inhibitor), but not by rottlerinTM (a PKCdelta-selective inhibitor), indicating that PKCalpha may be selectively involved in neurite outgrowth and cytoskeletal changes of filamentous actin and beta-tubulin. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 168-176 12472895-2 2002 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced neurite outgrowth and growth cone formation, effects that were blocked by GF 109203X (a PKC inhibitor), safingolTM(a PKCalpha-selective inhibitor), but not by rottlerinTM (a PKCdelta-selective inhibitor), indicating that PKCalpha may be selectively involved in neurite outgrowth and cytoskeletal changes of filamentous actin and beta-tubulin. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 272-280 12472895-2 2002 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced neurite outgrowth and growth cone formation, effects that were blocked by GF 109203X (a PKC inhibitor), safingolTM(a PKCalpha-selective inhibitor), but not by rottlerinTM (a PKCdelta-selective inhibitor), indicating that PKCalpha may be selectively involved in neurite outgrowth and cytoskeletal changes of filamentous actin and beta-tubulin. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 139-142 12472895-2 2002 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced neurite outgrowth and growth cone formation, effects that were blocked by GF 109203X (a PKC inhibitor), safingolTM(a PKCalpha-selective inhibitor), but not by rottlerinTM (a PKCdelta-selective inhibitor), indicating that PKCalpha may be selectively involved in neurite outgrowth and cytoskeletal changes of filamentous actin and beta-tubulin. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 168-176 12472895-2 2002 12-O-Tetradecanoylphorbol-13-acetate (TPA) induced neurite outgrowth and growth cone formation, effects that were blocked by GF 109203X (a PKC inhibitor), safingolTM(a PKCalpha-selective inhibitor), but not by rottlerinTM (a PKCdelta-selective inhibitor), indicating that PKCalpha may be selectively involved in neurite outgrowth and cytoskeletal changes of filamentous actin and beta-tubulin. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 272-280 12472895-4 2002 TPA treatment induced relocalization of PKCalpha-EGFP to growth cones and cell-cell adhesion sites, PKCgamma-EGFP to the nucleus, and PKCdelta-EGFP to the membrane ruffle, respectively. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 40-48 12472895-9 2002 Specific inhibition of PKCalpha with safingol blocked the phosphorylation of ERK induced by TPA. Tetradecanoylphorbol Acetate 92-95 protein kinase C alpha Homo sapiens 23-31 12631114-21 2003 The phorbol ester, PMA (phorbol 12-myristate 13-acetate), a PKC activator, mimicked the effect of PTH on chondrocyte differentiation. Tetradecanoylphorbol Acetate 19-22 protein kinase C alpha Homo sapiens 60-63 12631114-21 2003 The phorbol ester, PMA (phorbol 12-myristate 13-acetate), a PKC activator, mimicked the effect of PTH on chondrocyte differentiation. Tetradecanoylphorbol Acetate 24-55 protein kinase C alpha Homo sapiens 60-63 12454035-7 2002 Phorbol 12-myristate 13-acetate (PMA) caused PKC-alpha, -betaI, and - epsilon, initially present in the cytoplasm, to be translocated to the membrane and nuclear subcellular fractions and PKC-delta to be depleted from the cytoskeleton. Tetradecanoylphorbol Acetate 0-31 protein kinase C alpha Homo sapiens 45-54 12454035-7 2002 Phorbol 12-myristate 13-acetate (PMA) caused PKC-alpha, -betaI, and - epsilon, initially present in the cytoplasm, to be translocated to the membrane and nuclear subcellular fractions and PKC-delta to be depleted from the cytoskeleton. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 45-54 12381534-8 2002 Treatment with PMA induced translocation of PKC-alpha, -delta, and -mu from cytosol to membrane. Tetradecanoylphorbol Acetate 15-18 protein kinase C alpha Homo sapiens 44-70 12372816-2 2002 We recently showed that the phorbol ester PMA (100 nM) induces prompt activation of the novel isoform PKCepsilon followed by late activation of the conventional isoform PKCalpha in T84 intestinal epithelia. Tetradecanoylphorbol Acetate 42-45 protein kinase C alpha Homo sapiens 169-177 12372816-9 2002 The Ca2+ agonist thapsigargin (5 microM) induced early activation of PKC when added simultaneously with PMA. Tetradecanoylphorbol Acetate 104-107 protein kinase C alpha Homo sapiens 69-72 12372810-2 2002 The effect of the phorbol ester phorbol 12-myristate 13-acetate (PMA), an in vitro PKC agonist, on OH- gradient-driven 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid (DIDS)-sensitive 36Cl uptake in Caco-2 cells was assessed. Tetradecanoylphorbol Acetate 32-63 protein kinase C alpha Homo sapiens 83-86 12381534-10 2002 Addition of PKC-alpha inhibitor Go-6976 at a nanomolar concentration, other PKC inhibitors Go-6983 and GF-109203X, or PKC-delta-specific inhibitor rottlerin significantly inhibited PMA-mediated NT release. Tetradecanoylphorbol Acetate 181-184 protein kinase C alpha Homo sapiens 12-21 12381534-10 2002 Addition of PKC-alpha inhibitor Go-6976 at a nanomolar concentration, other PKC inhibitors Go-6983 and GF-109203X, or PKC-delta-specific inhibitor rottlerin significantly inhibited PMA-mediated NT release. Tetradecanoylphorbol Acetate 181-184 protein kinase C alpha Homo sapiens 12-15 12376314-1 2002 Culturing clonal beta-cells (HIT-T15) overnight in the presence of phorbol ester [phorbol myristate acetate (PMA)] enhanced insulin secretion while causing downregulation of some protein kinase C (PKC) isoforms and most PKC activity. Tetradecanoylphorbol Acetate 82-107 protein kinase C alpha Homo sapiens 197-200 12186945-1 2002 We have previously suggested that PKCalpha has a role in 12-O-Tetradecanoylphorbol-13-acetate (TPA)-mediated growth arrest and myogenic differentiation in human embryonal rhabdomyosarcoma cells (RD). Tetradecanoylphorbol Acetate 57-93 protein kinase C alpha Homo sapiens 34-42 12376314-1 2002 Culturing clonal beta-cells (HIT-T15) overnight in the presence of phorbol ester [phorbol myristate acetate (PMA)] enhanced insulin secretion while causing downregulation of some protein kinase C (PKC) isoforms and most PKC activity. Tetradecanoylphorbol Acetate 82-107 protein kinase C alpha Homo sapiens 220-223 12376314-1 2002 Culturing clonal beta-cells (HIT-T15) overnight in the presence of phorbol ester [phorbol myristate acetate (PMA)] enhanced insulin secretion while causing downregulation of some protein kinase C (PKC) isoforms and most PKC activity. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 197-200 12376314-1 2002 Culturing clonal beta-cells (HIT-T15) overnight in the presence of phorbol ester [phorbol myristate acetate (PMA)] enhanced insulin secretion while causing downregulation of some protein kinase C (PKC) isoforms and most PKC activity. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 220-223 12376314-7 2002 Therefore, stimulation of insulin secretion by PMA, and presumably by endogenous diacylglycerol, involves the activation of PKC isoforms delta and/or mu, and also PKC-alpha. Tetradecanoylphorbol Acetate 47-50 protein kinase C alpha Homo sapiens 163-172 12149272-2 2002 Previous studies demonstrated an inhibition of LPL activity and synthesis following depletion of protein kinase C (PKC) isoforms with long term treatment of 3T3-F442A adipocytes with 12-O-tetradecanoylphorbol-13-acetate. Tetradecanoylphorbol Acetate 183-219 protein kinase C alpha Homo sapiens 115-118 12186945-1 2002 We have previously suggested that PKCalpha has a role in 12-O-Tetradecanoylphorbol-13-acetate (TPA)-mediated growth arrest and myogenic differentiation in human embryonal rhabdomyosarcoma cells (RD). Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 34-42 12186945-2 2002 Here, by monitoring the signalling pathways triggered by TPA, we demonstrate that PKCalpha mediates these effects by inducing transient activation of c-Jun N-terminal protein kinases (JNKs) and sustained activation of both p38 kinase and extracellular signal-regulated kinases (ERKs) (all referred to as MAPKs). Tetradecanoylphorbol Acetate 57-60 protein kinase C alpha Homo sapiens 82-90 12110540-4 2002 Phorbol 12-myristrate 13-acetate (PMA) activated PKC-alpha and exogenous PKC-delta but not atypical PKC-lambda/zeta. Tetradecanoylphorbol Acetate 34-37 protein kinase C alpha Homo sapiens 49-58 12490289-7 2002 In parallel a greater increase of PKCalpha translocation after PMA treatment compared to controls was observed. Tetradecanoylphorbol Acetate 63-66 protein kinase C alpha Homo sapiens 34-42 12167592-10 2002 The stimulatory effects of LDL on PAI-1, tPA, and uPA gene regulation in HMC were blocked by the inhibition of PKC using GF-109203X 12 h after treatment with LDL or downregulation of PKC using phorbol myristate acetate. Tetradecanoylphorbol Acetate 193-218 protein kinase C alpha Homo sapiens 111-114 12205039-4 2002 BK-induced COX-2 expression and prostaglandin E2 (PGE2) accumulation were mimicked by the direct PKC activator phorbol 12-myristate 13-acetate (PMA) and inhibited by the broad spectrum PKC inhibitor bisindolylmaleimide I. Tetradecanoylphorbol Acetate 111-142 protein kinase C alpha Homo sapiens 97-100 12205039-4 2002 BK-induced COX-2 expression and prostaglandin E2 (PGE2) accumulation were mimicked by the direct PKC activator phorbol 12-myristate 13-acetate (PMA) and inhibited by the broad spectrum PKC inhibitor bisindolylmaleimide I. Tetradecanoylphorbol Acetate 144-147 protein kinase C alpha Homo sapiens 97-100 12205039-4 2002 BK-induced COX-2 expression and prostaglandin E2 (PGE2) accumulation were mimicked by the direct PKC activator phorbol 12-myristate 13-acetate (PMA) and inhibited by the broad spectrum PKC inhibitor bisindolylmaleimide I. Tetradecanoylphorbol Acetate 144-147 protein kinase C alpha Homo sapiens 185-188 11997388-7 2002 The ionomycin-induced transient translocation of PKCalpha-GFP was prolonged by staurosporine, diacylglycerol, and phorbol myristate acetate. Tetradecanoylphorbol Acetate 114-139 protein kinase C alpha Homo sapiens 49-57 12187329-8 2002 While TPA treatment resulted in translocation of the PKC isoforms alpha, delta and epsilon, SC-10 and FTT failed to induce alterations in the PKC content of the membrane and cytosolic fractions, respectively. Tetradecanoylphorbol Acetate 6-9 protein kinase C alpha Homo sapiens 53-97 12187329-8 2002 While TPA treatment resulted in translocation of the PKC isoforms alpha, delta and epsilon, SC-10 and FTT failed to induce alterations in the PKC content of the membrane and cytosolic fractions, respectively. Tetradecanoylphorbol Acetate 6-9 protein kinase C alpha Homo sapiens 53-56 12110540-9 2002 These findings demonstrate that both conventional and novel PKC isoforms are involved in PMA-stimulated glucose transport and that other novel PKC isoforms could participate in PMA-stimulated and insulin-stimulated glucose transport. Tetradecanoylphorbol Acetate 89-92 protein kinase C alpha Homo sapiens 60-63 12110540-9 2002 These findings demonstrate that both conventional and novel PKC isoforms are involved in PMA-stimulated glucose transport and that other novel PKC isoforms could participate in PMA-stimulated and insulin-stimulated glucose transport. Tetradecanoylphorbol Acetate 177-180 protein kinase C alpha Homo sapiens 143-146 12130708-4 2002 Furthermore, depletion of PKC by 12-O-tetradecanoylphorbol-13-acetate exposure (48 h, 1 microM) also prevented OFQ/N-mediated mu and ORL1 desensitization. Tetradecanoylphorbol Acetate 33-69 protein kinase C alpha Homo sapiens 26-29 12083800-7 2002 Following treatment with a PKC activator, phorbol 12-myristate 13-acetate (PMA), CGs were released and PKCalpha and -gamma were translocated to the membrane. Tetradecanoylphorbol Acetate 42-73 protein kinase C alpha Homo sapiens 27-30 12203369-3 2002 Two protein kinase C (PKC) isoforms, conventional PKC (cPKC) and novel PKC (nPKC), but not apical PKC, translocated from the cytosolic to the particulate fraction upon TPA treatment. Tetradecanoylphorbol Acetate 168-171 protein kinase C alpha Homo sapiens 22-25 12203369-3 2002 Two protein kinase C (PKC) isoforms, conventional PKC (cPKC) and novel PKC (nPKC), but not apical PKC, translocated from the cytosolic to the particulate fraction upon TPA treatment. Tetradecanoylphorbol Acetate 168-171 protein kinase C alpha Homo sapiens 50-53 12203369-3 2002 Two protein kinase C (PKC) isoforms, conventional PKC (cPKC) and novel PKC (nPKC), but not apical PKC, translocated from the cytosolic to the particulate fraction upon TPA treatment. Tetradecanoylphorbol Acetate 168-171 protein kinase C alpha Homo sapiens 50-53 12203369-3 2002 Two protein kinase C (PKC) isoforms, conventional PKC (cPKC) and novel PKC (nPKC), but not apical PKC, translocated from the cytosolic to the particulate fraction upon TPA treatment. Tetradecanoylphorbol Acetate 168-171 protein kinase C alpha Homo sapiens 50-53 12203369-8 2002 Furthermore, PKC inhibitors or an MEK inhibitor completely suppressed both TPA-induced activation of MAPK and promotion of anchorage-independent growth, but a cPKC-selective inhibitor partially suppressed TPA-induced promotion of the growth. Tetradecanoylphorbol Acetate 75-78 protein kinase C alpha Homo sapiens 13-16 12083800-7 2002 Following treatment with a PKC activator, phorbol 12-myristate 13-acetate (PMA), CGs were released and PKCalpha and -gamma were translocated to the membrane. Tetradecanoylphorbol Acetate 42-73 protein kinase C alpha Homo sapiens 103-122 12083800-7 2002 Following treatment with a PKC activator, phorbol 12-myristate 13-acetate (PMA), CGs were released and PKCalpha and -gamma were translocated to the membrane. Tetradecanoylphorbol Acetate 75-78 protein kinase C alpha Homo sapiens 27-30 12083800-7 2002 Following treatment with a PKC activator, phorbol 12-myristate 13-acetate (PMA), CGs were released and PKCalpha and -gamma were translocated to the membrane. Tetradecanoylphorbol Acetate 75-78 protein kinase C alpha Homo sapiens 103-122 12074591-2 2002 In G361 cell line, which lacks PKCalpha, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced PLD activation was potentiated by introducing PKCalpha by the adenovirus vector. Tetradecanoylphorbol Acetate 41-77 protein kinase C alpha Homo sapiens 31-39 12110618-2 2002 The phorbol ester TPA, an activator of protein kinase C (PKC), inhibits cholinergic stimulation of gastric acid secretion but increases basal H(+) secretion. Tetradecanoylphorbol Acetate 18-21 protein kinase C alpha Homo sapiens 57-60 12074591-2 2002 In G361 cell line, which lacks PKCalpha, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced PLD activation was potentiated by introducing PKCalpha by the adenovirus vector. Tetradecanoylphorbol Acetate 41-77 protein kinase C alpha Homo sapiens 138-146 12074591-2 2002 In G361 cell line, which lacks PKCalpha, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced PLD activation was potentiated by introducing PKCalpha by the adenovirus vector. Tetradecanoylphorbol Acetate 79-82 protein kinase C alpha Homo sapiens 31-39 12074591-2 2002 In G361 cell line, which lacks PKCalpha, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced PLD activation was potentiated by introducing PKCalpha by the adenovirus vector. Tetradecanoylphorbol Acetate 79-82 protein kinase C alpha Homo sapiens 138-146 12074591-3 2002 The kinase-negative PKCalpha elevated TPA-induced PLD activity less significantly than the wild type. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 20-28 12074591-6 2002 Furthermore, the TPA treatment increased the association of PKCalpha, PKCbetaII, and their kinase-negative mutants with PLD1 in melanoma cells. Tetradecanoylphorbol Acetate 17-20 protein kinase C alpha Homo sapiens 60-68 18759046-3 2002 Treatment of cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in the translocation of PKCalpha from both mitochondria and cytosol to nucleus as clearly shown by laserscanningconfocal microscopy, while the protein level of PKCalpha was not changed by TPA treatment as detected by Western blot. Tetradecanoylphorbol Acetate 24-60 protein kinase C alpha Homo sapiens 100-108 12191496-3 2002 Here we report that secretion and expression of HGF in U87 astrocytoma is increased by a PKC activator, PMA, an effect which is abolished by a PKC inhibitor, Go6976, specific for PKCalpha and PKCbeta1. Tetradecanoylphorbol Acetate 104-107 protein kinase C alpha Homo sapiens 89-92 12191496-3 2002 Here we report that secretion and expression of HGF in U87 astrocytoma is increased by a PKC activator, PMA, an effect which is abolished by a PKC inhibitor, Go6976, specific for PKCalpha and PKCbeta1. Tetradecanoylphorbol Acetate 104-107 protein kinase C alpha Homo sapiens 143-146 12191496-3 2002 Here we report that secretion and expression of HGF in U87 astrocytoma is increased by a PKC activator, PMA, an effect which is abolished by a PKC inhibitor, Go6976, specific for PKCalpha and PKCbeta1. Tetradecanoylphorbol Acetate 104-107 protein kinase C alpha Homo sapiens 179-187 12191496-7 2002 In addition, such effect of PKC is Ras-dependent as specific Ras inhibitor L-744,832 attenuated both PMA mediated induction of Erk 1/2 phosphorylation as well as HGF secretion. Tetradecanoylphorbol Acetate 101-104 protein kinase C alpha Homo sapiens 28-31 18759046-3 2002 Treatment of cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in the translocation of PKCalpha from both mitochondria and cytosol to nucleus as clearly shown by laserscanningconfocal microscopy, while the protein level of PKCalpha was not changed by TPA treatment as detected by Western blot. Tetradecanoylphorbol Acetate 24-60 protein kinase C alpha Homo sapiens 236-244 18759046-3 2002 Treatment of cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in the translocation of PKCalpha from both mitochondria and cytosol to nucleus as clearly shown by laserscanningconfocal microscopy, while the protein level of PKCalpha was not changed by TPA treatment as detected by Western blot. Tetradecanoylphorbol Acetate 62-65 protein kinase C alpha Homo sapiens 100-108 18759046-3 2002 Treatment of cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in the translocation of PKCalpha from both mitochondria and cytosol to nucleus as clearly shown by laserscanningconfocal microscopy, while the protein level of PKCalpha was not changed by TPA treatment as detected by Western blot. Tetradecanoylphorbol Acetate 62-65 protein kinase C alpha Homo sapiens 236-244 18759046-3 2002 Treatment of cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) resulted in the translocation of PKCalpha from both mitochondria and cytosol to nucleus as clearly shown by laserscanningconfocal microscopy, while the protein level of PKCalpha was not changed by TPA treatment as detected by Western blot. Tetradecanoylphorbol Acetate 264-267 protein kinase C alpha Homo sapiens 100-108 18759046-4 2002 The results also revealed that TPA-induced translocation of PKCalpha was in close association with apoptosis induction, and such association was further affirmed by other experiments where various apoptotic stimuli and specific inhibitors of PKC were used. Tetradecanoylphorbol Acetate 31-34 protein kinase C alpha Homo sapiens 60-68 18759046-4 2002 The results also revealed that TPA-induced translocation of PKCalpha was in close association with apoptosis induction, and such association was further affirmed by other experiments where various apoptotic stimuli and specific inhibitors of PKC were used. Tetradecanoylphorbol Acetate 31-34 protein kinase C alpha Homo sapiens 60-63 11950946-5 2002 Down-regulation of diacylglycerol-sensitive types of protein kinase C (PKC) by pretreatment with phorbol 12-myristate 13-acetate or inhibition with bisindolylmaleimide prevented the DA-mediated increase in Na,K-ATPase activity and exocytosis of Na,K-pumps to the BLM. Tetradecanoylphorbol Acetate 97-128 protein kinase C alpha Homo sapiens 71-74 11907165-3 2002 In this study, by using the primary cultures of hypothalamic neurons, we tested the effects of PKC stimulator phorbol ester 4 beta-phorbol 12-myristate-13-acetate (PMA) and PKC inhibitor chelerythrine chloride on ethanol-induced IR-beta-EP release. Tetradecanoylphorbol Acetate 164-167 protein kinase C alpha Homo sapiens 95-98 11751911-11 2002 However, cotransfection with dominant negative mutants of PKCalpha or c-Src inhibited both IFN-gamma- and TPA-induced ICAM-1 promoter activity. Tetradecanoylphorbol Acetate 106-109 protein kinase C alpha Homo sapiens 58-66 11751911-6 2002 12-O-Tetradecanoylphorbol-13-acetate (TPA), a PKC activator, stimulated ICAM-1 expression; this effect was inhibited by tyrosine kinase or Src inhibitor. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 46-49 11751911-6 2002 12-O-Tetradecanoylphorbol-13-acetate (TPA), a PKC activator, stimulated ICAM-1 expression; this effect was inhibited by tyrosine kinase or Src inhibitor. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 46-49 11864993-7 2002 A mechanism whereby PKC alpha might regulate hypertrophy was suggested by the observations that wild-type PKC alpha induced extracellular signal-regulated kinase1/2 (ERK1/2), that dominant negative PKC alpha inhibited PMA-induced ERK1/2 activation, and that dominant negative MEK1 (up-stream of ERK1/2) inhibited wild-type PKC alpha-induced hypertrophic growth. Tetradecanoylphorbol Acetate 218-221 protein kinase C alpha Homo sapiens 20-29 11864993-7 2002 A mechanism whereby PKC alpha might regulate hypertrophy was suggested by the observations that wild-type PKC alpha induced extracellular signal-regulated kinase1/2 (ERK1/2), that dominant negative PKC alpha inhibited PMA-induced ERK1/2 activation, and that dominant negative MEK1 (up-stream of ERK1/2) inhibited wild-type PKC alpha-induced hypertrophic growth. Tetradecanoylphorbol Acetate 218-221 protein kinase C alpha Homo sapiens 106-115 11864993-7 2002 A mechanism whereby PKC alpha might regulate hypertrophy was suggested by the observations that wild-type PKC alpha induced extracellular signal-regulated kinase1/2 (ERK1/2), that dominant negative PKC alpha inhibited PMA-induced ERK1/2 activation, and that dominant negative MEK1 (up-stream of ERK1/2) inhibited wild-type PKC alpha-induced hypertrophic growth. Tetradecanoylphorbol Acetate 218-221 protein kinase C alpha Homo sapiens 106-115 11864993-7 2002 A mechanism whereby PKC alpha might regulate hypertrophy was suggested by the observations that wild-type PKC alpha induced extracellular signal-regulated kinase1/2 (ERK1/2), that dominant negative PKC alpha inhibited PMA-induced ERK1/2 activation, and that dominant negative MEK1 (up-stream of ERK1/2) inhibited wild-type PKC alpha-induced hypertrophic growth. Tetradecanoylphorbol Acetate 218-221 protein kinase C alpha Homo sapiens 106-115 11861786-4 2002 This effect was significantly reduced by the PKC-specific inhibitor bisindolylmaleimide (GF109203X), by down-regulation of PKC with 12-O-tetradecanoyl-phorbol 13-acetate, by a pseudosubstrate to PKCalpha, and by selective down-regulation of PKCalpha by prior lead exposure. Tetradecanoylphorbol Acetate 132-169 protein kinase C alpha Homo sapiens 45-48 11861786-4 2002 This effect was significantly reduced by the PKC-specific inhibitor bisindolylmaleimide (GF109203X), by down-regulation of PKC with 12-O-tetradecanoyl-phorbol 13-acetate, by a pseudosubstrate to PKCalpha, and by selective down-regulation of PKCalpha by prior lead exposure. Tetradecanoylphorbol Acetate 132-169 protein kinase C alpha Homo sapiens 123-126 11861786-4 2002 This effect was significantly reduced by the PKC-specific inhibitor bisindolylmaleimide (GF109203X), by down-regulation of PKC with 12-O-tetradecanoyl-phorbol 13-acetate, by a pseudosubstrate to PKCalpha, and by selective down-regulation of PKCalpha by prior lead exposure. Tetradecanoylphorbol Acetate 132-169 protein kinase C alpha Homo sapiens 241-249 11744714-8 2002 12-O-Tetradecanoyl phorbol 13-acetate (16 nm), a PKC activator, reproduced the effects of gp160 in untreated cells. Tetradecanoylphorbol Acetate 0-37 protein kinase C alpha Homo sapiens 49-52 11952172-7 2002 In our experimental conditions phorbol myristate acetate (PMA) induced a rapid depletion of PKCalpha in the cytosolic fraction and its translocation toward the particulate fraction. Tetradecanoylphorbol Acetate 31-56 protein kinase C alpha Homo sapiens 92-100 11952825-3 2002 An overnight treatment of isolated HaCaT keratinocytes with phorbol 12-myristate 13-acetate (PMA) selectively downregulated the classical, calcium-dependent protein kinase C (PKC) isoenzyme PKC alpha in preconfluent cells. Tetradecanoylphorbol Acetate 60-91 protein kinase C alpha Homo sapiens 175-178 11952825-3 2002 An overnight treatment of isolated HaCaT keratinocytes with phorbol 12-myristate 13-acetate (PMA) selectively downregulated the classical, calcium-dependent protein kinase C (PKC) isoenzyme PKC alpha in preconfluent cells. Tetradecanoylphorbol Acetate 60-91 protein kinase C alpha Homo sapiens 190-199 11952825-3 2002 An overnight treatment of isolated HaCaT keratinocytes with phorbol 12-myristate 13-acetate (PMA) selectively downregulated the classical, calcium-dependent protein kinase C (PKC) isoenzyme PKC alpha in preconfluent cells. Tetradecanoylphorbol Acetate 93-96 protein kinase C alpha Homo sapiens 175-178 11952825-3 2002 An overnight treatment of isolated HaCaT keratinocytes with phorbol 12-myristate 13-acetate (PMA) selectively downregulated the classical, calcium-dependent protein kinase C (PKC) isoenzyme PKC alpha in preconfluent cells. Tetradecanoylphorbol Acetate 93-96 protein kinase C alpha Homo sapiens 190-199 11952172-7 2002 In our experimental conditions phorbol myristate acetate (PMA) induced a rapid depletion of PKCalpha in the cytosolic fraction and its translocation toward the particulate fraction. Tetradecanoylphorbol Acetate 58-61 protein kinase C alpha Homo sapiens 92-100 11952172-8 2002 Long term exposure of myotubes in the presence of PMA induced down-regulation of PKCalpha, this process being partially blocked by calpain inhibitors (CS peptide and inhibitor II) and antisense oligonucleotides for the two major ubiquitous calpain isoforms (m- and micro-calpains). Tetradecanoylphorbol Acetate 50-53 protein kinase C alpha Homo sapiens 81-89 11726535-6 2001 Three DAG species significantly curtailed the PMA-induced activation of beta Iota, gamma, and delta, but not of alpha and epsilon, isoforms of PKC. Tetradecanoylphorbol Acetate 46-49 protein kinase C alpha Homo sapiens 143-146 11584014-5 2002 Moreover, different PKC isozymes were found to mediate the apoptotic effect of phorbol 12-myristate 13-acetate (PMA) and HK654 in LNCaP cells. Tetradecanoylphorbol Acetate 79-110 protein kinase C alpha Homo sapiens 20-23 11584014-5 2002 Moreover, different PKC isozymes were found to mediate the apoptotic effect of phorbol 12-myristate 13-acetate (PMA) and HK654 in LNCaP cells. Tetradecanoylphorbol Acetate 112-115 protein kinase C alpha Homo sapiens 20-23 11584014-6 2002 Using PKC inhibitors and dominant negative PKC isoforms, we found that both PKCalpha and PKCdelta mediated the apoptotic effect of PMA, whereas only PKCalpha was involved in the effect of the DAG-lactone. Tetradecanoylphorbol Acetate 131-134 protein kinase C alpha Homo sapiens 6-9 11584014-6 2002 Using PKC inhibitors and dominant negative PKC isoforms, we found that both PKCalpha and PKCdelta mediated the apoptotic effect of PMA, whereas only PKCalpha was involved in the effect of the DAG-lactone. Tetradecanoylphorbol Acetate 131-134 protein kinase C alpha Homo sapiens 43-46 11584014-6 2002 Using PKC inhibitors and dominant negative PKC isoforms, we found that both PKCalpha and PKCdelta mediated the apoptotic effect of PMA, whereas only PKCalpha was involved in the effect of the DAG-lactone. Tetradecanoylphorbol Acetate 131-134 protein kinase C alpha Homo sapiens 76-84 11669302-9 2001 PKC alpha was the only isoform that translocated to the membrane upon stimulation with phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 87-112 protein kinase C alpha Homo sapiens 0-9 11600418-5 2001 The mRNA levels of the NHE isoforms in Caco-2 cells were initially measured by a semiquantitative RT-PCR technique in response to PKC downregulation by long-term exposure to 1 microM 12-O-tetradecanoylphorbol-13-acetate (TPA) for 24 h. PKC downregulation resulted in an approximately 60% increase in the mRNA level for NHE3, but not for NHE1 or NHE2. Tetradecanoylphorbol Acetate 183-219 protein kinase C alpha Homo sapiens 130-133 11600418-5 2001 The mRNA levels of the NHE isoforms in Caco-2 cells were initially measured by a semiquantitative RT-PCR technique in response to PKC downregulation by long-term exposure to 1 microM 12-O-tetradecanoylphorbol-13-acetate (TPA) for 24 h. PKC downregulation resulted in an approximately 60% increase in the mRNA level for NHE3, but not for NHE1 or NHE2. Tetradecanoylphorbol Acetate 221-224 protein kinase C alpha Homo sapiens 130-133 11600418-7 2001 Consistent with the mRNA results, our data showed that amiloride-sensitive (22)Na(+) uptake was increased after incubation of Caco-2 cells with 1 microM TPA for 24 h. To elucidate the role of PKC-alpha, an isoform downregulated by TPA, the relative abundance of NHE isoform mRNA levels and the apical NHE activity were assessed in Caco-2 cells over- and underexpressing PKC-alpha. Tetradecanoylphorbol Acetate 153-156 protein kinase C alpha Homo sapiens 192-201 11600418-7 2001 Consistent with the mRNA results, our data showed that amiloride-sensitive (22)Na(+) uptake was increased after incubation of Caco-2 cells with 1 microM TPA for 24 h. To elucidate the role of PKC-alpha, an isoform downregulated by TPA, the relative abundance of NHE isoform mRNA levels and the apical NHE activity were assessed in Caco-2 cells over- and underexpressing PKC-alpha. Tetradecanoylphorbol Acetate 153-156 protein kinase C alpha Homo sapiens 370-379 11669302-9 2001 PKC alpha was the only isoform that translocated to the membrane upon stimulation with phorbol myristate acetate (PMA). Tetradecanoylphorbol Acetate 114-117 protein kinase C alpha Homo sapiens 0-9 11413129-5 2001 Pre-incubation with selective protein kinase C (PKC) inhibitors GF109203X and Go6983, or transfection of dominant negative (DN)-PKC alpha, abolished phorbol 12-myristate 13-acetate-mediated c-Jun N-terminal kinase activity, although it only partially inhibited the response to trypsin. Tetradecanoylphorbol Acetate 149-180 protein kinase C alpha Homo sapiens 48-51 11532083-9 2001 In BS/GS, PKC stimulation with PMA dose dependently reduced ecNOS gene expression (from 0.80 +/- 0.05 to 0.78 +/- 0.03 densitometric units; PMA 50 nmol/L, P = NS; to 0.55 +/- 0.07, PMA 100 nmol/L, P < 0.001) to an undetectable expression (PMA 200 nmol/L). Tetradecanoylphorbol Acetate 31-34 protein kinase C alpha Homo sapiens 10-13 11532083-9 2001 In BS/GS, PKC stimulation with PMA dose dependently reduced ecNOS gene expression (from 0.80 +/- 0.05 to 0.78 +/- 0.03 densitometric units; PMA 50 nmol/L, P = NS; to 0.55 +/- 0.07, PMA 100 nmol/L, P < 0.001) to an undetectable expression (PMA 200 nmol/L). Tetradecanoylphorbol Acetate 140-143 protein kinase C alpha Homo sapiens 10-13 11532083-9 2001 In BS/GS, PKC stimulation with PMA dose dependently reduced ecNOS gene expression (from 0.80 +/- 0.05 to 0.78 +/- 0.03 densitometric units; PMA 50 nmol/L, P = NS; to 0.55 +/- 0.07, PMA 100 nmol/L, P < 0.001) to an undetectable expression (PMA 200 nmol/L). Tetradecanoylphorbol Acetate 140-143 protein kinase C alpha Homo sapiens 10-13 11413129-5 2001 Pre-incubation with selective protein kinase C (PKC) inhibitors GF109203X and Go6983, or transfection of dominant negative (DN)-PKC alpha, abolished phorbol 12-myristate 13-acetate-mediated c-Jun N-terminal kinase activity, although it only partially inhibited the response to trypsin. Tetradecanoylphorbol Acetate 149-180 protein kinase C alpha Homo sapiens 128-137 11443064-4 2001 By subcellular fractionation and Western blot, PMA (100 nM) induced sequential membrane translocation of the novel PKC epsilon followed by the conventional PKC alpha and activated both isozymes by in vitro kinase assay. Tetradecanoylphorbol Acetate 47-50 protein kinase C alpha Homo sapiens 156-165 11443050-3 2001 In neutrophilic HL60 cells, the PKC activator phorbol myristate acetate (PMA) activates multiple PKC isotypes, PKC-alpha, PKC-beta, and PKC-delta, and inhibits ligand-initiated mobilization of intracellular Ca(2+) and uptake of extracellular Ca(2+). Tetradecanoylphorbol Acetate 46-71 protein kinase C alpha Homo sapiens 32-35 11443064-7 2001 Inhibition of I(sc) by PMA was prevented by the conventional and novel PKC inhibitor Go-6850 (5 microM) but not the conventional isoform inhibitor Go-6976 (5 microM) or the PKC delta inhibitor rottlerin (10 microM), implicating PKC epsilon in inhibition of Cl(-) secretion. Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 71-74 11443050-3 2001 In neutrophilic HL60 cells, the PKC activator phorbol myristate acetate (PMA) activates multiple PKC isotypes, PKC-alpha, PKC-beta, and PKC-delta, and inhibits ligand-initiated mobilization of intracellular Ca(2+) and uptake of extracellular Ca(2+). Tetradecanoylphorbol Acetate 46-71 protein kinase C alpha Homo sapiens 97-100 11443050-3 2001 In neutrophilic HL60 cells, the PKC activator phorbol myristate acetate (PMA) activates multiple PKC isotypes, PKC-alpha, PKC-beta, and PKC-delta, and inhibits ligand-initiated mobilization of intracellular Ca(2+) and uptake of extracellular Ca(2+). Tetradecanoylphorbol Acetate 46-71 protein kinase C alpha Homo sapiens 111-120 11443050-3 2001 In neutrophilic HL60 cells, the PKC activator phorbol myristate acetate (PMA) activates multiple PKC isotypes, PKC-alpha, PKC-beta, and PKC-delta, and inhibits ligand-initiated mobilization of intracellular Ca(2+) and uptake of extracellular Ca(2+). Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 32-35 11443050-3 2001 In neutrophilic HL60 cells, the PKC activator phorbol myristate acetate (PMA) activates multiple PKC isotypes, PKC-alpha, PKC-beta, and PKC-delta, and inhibits ligand-initiated mobilization of intracellular Ca(2+) and uptake of extracellular Ca(2+). Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 97-100 11443050-3 2001 In neutrophilic HL60 cells, the PKC activator phorbol myristate acetate (PMA) activates multiple PKC isotypes, PKC-alpha, PKC-beta, and PKC-delta, and inhibits ligand-initiated mobilization of intracellular Ca(2+) and uptake of extracellular Ca(2+). Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 111-120 11488907-6 2001 Treatment of these cells with ponasterone A induced expression of PKC that was catalytically active and underwent translocation and down-regulation on exposure to 12-O-tetradecanoyl-13-phorbol acetate (TPA). Tetradecanoylphorbol Acetate 202-205 protein kinase C alpha Homo sapiens 66-69 11483407-7 2001 12-O-Tetradecanoylphorbol-13-acetate (TPA), a PKC activator, stimulated ICAM-1 expression, this effect was inhibited by genistein or tyrphostin 23. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 46-49 11483407-7 2001 12-O-Tetradecanoylphorbol-13-acetate (TPA), a PKC activator, stimulated ICAM-1 expression, this effect was inhibited by genistein or tyrphostin 23. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 46-49 11483407-13 2001 TNF-alpha- or TPA-induced ICAM-1 promoter activity was inhibited by dominant negative PKCalpha or IKK2, but not IKK1 mutant. Tetradecanoylphorbol Acetate 14-17 protein kinase C alpha Homo sapiens 86-94 11488907-8 2001 In PKC-alpha expressing cells TPA caused activation of all promoter fragments to -29 bp. Tetradecanoylphorbol Acetate 30-33 protein kinase C alpha Homo sapiens 3-12 11488907-9 2001 This finding suggests that TPA-inducible MDR1 transcription mediated through the TPA responsive factor early growth response 1 (EGR-1) in this region of the promoter may be due to activation of PKC-alpha. Tetradecanoylphorbol Acetate 27-30 protein kinase C alpha Homo sapiens 194-203 11488907-9 2001 This finding suggests that TPA-inducible MDR1 transcription mediated through the TPA responsive factor early growth response 1 (EGR-1) in this region of the promoter may be due to activation of PKC-alpha. Tetradecanoylphorbol Acetate 81-84 protein kinase C alpha Homo sapiens 194-203 11488907-11 2001 The effect of TPA on reporter gene expression was attenuated by the PKC inhibitor GF 109203X. Tetradecanoylphorbol Acetate 14-17 protein kinase C alpha Homo sapiens 68-71 11466413-3 2001 The formation of PICK1-PKCalpha complexes is strongly induced by TPA, and PICK1-PKCalpha complexes are cotargeted with PICK1-GluR2 complexes to spines, where GluR2 is found to be phosphorylated by PKC on serine 880. Tetradecanoylphorbol Acetate 65-68 protein kinase C alpha Homo sapiens 23-31 11460267-6 2001 Pretreatment of cells with the protein kinase C (PKC) inhibitor bisindolylmaleimide I, or downregulation of PKC by 24-h treatment with the phorbol ester TPA inhibited carbachol-induced MAPK activation. Tetradecanoylphorbol Acetate 153-156 protein kinase C alpha Homo sapiens 108-111 11424083-8 2001 The PLC inhibitors, neomycin and U73,122, and PKC-alpha down regulator, phorbol 12-myristate 13-acetate (PMA), were able to prevent estradiol-induced DNA synthesis in hepatoma cells, but ineffective in mammary cells; wortmannin, an inhibitor of phosphoinositide 3-kinases (PI3-K), blocked DNA synthesis in both cell lines. Tetradecanoylphorbol Acetate 72-103 protein kinase C alpha Homo sapiens 46-55 11424083-8 2001 The PLC inhibitors, neomycin and U73,122, and PKC-alpha down regulator, phorbol 12-myristate 13-acetate (PMA), were able to prevent estradiol-induced DNA synthesis in hepatoma cells, but ineffective in mammary cells; wortmannin, an inhibitor of phosphoinositide 3-kinases (PI3-K), blocked DNA synthesis in both cell lines. Tetradecanoylphorbol Acetate 105-108 protein kinase C alpha Homo sapiens 46-55 11466413-3 2001 The formation of PICK1-PKCalpha complexes is strongly induced by TPA, and PICK1-PKCalpha complexes are cotargeted with PICK1-GluR2 complexes to spines, where GluR2 is found to be phosphorylated by PKC on serine 880. Tetradecanoylphorbol Acetate 65-68 protein kinase C alpha Homo sapiens 23-26 11547951-2 2001 In this study we investigated the effects of the PKC activator phorbol 12-myristate 13-acetate (PMA) on differentiation and on PKC isozymes of human skeletal muscle satellite cells. Tetradecanoylphorbol Acetate 63-94 protein kinase C alpha Homo sapiens 49-52 11467851-4 2001 Phorbol 12-myristate, 13-acetate (PMA)-stimulated APP secretion, which was reduced by a general PKC inhibitor bisindoylmaleimide I, but not by Go 6976, which inhibits PKCalpha, beta, gamma, and mu. Tetradecanoylphorbol Acetate 34-37 protein kinase C alpha Homo sapiens 96-99 11467851-4 2001 Phorbol 12-myristate, 13-acetate (PMA)-stimulated APP secretion, which was reduced by a general PKC inhibitor bisindoylmaleimide I, but not by Go 6976, which inhibits PKCalpha, beta, gamma, and mu. Tetradecanoylphorbol Acetate 34-37 protein kinase C alpha Homo sapiens 167-175 11547951-2 2001 In this study we investigated the effects of the PKC activator phorbol 12-myristate 13-acetate (PMA) on differentiation and on PKC isozymes of human skeletal muscle satellite cells. Tetradecanoylphorbol Acetate 96-99 protein kinase C alpha Homo sapiens 49-52 11547951-7 2001 Our findings, therefore, suggest that the PMA-induced inhibition of differentiation of human skeletal muscle cells is mediated by certain PKC isoforms. Tetradecanoylphorbol Acetate 42-45 protein kinase C alpha Homo sapiens 138-141 11329379-6 2001 This dissociation was not blocked by PP1 but was mimicked by the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 98-134 protein kinase C alpha Homo sapiens 83-86 11443195-9 2001 The change in PKC isoform in PKC-depleted cells (achieved by exposure to PMA for 18 h) was also examined. Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 14-17 11329379-6 2001 This dissociation was not blocked by PP1 but was mimicked by the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 136-139 protein kinase C alpha Homo sapiens 83-86 11329379-7 2001 Also, the PKC inhibitor GF109203X abolished both the LTD(4)- and the TPA-induced dissociation of vinculin from alpha-catenin. Tetradecanoylphorbol Acetate 69-72 protein kinase C alpha Homo sapiens 10-13 11152962-5 2000 Activation of the IKK complex in response to TPA is mediated by PKC-alpha, since both the PKC inhibitor GF109203 and a catalytically inactive PKC-alpha mutant inhibit activation of endogenous IKK by TPA, but not by tumor necrosis factor-alpha (TNF-alpha). Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 64-73 11313866-3 2001 TPA-induced differentiation and growth arrest of TSU-Pr1 cells were inhibited by treatment with Protein kinase C (PKC) inhibitor GF109203X and mitogen-activated protein (MAP) kinase inhibitor PD98059. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 114-117 11313866-4 2001 Treatment of TSU-Pr1 cells with TPA for 15 min or longer resulted in translocation of PKCalpha, PKCgamma, and PKCepsilon from cytosolic to membrane fraction. Tetradecanoylphorbol Acetate 32-35 protein kinase C alpha Homo sapiens 86-94 11313866-5 2001 Our results suggest that TPA-induced TSU-Pr1 cell differentiation is associated with activation of MAP kinase and PKCalpha, PKCgamma, and PKCepsilon. Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 114-122 11222091-0 2001 Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C. We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1). Tetradecanoylphorbol Acetate 76-112 protein kinase C alpha Homo sapiens 345-348 11222091-0 2001 Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C. We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1). Tetradecanoylphorbol Acetate 191-227 protein kinase C alpha Homo sapiens 345-348 11222091-1 2001 By employing the PKC inhibitor, bisindolylmaleimide I and cotransfecting the reporter LTR construct with a vector expressing PKC-alpha, we demonstrated, in the present study, that this effect of TPA was not only independent of, but actually antagonized by, PKC. Tetradecanoylphorbol Acetate 195-198 protein kinase C alpha Homo sapiens 17-20 11222091-1 2001 By employing the PKC inhibitor, bisindolylmaleimide I and cotransfecting the reporter LTR construct with a vector expressing PKC-alpha, we demonstrated, in the present study, that this effect of TPA was not only independent of, but actually antagonized by, PKC. Tetradecanoylphorbol Acetate 195-198 protein kinase C alpha Homo sapiens 125-134 11222091-1 2001 By employing the PKC inhibitor, bisindolylmaleimide I and cotransfecting the reporter LTR construct with a vector expressing PKC-alpha, we demonstrated, in the present study, that this effect of TPA was not only independent of, but actually antagonized by, PKC. Tetradecanoylphorbol Acetate 195-198 protein kinase C alpha Homo sapiens 125-128 11222091-8 2001 Therefore, we speculate that there might be several other PKC-independent biological effects of TPA which result from interaction of such Sp1-p53 complexes with Sp1 recognition sites residing in the promoters of a wide variety of cellular and viral genes. Tetradecanoylphorbol Acetate 96-99 protein kinase C alpha Homo sapiens 58-61 11230335-7 2001 Direct activation of PKC by phorbol 12-myristate13-acetate (PMA; 10(-7) mol/L) caused a contraction similar in magnitude and time course to ox-LDL-induced contraction and enhanced 5-HT- and KCl-induced contraction with no additional increases in [Ca(2+)](i). Tetradecanoylphorbol Acetate 28-58 protein kinase C alpha Homo sapiens 21-24 11230335-7 2001 Direct activation of PKC by phorbol 12-myristate13-acetate (PMA; 10(-7) mol/L) caused a contraction similar in magnitude and time course to ox-LDL-induced contraction and enhanced 5-HT- and KCl-induced contraction with no additional increases in [Ca(2+)](i). Tetradecanoylphorbol Acetate 60-63 protein kinase C alpha Homo sapiens 21-24 11230335-9 2001 Both ox-LDL and PMA caused an increase in PKC activity in the particulate fraction, a decrease in the cytosolic fraction, and an increase in the particulate/cytosolic PKC activity ratio. Tetradecanoylphorbol Acetate 16-19 protein kinase C alpha Homo sapiens 42-45 11230335-9 2001 Both ox-LDL and PMA caused an increase in PKC activity in the particulate fraction, a decrease in the cytosolic fraction, and an increase in the particulate/cytosolic PKC activity ratio. Tetradecanoylphorbol Acetate 16-19 protein kinase C alpha Homo sapiens 167-170 11182772-9 2001 The inhibition of the Na+/K+ATPase activity was dependent on protein kinase C (PKC) activation since PKC antagonists (calphostin C and staurosporine) abolished the inhibitory effect of Ang II, and the PKC activator phorbol 12-myristate 13-acetate reduced transporter activity. Tetradecanoylphorbol Acetate 215-246 protein kinase C alpha Homo sapiens 79-82 11182772-9 2001 The inhibition of the Na+/K+ATPase activity was dependent on protein kinase C (PKC) activation since PKC antagonists (calphostin C and staurosporine) abolished the inhibitory effect of Ang II, and the PKC activator phorbol 12-myristate 13-acetate reduced transporter activity. Tetradecanoylphorbol Acetate 215-246 protein kinase C alpha Homo sapiens 101-104 11182772-9 2001 The inhibition of the Na+/K+ATPase activity was dependent on protein kinase C (PKC) activation since PKC antagonists (calphostin C and staurosporine) abolished the inhibitory effect of Ang II, and the PKC activator phorbol 12-myristate 13-acetate reduced transporter activity. Tetradecanoylphorbol Acetate 215-246 protein kinase C alpha Homo sapiens 101-104 11133494-5 2001 Immunohistochemistry of feline pulmonary arterial smooth muscle cells demonstrated localization of PKC-alpha and -delta isozymes in response to phorbol 12-myristate 13-acetate and angiotensin II. Tetradecanoylphorbol Acetate 144-175 protein kinase C alpha Homo sapiens 99-119 11175257-2 2000 We show here that activation of the conventional and novel isoforms of PKC with 12-O-tetradecanoyl phorbol-13- ester (TPA) induces apoptosis in salivary acinar cells as indicated by DNA fragmentation and activation of caspase-3. Tetradecanoylphorbol Acetate 118-121 protein kinase C alpha Homo sapiens 71-74 11175257-4 2000 Analysis of PKC isoform expression by immunoblot shows that TPA-induced downregulation of PKC alpha and PKC delta is delayed in cells pre-treated with calpeptin, and that this correlates with an increase of these isoforms in the membrane fraction of cells. Tetradecanoylphorbol Acetate 60-63 protein kinase C alpha Homo sapiens 90-99 11175257-6 2000 Expression of constitutively activated PKC alpha or PKC delta, but not kinase negative mutants of these isoforms, or constitutively activated PKC epsilon, induces apoptosis in salivary acinar cells, suggesting a role for these isoforms in TPA-induced apoptosis. Tetradecanoylphorbol Acetate 239-242 protein kinase C alpha Homo sapiens 39-48 11313461-2 2001 We have previously shown that, upon treatment of the pituitary cell line GH3B6 with thyrotropin-releasing hormone (TRH) or phorbol 12-myristate 13-acetate (PMA), human PKCalpha (hPKCalpha) is selectively targeted to the cell-cell contacts (42). Tetradecanoylphorbol Acetate 123-154 protein kinase C alpha Homo sapiens 168-176 11313461-2 2001 We have previously shown that, upon treatment of the pituitary cell line GH3B6 with thyrotropin-releasing hormone (TRH) or phorbol 12-myristate 13-acetate (PMA), human PKCalpha (hPKCalpha) is selectively targeted to the cell-cell contacts (42). Tetradecanoylphorbol Acetate 123-154 protein kinase C alpha Homo sapiens 178-187 11152962-5 2000 Activation of the IKK complex in response to TPA is mediated by PKC-alpha, since both the PKC inhibitor GF109203 and a catalytically inactive PKC-alpha mutant inhibit activation of endogenous IKK by TPA, but not by tumor necrosis factor-alpha (TNF-alpha). Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 64-67 11152962-5 2000 Activation of the IKK complex in response to TPA is mediated by PKC-alpha, since both the PKC inhibitor GF109203 and a catalytically inactive PKC-alpha mutant inhibit activation of endogenous IKK by TPA, but not by tumor necrosis factor-alpha (TNF-alpha). Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 142-151 11152962-5 2000 Activation of the IKK complex in response to TPA is mediated by PKC-alpha, since both the PKC inhibitor GF109203 and a catalytically inactive PKC-alpha mutant inhibit activation of endogenous IKK by TPA, but not by tumor necrosis factor-alpha (TNF-alpha). Tetradecanoylphorbol Acetate 199-202 protein kinase C alpha Homo sapiens 64-73 11152962-5 2000 Activation of the IKK complex in response to TPA is mediated by PKC-alpha, since both the PKC inhibitor GF109203 and a catalytically inactive PKC-alpha mutant inhibit activation of endogenous IKK by TPA, but not by tumor necrosis factor-alpha (TNF-alpha). Tetradecanoylphorbol Acetate 199-202 protein kinase C alpha Homo sapiens 64-67 11152962-5 2000 Activation of the IKK complex in response to TPA is mediated by PKC-alpha, since both the PKC inhibitor GF109203 and a catalytically inactive PKC-alpha mutant inhibit activation of endogenous IKK by TPA, but not by tumor necrosis factor-alpha (TNF-alpha). Tetradecanoylphorbol Acetate 199-202 protein kinase C alpha Homo sapiens 142-151 10993217-3 2000 The dissociation constants (Kd"s) of TPA to PDI, histone H1 and PKCalpha were determined to be 1.03 x 10(-6) M, 5.70 x 10(-7) M, and 4.00 x 10(-7) m, respectively, by the surface plasmon resonance (SPR) method. Tetradecanoylphorbol Acetate 37-40 protein kinase C alpha Homo sapiens 64-72 11004668-2 2000 The PKC activator phorbol myristate acetate (PMA) induced the transition of elongated fibroblast-like cells into CS cells and stimulated locomotion. Tetradecanoylphorbol Acetate 18-43 protein kinase C alpha Homo sapiens 4-7 11004668-2 2000 The PKC activator phorbol myristate acetate (PMA) induced the transition of elongated fibroblast-like cells into CS cells and stimulated locomotion. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 4-7 11004668-5 2000 CS formation and stimulated locomotion correlated closely with a marked redistribution from the cytosol to the membrane of PKC isoforms alpha, beta1 and gamma in the early phase (0.5 to 2 hr) following activation with PMA. Tetradecanoylphorbol Acetate 218-221 protein kinase C alpha Homo sapiens 123-158 11093788-5 2000 TPA, a PKC activator, stimulated ICAM-1 expression as well, this effect being inhibited by tyrosine kinase inhibitors. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 7-10 11093788-10 2000 Dominant-negative PKCalpha, NIK, or IKK2, but not IKK1 mutant, inhibited IL-1beta- or TPA-induced ICAM-1 promoter activity. Tetradecanoylphorbol Acetate 86-89 protein kinase C alpha Homo sapiens 18-26 10976111-3 2000 The effect of TPA was specifically abolished by the PKC inhibitor GF109203X and by dominant negative PKCtheta, PKCepsilon, and PKCalpha, suggesting that novel and conventional PKC isoforms mediate phorbol ester action. Tetradecanoylphorbol Acetate 14-17 protein kinase C alpha Homo sapiens 52-55 10976111-3 2000 The effect of TPA was specifically abolished by the PKC inhibitor GF109203X and by dominant negative PKCtheta, PKCepsilon, and PKCalpha, suggesting that novel and conventional PKC isoforms mediate phorbol ester action. Tetradecanoylphorbol Acetate 14-17 protein kinase C alpha Homo sapiens 127-135 10976111-3 2000 The effect of TPA was specifically abolished by the PKC inhibitor GF109203X and by dominant negative PKCtheta, PKCepsilon, and PKCalpha, suggesting that novel and conventional PKC isoforms mediate phorbol ester action. Tetradecanoylphorbol Acetate 14-17 protein kinase C alpha Homo sapiens 101-104 10882716-5 2000 Lead induced VEGF mRNA 3-fold and VEGF protein approximately 2-fold with maximum mRNA induction following incubation with 10 micrometer lead acetate for 24 h. Phorbol 12-myristate 13-acetate (PMA), a potent protein kinase C (PKC) activator, increased VEGF mRNA 2-fold and PKC inhibition by GF-109203 completely blocked VEGF induction by lead. Tetradecanoylphorbol Acetate 159-190 protein kinase C alpha Homo sapiens 225-228 10882716-5 2000 Lead induced VEGF mRNA 3-fold and VEGF protein approximately 2-fold with maximum mRNA induction following incubation with 10 micrometer lead acetate for 24 h. Phorbol 12-myristate 13-acetate (PMA), a potent protein kinase C (PKC) activator, increased VEGF mRNA 2-fold and PKC inhibition by GF-109203 completely blocked VEGF induction by lead. Tetradecanoylphorbol Acetate 159-190 protein kinase C alpha Homo sapiens 272-275 10899038-7 2000 cis-UFA also interacted synergistically with the PKC activator phorbol 12-myristate 13-acetate to promote positive inotropic responses. Tetradecanoylphorbol Acetate 63-94 protein kinase C alpha Homo sapiens 49-52 10934041-3 2000 TPA treatment resulted in transient PKC(&agr;) activation accompanied by translocation of the enzyme into membrane and nuclear compartments, and was followed by subsequent downregulation. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 36-39 10934041-4 2000 TPA-induced inhibition of DNA synthesis was prevented by a PKC-antagonist and was reproduced by microinjection of recombinant PKCalpha, indicating that activation of this isoenzyme was required and sufficient for growth inhibitory effects. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 59-62 10934041-4 2000 TPA-induced inhibition of DNA synthesis was prevented by a PKC-antagonist and was reproduced by microinjection of recombinant PKCalpha, indicating that activation of this isoenzyme was required and sufficient for growth inhibitory effects. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 126-134 10947075-1 2000 We have treated Jurkat T lymphocytes with a concentration (160 nM) of phorbol myristyl acetate (PMA) that down-regulates conventional and novel protein kinase C (PKC) isozymes and we have investigated the effects on Ca2+ signaling and protein tyrosine phosphorylation using mAb (C305) directed against the beta-subunit of the Ti heterodimer or the epsilon/delta-component of the CD3 complex (mAb Leu 4 or OKT 3). Tetradecanoylphorbol Acetate 96-99 protein kinase C alpha Homo sapiens 162-165 10947075-2 2000 The levels of expression of PKC alpha, betaI, betaII, and delta were reduced by 90% or more in PMA-treated cells, whereas the expression of PKCtheta decreased by approximately 30%. Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 28-37 10912793-3 2000 PMA but not phenylephrine rapidly activated PKCalpha in TFG2 cells, and the highly selective PKC inhibitor bisindolylmaleimide (GFX) completely abolished PMA-induced but not PE-induced scattering. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 44-52 10912793-3 2000 PMA but not phenylephrine rapidly activated PKCalpha in TFG2 cells, and the highly selective PKC inhibitor bisindolylmaleimide (GFX) completely abolished PMA-induced but not PE-induced scattering. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 44-47 10681596-2 2000 We found that upon thyrotropin-releasing hormone (TRH) or phorbol 12-myristate 13-acetate stimulation, hPKCalpha-GFP was localized exclusively in regions of cell-cell contacts. Tetradecanoylphorbol Acetate 58-89 protein kinase C alpha Homo sapiens 103-112 10848585-3 2000 Of the six PKC isoforms that were present in glioma cells, PKC alpha was both necessary and sufficient to promote cell cycle progression when stimulated with phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 158-189 protein kinase C alpha Homo sapiens 11-14 10848585-3 2000 Of the six PKC isoforms that were present in glioma cells, PKC alpha was both necessary and sufficient to promote cell cycle progression when stimulated with phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 158-189 protein kinase C alpha Homo sapiens 59-68 10825394-1 2000 Previously, we reported that 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced apoptosis of LNCaP human prostate cancer cells was accompanied by prolonged translocation of protein kinase C (PKC)alpha to non-nuclear membranes and that TPA-resistant LNCaP cells had down-regulated PKCalpha. Tetradecanoylphorbol Acetate 29-65 protein kinase C alpha Homo sapiens 191-200 10825394-1 2000 Previously, we reported that 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced apoptosis of LNCaP human prostate cancer cells was accompanied by prolonged translocation of protein kinase C (PKC)alpha to non-nuclear membranes and that TPA-resistant LNCaP cells had down-regulated PKCalpha. Tetradecanoylphorbol Acetate 29-65 protein kinase C alpha Homo sapiens 280-288 10825394-1 2000 Previously, we reported that 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced apoptosis of LNCaP human prostate cancer cells was accompanied by prolonged translocation of protein kinase C (PKC)alpha to non-nuclear membranes and that TPA-resistant LNCaP cells had down-regulated PKCalpha. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 191-200 10825394-1 2000 Previously, we reported that 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced apoptosis of LNCaP human prostate cancer cells was accompanied by prolonged translocation of protein kinase C (PKC)alpha to non-nuclear membranes and that TPA-resistant LNCaP cells had down-regulated PKCalpha. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 280-288 10825394-1 2000 Previously, we reported that 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced apoptosis of LNCaP human prostate cancer cells was accompanied by prolonged translocation of protein kinase C (PKC)alpha to non-nuclear membranes and that TPA-resistant LNCaP cells had down-regulated PKCalpha. Tetradecanoylphorbol Acetate 235-238 protein kinase C alpha Homo sapiens 191-200 10825394-6 2000 Immunoblot analysis revealed that TPA induced prolonged hyperphosphorylation of Raf-1 and activation of extracellular-regulated/mitogen-activated protein kinases 1 and 2 in untransfected LNCaP cells, as did bryostatin 1 in PKCalpha-overexpressing cells. Tetradecanoylphorbol Acetate 34-37 protein kinase C alpha Homo sapiens 223-231 10862715-3 2000 It is demonstrated here that acute TPA exposure induces the transport of activated PKC(alpha) from the plasma membrane to endosomes. Tetradecanoylphorbol Acetate 35-38 protein kinase C alpha Homo sapiens 83-93 10775457-2 2000 Now we report that addition of a PKC-alpha-enriched purified PKC preparation or recombinant PKC-alpha to a plasma membrane-enriched membrane fraction, isolated from leukemic HL60 cells, greatly ( approximately 6.5-fold stimulation) enhanced PtdEtn hydrolysis if the PKC activator phorbol 12-myristate 13-acetate (PMA) and ATP were both present; this was accompanied by PKC-mediated phosphorylation of several membrane proteins. Tetradecanoylphorbol Acetate 280-311 protein kinase C alpha Homo sapiens 33-42 10775457-2 2000 Now we report that addition of a PKC-alpha-enriched purified PKC preparation or recombinant PKC-alpha to a plasma membrane-enriched membrane fraction, isolated from leukemic HL60 cells, greatly ( approximately 6.5-fold stimulation) enhanced PtdEtn hydrolysis if the PKC activator phorbol 12-myristate 13-acetate (PMA) and ATP were both present; this was accompanied by PKC-mediated phosphorylation of several membrane proteins. Tetradecanoylphorbol Acetate 280-311 protein kinase C alpha Homo sapiens 33-36 10775457-2 2000 Now we report that addition of a PKC-alpha-enriched purified PKC preparation or recombinant PKC-alpha to a plasma membrane-enriched membrane fraction, isolated from leukemic HL60 cells, greatly ( approximately 6.5-fold stimulation) enhanced PtdEtn hydrolysis if the PKC activator phorbol 12-myristate 13-acetate (PMA) and ATP were both present; this was accompanied by PKC-mediated phosphorylation of several membrane proteins. Tetradecanoylphorbol Acetate 280-311 protein kinase C alpha Homo sapiens 92-101 10775457-2 2000 Now we report that addition of a PKC-alpha-enriched purified PKC preparation or recombinant PKC-alpha to a plasma membrane-enriched membrane fraction, isolated from leukemic HL60 cells, greatly ( approximately 6.5-fold stimulation) enhanced PtdEtn hydrolysis if the PKC activator phorbol 12-myristate 13-acetate (PMA) and ATP were both present; this was accompanied by PKC-mediated phosphorylation of several membrane proteins. Tetradecanoylphorbol Acetate 280-311 protein kinase C alpha Homo sapiens 61-64 10775457-2 2000 Now we report that addition of a PKC-alpha-enriched purified PKC preparation or recombinant PKC-alpha to a plasma membrane-enriched membrane fraction, isolated from leukemic HL60 cells, greatly ( approximately 6.5-fold stimulation) enhanced PtdEtn hydrolysis if the PKC activator phorbol 12-myristate 13-acetate (PMA) and ATP were both present; this was accompanied by PKC-mediated phosphorylation of several membrane proteins. Tetradecanoylphorbol Acetate 313-316 protein kinase C alpha Homo sapiens 33-42 10775457-2 2000 Now we report that addition of a PKC-alpha-enriched purified PKC preparation or recombinant PKC-alpha to a plasma membrane-enriched membrane fraction, isolated from leukemic HL60 cells, greatly ( approximately 6.5-fold stimulation) enhanced PtdEtn hydrolysis if the PKC activator phorbol 12-myristate 13-acetate (PMA) and ATP were both present; this was accompanied by PKC-mediated phosphorylation of several membrane proteins. Tetradecanoylphorbol Acetate 313-316 protein kinase C alpha Homo sapiens 33-36 10775457-2 2000 Now we report that addition of a PKC-alpha-enriched purified PKC preparation or recombinant PKC-alpha to a plasma membrane-enriched membrane fraction, isolated from leukemic HL60 cells, greatly ( approximately 6.5-fold stimulation) enhanced PtdEtn hydrolysis if the PKC activator phorbol 12-myristate 13-acetate (PMA) and ATP were both present; this was accompanied by PKC-mediated phosphorylation of several membrane proteins. Tetradecanoylphorbol Acetate 313-316 protein kinase C alpha Homo sapiens 92-101 10775457-2 2000 Now we report that addition of a PKC-alpha-enriched purified PKC preparation or recombinant PKC-alpha to a plasma membrane-enriched membrane fraction, isolated from leukemic HL60 cells, greatly ( approximately 6.5-fold stimulation) enhanced PtdEtn hydrolysis if the PKC activator phorbol 12-myristate 13-acetate (PMA) and ATP were both present; this was accompanied by PKC-mediated phosphorylation of several membrane proteins. Tetradecanoylphorbol Acetate 313-316 protein kinase C alpha Homo sapiens 61-64 10627456-9 2000 Down-regulation of the PKC-alpha, PKC-beta2, and PKC-epsilon expression by TPA pretreatment, or the down-regulation of PKC-alpha with a specific ribozyme, also inhibited the EPO-induced erythroid differentiation of CD34(+) cells. Tetradecanoylphorbol Acetate 75-78 protein kinase C alpha Homo sapiens 23-32 10651808-9 2000 Measurement of PKC activity in the cytosolic and membrane fractions showed that pretreatment of PMNs with ethanol increased twofold the PMA-stimulated PKC activity in the membrane fraction. Tetradecanoylphorbol Acetate 136-139 protein kinase C alpha Homo sapiens 15-18 10651808-9 2000 Measurement of PKC activity in the cytosolic and membrane fractions showed that pretreatment of PMNs with ethanol increased twofold the PMA-stimulated PKC activity in the membrane fraction. Tetradecanoylphorbol Acetate 136-139 protein kinase C alpha Homo sapiens 151-154 10651808-11 2000 These results suggest that ethanol potentiates PMA-induced O-2 production through increasing PKC translocation and activity in PMNs. Tetradecanoylphorbol Acetate 47-50 protein kinase C alpha Homo sapiens 93-96 10638963-1 2000 Down-regulation of protein kinase C (PKC) by 12-Otetradecanoylphorbol-13-acetate (TPA) enhances the sensitivity of human ovarian carcinoma 2008 cells to various types of platinum compounds such as cisplatin (DDP), carboplatin and (-)-(R)-2-aminomethylpyrrolidine (1,1-cyclobutanedicarboxylato)-platinum(II) monohydrate (DWA) by a factor of two- to threefold. Tetradecanoylphorbol Acetate 45-80 protein kinase C alpha Homo sapiens 37-40 10638963-0 2000 Depletion of protein kinase C (PKC) by 12-O-tetradecanoylphorbol-13-acetate (TPA) enhances platinum drug sensitivity in human ovarian carcinoma cells. Tetradecanoylphorbol Acetate 77-80 protein kinase C alpha Homo sapiens 31-34 10638963-1 2000 Down-regulation of protein kinase C (PKC) by 12-Otetradecanoylphorbol-13-acetate (TPA) enhances the sensitivity of human ovarian carcinoma 2008 cells to various types of platinum compounds such as cisplatin (DDP), carboplatin and (-)-(R)-2-aminomethylpyrrolidine (1,1-cyclobutanedicarboxylato)-platinum(II) monohydrate (DWA) by a factor of two- to threefold. Tetradecanoylphorbol Acetate 82-85 protein kinase C alpha Homo sapiens 37-40 10638963-0 2000 Depletion of protein kinase C (PKC) by 12-O-tetradecanoylphorbol-13-acetate (TPA) enhances platinum drug sensitivity in human ovarian carcinoma cells. Tetradecanoylphorbol Acetate 39-75 protein kinase C alpha Homo sapiens 31-34 10638963-3 2000 The extent of PKC down-regulation and drug sensitization depended on the duration of TPA exposure; maximum effect was achieved with a 48 h pretreatment. Tetradecanoylphorbol Acetate 85-88 protein kinase C alpha Homo sapiens 14-17 10638963-6 2000 Western blot analysis revealed that whereas the expression of PKCalpha was reduced by TPA the level of PKCzeta was not affected. Tetradecanoylphorbol Acetate 86-89 protein kinase C alpha Homo sapiens 62-70 10638963-7 2000 These results suggest that PKCalpha is the isotype responsive to TPA in these cells and that platinum drug sensitivity can be modulated by this isoform alone. Tetradecanoylphorbol Acetate 65-68 protein kinase C alpha Homo sapiens 27-35 10638963-8 2000 In parallel to its effect on PKCalpha, TPA decreased cellular glutathione content by 30 +/- 3 (standard deviation (s.d.) Tetradecanoylphorbol Acetate 39-42 protein kinase C alpha Homo sapiens 29-37 10638963-13 2000 Although the mechanism of TPA induced sensitization is not yet fully understood, this study points to a central role for PKCalpha in modulating platinum drug sensitivity. Tetradecanoylphorbol Acetate 26-29 protein kinase C alpha Homo sapiens 121-129 10614786-2 1999 Three agonists known to stimulate PLD activity, fMet-Leu-Phe (fMLP), phorbol 12-myristate 13-acetate (PMA) and V4+-OOH, induced a differential translocation of ADP-ribosylation factor (ARF), RhoA, and protein kinase Calpha (PKCalpha), all cofactors for PLD activation. Tetradecanoylphorbol Acetate 69-100 protein kinase C alpha Homo sapiens 201-222 10618645-4 1999 Exploratory studies confirmed the anti-PKC effects of CalC, as equal molar concentrations of CalC blocked the PMA-induced translocation of PKC-alpha from the cytosolic to the membrane fraction. Tetradecanoylphorbol Acetate 110-113 protein kinase C alpha Homo sapiens 39-42 10618645-4 1999 Exploratory studies confirmed the anti-PKC effects of CalC, as equal molar concentrations of CalC blocked the PMA-induced translocation of PKC-alpha from the cytosolic to the membrane fraction. Tetradecanoylphorbol Acetate 110-113 protein kinase C alpha Homo sapiens 139-148 12058180-2 2000 Here, the regulatory effect of phorbol 12-myristate 13-acetate(PMA)on the several PKC isozymes in the human lung carcinoma cells A-549 was studied. Tetradecanoylphorbol Acetate 31-62 protein kinase C alpha Homo sapiens 82-85 12058180-2 2000 Here, the regulatory effect of phorbol 12-myristate 13-acetate(PMA)on the several PKC isozymes in the human lung carcinoma cells A-549 was studied. Tetradecanoylphorbol Acetate 63-66 protein kinase C alpha Homo sapiens 82-85 12058180-5 2000 Short-term treatment of cells with PMA led to the translocation of these PKC isozymes, to different extent, from cytosol to cell membrane. Tetradecanoylphorbol Acetate 35-38 protein kinase C alpha Homo sapiens 73-76 10614786-3 1999 Whereas fMLP recruited all three proteins to membranes, V4+-OOH only elicited RhoA translocation and PMA induced ARF and PKCalpha translocation. Tetradecanoylphorbol Acetate 101-104 protein kinase C alpha Homo sapiens 121-129 10614786-2 1999 Three agonists known to stimulate PLD activity, fMet-Leu-Phe (fMLP), phorbol 12-myristate 13-acetate (PMA) and V4+-OOH, induced a differential translocation of ADP-ribosylation factor (ARF), RhoA, and protein kinase Calpha (PKCalpha), all cofactors for PLD activation. Tetradecanoylphorbol Acetate 69-100 protein kinase C alpha Homo sapiens 224-232 10547271-3 1999 It is reported that in monocytes treated with phorbol ester (PMA), translocation of PKC isoforms alpha, betaII, delta and epsilon precede cytokine synthesis. Tetradecanoylphorbol Acetate 61-64 protein kinase C alpha Homo sapiens 84-117 10523655-6 1999 In contrast with expectations, downregulation of PKC isoforms with TPA did not transform the EGFR cells; however, treatment with EGF did transform these cells. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 49-52 10523655-7 1999 Since TPA downregulates all phorbol ester-responsive PKC isoforms, we examined the effects of PKC delta- and PKC alpha-specific inhibitors and the expression of dominant negative mutants for both PKC delta and alpha. Tetradecanoylphorbol Acetate 6-9 protein kinase C alpha Homo sapiens 53-56 10510401-12 1999 We conclude that conventional PKC isoforms (PKC-alpha and/or PKC-betaII) may regulate PMA-stimulated cytoskeletal association and activation of NADPH oxidase. Tetradecanoylphorbol Acetate 86-89 protein kinase C alpha Homo sapiens 30-33 10510401-12 1999 We conclude that conventional PKC isoforms (PKC-alpha and/or PKC-betaII) may regulate PMA-stimulated cytoskeletal association and activation of NADPH oxidase. Tetradecanoylphorbol Acetate 86-89 protein kinase C alpha Homo sapiens 44-53 10529207-9 1999 After phorbol ester (TPA) application, PKC activation was characterized by biexponential kinetics, including a rapid phase completed within 5 min and a slow phase lasting at least 30 min, which reflected several activation steps. Tetradecanoylphorbol Acetate 21-24 protein kinase C alpha Homo sapiens 39-42 10523856-13 1999 These data demonstrate that MDR1 induction by TPA occurs via a PKC-dependent mechanism that operates independently of ERK, p38 or JNK pathways, and thus have important implications for understanding the mechanisms of MDR1 induction by extracellular stimuli. Tetradecanoylphorbol Acetate 46-49 protein kinase C alpha Homo sapiens 63-66 10523856-3 1999 Downstream of protein kinase C (PKC), the effects of TPA are often mediated by the Raf-1/MEK/ERK mitogen-activated protein kinase (MAPK) cascade, and Raf-1 has been implicated in MDR1 induction by serum and mitogens. Tetradecanoylphorbol Acetate 53-56 protein kinase C alpha Homo sapiens 32-35 10523856-6 1999 TPA-mediated MDR1 induction was inhibited by several PKC inhibitors including staurosporine, H7 and calphostin C. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 53-56 10523856-7 1999 TPA stimulated the subcellular translocation of PKCalpha from the cytosol to the membrane and nucleus but did not affect other PKC isozymes. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 48-56 10523856-7 1999 TPA stimulated the subcellular translocation of PKCalpha from the cytosol to the membrane and nucleus but did not affect other PKC isozymes. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 48-51 10523856-10 1999 The MEK inhibitor PD 098059, as well as the PKC inhibitors, completely blocked TPA-mediated ERK activation. Tetradecanoylphorbol Acetate 79-82 protein kinase C alpha Homo sapiens 44-47 10529207-10 1999 Two different binding sites for TPA were revealed on membrane-associated PKCalpha (EC(50) = 31 +/- 12 and 580 +/- 170 nM), and their modulation by phosphatidylserine and Ca2+ was characterized. Tetradecanoylphorbol Acetate 32-35 protein kinase C alpha Homo sapiens 73-81 10529207-12 1999 Our study shows that binding of low concentrations of TPA triggers conformational changes in the soluble PKCalpha, which affect the microenvironment of its catalytic domain. Tetradecanoylphorbol Acetate 54-57 protein kinase C alpha Homo sapiens 105-113 10625951-7 1999 Furthermore, we have investigated the role of PKC and its isozymes in the synergistic induction of PI-3 K by TPA and insulin and found that bisindolylmaleimide, a PKC inhibitor, inhibits TPA-induced PI-3 K. Overexpression of a dominant negative PKC epsilon, but not dominant negative PKC alpha, blocks the TPA- or TPA plus insulin-induced PI-3 K activity. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 46-49 10484520-7 1999 The stimulatory effects of LDL on collagen gene regulation in HMC were blocked by the inhibition of PKC using GF-109203X (GFX) or the downregulation of PKC using phorbol myristate acetate. Tetradecanoylphorbol Acetate 162-187 protein kinase C alpha Homo sapiens 152-155 10523838-3 1999 Here we found that a protein kinase C (PKC) activator phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) promoted cell death in human gastric cancer cell lines MKN45 and MKN74 only when they lost anchorage. Tetradecanoylphorbol Acetate 68-105 protein kinase C alpha Homo sapiens 39-42 10523838-3 1999 Here we found that a protein kinase C (PKC) activator phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) promoted cell death in human gastric cancer cell lines MKN45 and MKN74 only when they lost anchorage. Tetradecanoylphorbol Acetate 107-110 protein kinase C alpha Homo sapiens 39-42 10523838-4 1999 Loss of anchorage slightly increased enzymatic activity of PKCalpha, and an addition of TPA promoted cell death with further increase of PKCalpha activity, but not PKCbeta in MKN45 cells, implicating an involvement of PKCalpha in anoikis. Tetradecanoylphorbol Acetate 88-91 protein kinase C alpha Homo sapiens 137-145 10523838-4 1999 Loss of anchorage slightly increased enzymatic activity of PKCalpha, and an addition of TPA promoted cell death with further increase of PKCalpha activity, but not PKCbeta in MKN45 cells, implicating an involvement of PKCalpha in anoikis. Tetradecanoylphorbol Acetate 88-91 protein kinase C alpha Homo sapiens 137-145 10625951-7 1999 Furthermore, we have investigated the role of PKC and its isozymes in the synergistic induction of PI-3 K by TPA and insulin and found that bisindolylmaleimide, a PKC inhibitor, inhibits TPA-induced PI-3 K. Overexpression of a dominant negative PKC epsilon, but not dominant negative PKC alpha, blocks the TPA- or TPA plus insulin-induced PI-3 K activity. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 163-166 10625951-7 1999 Furthermore, we have investigated the role of PKC and its isozymes in the synergistic induction of PI-3 K by TPA and insulin and found that bisindolylmaleimide, a PKC inhibitor, inhibits TPA-induced PI-3 K. Overexpression of a dominant negative PKC epsilon, but not dominant negative PKC alpha, blocks the TPA- or TPA plus insulin-induced PI-3 K activity. Tetradecanoylphorbol Acetate 109-112 protein kinase C alpha Homo sapiens 284-293 10625951-7 1999 Furthermore, we have investigated the role of PKC and its isozymes in the synergistic induction of PI-3 K by TPA and insulin and found that bisindolylmaleimide, a PKC inhibitor, inhibits TPA-induced PI-3 K. Overexpression of a dominant negative PKC epsilon, but not dominant negative PKC alpha, blocks the TPA- or TPA plus insulin-induced PI-3 K activity. Tetradecanoylphorbol Acetate 187-190 protein kinase C alpha Homo sapiens 46-49 10625951-7 1999 Furthermore, we have investigated the role of PKC and its isozymes in the synergistic induction of PI-3 K by TPA and insulin and found that bisindolylmaleimide, a PKC inhibitor, inhibits TPA-induced PI-3 K. Overexpression of a dominant negative PKC epsilon, but not dominant negative PKC alpha, blocks the TPA- or TPA plus insulin-induced PI-3 K activity. Tetradecanoylphorbol Acetate 187-190 protein kinase C alpha Homo sapiens 46-49 10455033-7 1999 Furthermore, sucrose-density-gradient centrifugation and immunofluorescence microscopy demonstrated that PKCalpha was translocated to the endoplasmic reticulum membrane in cells expressing GPI-PLD, in contrast with its association with the plasma membrane in cells treated with PMA. Tetradecanoylphorbol Acetate 278-281 protein kinase C alpha Homo sapiens 105-113 10625951-7 1999 Furthermore, we have investigated the role of PKC and its isozymes in the synergistic induction of PI-3 K by TPA and insulin and found that bisindolylmaleimide, a PKC inhibitor, inhibits TPA-induced PI-3 K. Overexpression of a dominant negative PKC epsilon, but not dominant negative PKC alpha, blocks the TPA- or TPA plus insulin-induced PI-3 K activity. Tetradecanoylphorbol Acetate 187-190 protein kinase C alpha Homo sapiens 46-49 10198345-14 1999 These findings, taken together with those of the accompanying paper, indicate that although 1,25(OH)2D3 and TPA each activate PLD in Caco-2 cells in part via PKC-alpha, their stimulation of PLD differs in a number of important aspects, including the requirement for pp60(c-src) and RhoA in the activation of PLD by 1,25(OH)2D3, but not TPA. Tetradecanoylphorbol Acetate 108-111 protein kinase C alpha Homo sapiens 158-167 10413111-1 1999 ET-18-OCH3, but not ELL-12, blunted the increase in membrane protein kinase C (PKC) activity induced by 12-O-tetradecanoylphorbol 13-myristate (TPA) and markedly reduced levels of PKC alpha in NIH 3T3 fibroblasts. Tetradecanoylphorbol Acetate 144-147 protein kinase C alpha Homo sapiens 79-82 10545022-8 1999 Only a combination of depletion of PKC by prolonged stimulation with a high concentration of phorbol 12,13 dibutyrate (PDBu) and treatment with antisense ODNs effectively inhibited L-10 cell invasion even in the presence of TPA. Tetradecanoylphorbol Acetate 224-227 protein kinase C alpha Homo sapiens 35-38 10209967-5 1999 Exposure to the PKC inhibitors GF109203X, Go 6976 or Go 6983 caused a decrease whereas activation of PKC with 12-O-tetradecanoyl phorbol 13-acetate caused an increase in the number of neuroblastoma cells. Tetradecanoylphorbol Acetate 110-147 protein kinase C alpha Homo sapiens 101-104 10545022-0 1999 TPA-enhanced motility and invasion in a highly metastatic variant (L-10) of human rectal adenocarcinoma cell line RCM-1: selective role of PKC-alpha and its inhibition by a combination of PDBu-induced PKC downregulation and antisense oligonucleotides treatment. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 139-148 10545022-0 1999 TPA-enhanced motility and invasion in a highly metastatic variant (L-10) of human rectal adenocarcinoma cell line RCM-1: selective role of PKC-alpha and its inhibition by a combination of PDBu-induced PKC downregulation and antisense oligonucleotides treatment. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 139-142 10545022-1 1999 We previously found that 12-O-tetradecanoylphorbol-13-acetate (TPA)-enhanced invasiveness was associated with augmentation of cell motility but not that of metalloproteinase activity in a highly metastatic variant (L-10) of the human colon adenocarcinoma cell line RCM-1 and that this enhancement was possibly mediated by protein kinase C (PKC). Tetradecanoylphorbol Acetate 25-61 protein kinase C alpha Homo sapiens 340-343 10545022-1 1999 We previously found that 12-O-tetradecanoylphorbol-13-acetate (TPA)-enhanced invasiveness was associated with augmentation of cell motility but not that of metalloproteinase activity in a highly metastatic variant (L-10) of the human colon adenocarcinoma cell line RCM-1 and that this enhancement was possibly mediated by protein kinase C (PKC). Tetradecanoylphorbol Acetate 63-66 protein kinase C alpha Homo sapiens 340-343 10545022-2 1999 In this study, we first intended to determine the specific isoforms of PKC involved in this TPA-enhanced L-10 cell motility that leads to invasion, and then investigated the way to inhibit the enhanced motility and invasion by using antisense oligodeoxynucleotides (ODN) targeting the isoform. Tetradecanoylphorbol Acetate 92-95 protein kinase C alpha Homo sapiens 71-74 10545022-4 1999 TPA treatment induced a shift of PKC-alpha, but not other isoforms, from the cytosol to the membrane fraction, indicating the activation of the isoform. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 33-42 10545022-6 1999 Antisense ODNs specific for PKC-alpha efficiently reduced its expression at the protein levels and inhibited L-10 cell motility in the absence of TPA. Tetradecanoylphorbol Acetate 146-149 protein kinase C alpha Homo sapiens 28-37 10545022-7 1999 With TPA treatment, however, the remaining PKC-alpha was sufficient for activation leading to enhanced invasion. Tetradecanoylphorbol Acetate 5-8 protein kinase C alpha Homo sapiens 43-52 10325235-5 1999 Phorbol ester-sensitive PKC isoforms were detected at very low levels in caveolae fractions prepared from unstimulated cardiomyocytes; phorbol 12-myristate 13-acetate (PMA) (but not 4alpha-PMA, which does not activate PKC) recruited calcium-sensitive PKCalpha and novel PKCdelta and PKCepsilon to this compartment. Tetradecanoylphorbol Acetate 135-166 protein kinase C alpha Homo sapiens 24-27 10049506-1 1999 In fibroblasts, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) stimulates phospholipase D (PLD)-mediated hydrolysis of both phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) by PKC-alpha-mediated nonphosphorylating and phosphorylating mechanisms. Tetradecanoylphorbol Acetate 53-84 protein kinase C alpha Homo sapiens 38-41 10198344-3 1999 1,25(OH)2D3 activated PKC-alpha, but not PKC-beta1, -betaII, -delta, or -zeta, whereas TPA activated PKC-alpha, -beta1, and -delta. Tetradecanoylphorbol Acetate 87-90 protein kinase C alpha Homo sapiens 101-110 10198344-4 1999 Chronic treatment with TPA (1 microM, 24 h) significantly reduced the expression of PKC-alpha, -betaI, and -delta and markedly reduced the ability of 1,25(OH)2D3 or TPA to acutely stimulate PLD. Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 84-113 10198344-7 1999 In addition, the activation of PLD by 1,25(OH)2D3 or TPA was markedly reduced or accentuated in stably transfected cells with inhibited or amplified PKC-alpha expression, respectively. Tetradecanoylphorbol Acetate 53-56 protein kinase C alpha Homo sapiens 149-158 10198344-8 1999 Taken together, these observations indicate that PKC-alpha is intimately involved in the stimulation of PLD in Caco-2 cells by 1,25(OH)2D3 or TPA. Tetradecanoylphorbol Acetate 142-145 protein kinase C alpha Homo sapiens 49-58 10198345-5 1999 39): G993-G1004, 1999], activation of protein kinase C-alpha (PKC-alpha) was shown to be involved in the stimulation of phospholipase D (PLD) by 1,25-dihydroxyvitamin D3 [1, 25(OH)2D3] and 12-O-tetradecanoylphorbol 13-acetate (TPA) in Caco-2 cells. Tetradecanoylphorbol Acetate 189-225 protein kinase C alpha Homo sapiens 62-71 10198345-5 1999 39): G993-G1004, 1999], activation of protein kinase C-alpha (PKC-alpha) was shown to be involved in the stimulation of phospholipase D (PLD) by 1,25-dihydroxyvitamin D3 [1, 25(OH)2D3] and 12-O-tetradecanoylphorbol 13-acetate (TPA) in Caco-2 cells. Tetradecanoylphorbol Acetate 227-230 protein kinase C alpha Homo sapiens 62-71 10090770-6 1999 The association of PKCalpha with membranes containing 12-O-tetradecanoylphorbol 13-acetate (TPA) or 1, 2-dioleoylglycerol (DAG), determined from tryptophan to dansyl-PE resonance energy transfer (RET) measurements, was found to occur at relatively low Ca2+ levels (</=1 microM). Tetradecanoylphorbol Acetate 54-90 protein kinase C alpha Homo sapiens 19-27 10090770-6 1999 The association of PKCalpha with membranes containing 12-O-tetradecanoylphorbol 13-acetate (TPA) or 1, 2-dioleoylglycerol (DAG), determined from tryptophan to dansyl-PE resonance energy transfer (RET) measurements, was found to occur at relatively low Ca2+ levels (</=1 microM). Tetradecanoylphorbol Acetate 92-95 protein kinase C alpha Homo sapiens 19-27 10090770-10 1999 Also, it was found that incubation of the enzyme with TPA alone resulted in a time-dependent increase in the Ca2+-independent PKCalpha activity, the rate and extent of which was further enhanced upon coaddition with DAG. Tetradecanoylphorbol Acetate 54-57 protein kinase C alpha Homo sapiens 126-134 10090770-11 1999 Tauhe results suggest that the enhanced level of activity induced by coaddition of DAG and TPA involves both Ca2+-dependent and Ca2+-independent activating conformational changes which result in active conformers of PKCalpha distinct from those formed by interaction with either activator separately. Tetradecanoylphorbol Acetate 91-94 protein kinase C alpha Homo sapiens 216-224 10049506-1 1999 In fibroblasts, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) stimulates phospholipase D (PLD)-mediated hydrolysis of both phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) by PKC-alpha-mediated nonphosphorylating and phosphorylating mechanisms. Tetradecanoylphorbol Acetate 53-84 protein kinase C alpha Homo sapiens 222-231 10049506-1 1999 In fibroblasts, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) stimulates phospholipase D (PLD)-mediated hydrolysis of both phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) by PKC-alpha-mediated nonphosphorylating and phosphorylating mechanisms. Tetradecanoylphorbol Acetate 86-89 protein kinase C alpha Homo sapiens 38-41 10049506-1 1999 In fibroblasts, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) stimulates phospholipase D (PLD)-mediated hydrolysis of both phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) by PKC-alpha-mediated nonphosphorylating and phosphorylating mechanisms. Tetradecanoylphorbol Acetate 86-89 protein kinase C alpha Homo sapiens 222-231 10049506-7 1999 Interestingly, although PKC-alpha also mediates the stimulatory effect of PMA on the synthesis of PtdCho by a phosphorylation mechanism, overexpression of holo PKC-epsilon or its regulatory domain fragments did not affect PMA-induced PtdCho synthesis. Tetradecanoylphorbol Acetate 74-77 protein kinase C alpha Homo sapiens 24-33 9794414-5 1998 Western analysis performed on cellular fractions of resting cells and of TPA-activated cells revealed abundant expression of classical PKC-alpha (cPKC-alpha), cPKC-betaII, and atypical PKC-zeta isoforms and identified a sustained translocation of cPKC-alpha and cPKC-betaII from the cytosolic compartment to membranes. Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 135-144 9925750-6 1999 The ability of phorbol myristate acetate to preferentially diminish protein kinase Calpha-protein localization to the nucleus by 24 h and thereby block differentiation induced by hexamethylene bisacetamide was paralleled by the ability of protein kinase Calpha antisense transfection to block differentiation. Tetradecanoylphorbol Acetate 15-40 protein kinase C alpha Homo sapiens 68-89 9925750-6 1999 The ability of phorbol myristate acetate to preferentially diminish protein kinase Calpha-protein localization to the nucleus by 24 h and thereby block differentiation induced by hexamethylene bisacetamide was paralleled by the ability of protein kinase Calpha antisense transfection to block differentiation. Tetradecanoylphorbol Acetate 15-40 protein kinase C alpha Homo sapiens 239-260 9935190-9 1999 TPA treatment causes rapid translocation of PKC-alpha to the insoluble fraction. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 44-53 9844735-4 1998 Immunoblot analysis of membrane fractions showed increases in PKC alpha and beta immunoreactivities after treatment with 5 mM, 20 mM glucose and 1 microM TPA. Tetradecanoylphorbol Acetate 154-157 protein kinase C alpha Homo sapiens 62-71 9844735-5 1998 Translocations of PKC alpha after treatment with glucose and TPA were greater than those of PKC beta in membrane fractions. Tetradecanoylphorbol Acetate 61-64 protein kinase C alpha Homo sapiens 18-27 9852137-10 1998 Down-regulation of PKC by prolonged treatment with phorbol 12-myristate 13-acetate (PMA) also inhibited induction of MnSOD by anticancer drugs, indicating an important role of PKC in MnSOD signaling by these agents. Tetradecanoylphorbol Acetate 51-82 protein kinase C alpha Homo sapiens 19-22 9852137-10 1998 Down-regulation of PKC by prolonged treatment with phorbol 12-myristate 13-acetate (PMA) also inhibited induction of MnSOD by anticancer drugs, indicating an important role of PKC in MnSOD signaling by these agents. Tetradecanoylphorbol Acetate 84-87 protein kinase C alpha Homo sapiens 19-22 9852137-10 1998 Down-regulation of PKC by prolonged treatment with phorbol 12-myristate 13-acetate (PMA) also inhibited induction of MnSOD by anticancer drugs, indicating an important role of PKC in MnSOD signaling by these agents. Tetradecanoylphorbol Acetate 84-87 protein kinase C alpha Homo sapiens 176-179 9794414-10 1998 Together, these results show that activated HLA-DRA expression in response to TPA treatment is strictly dependent on PKC activation acting on the X2 box of the DRA promoter and that selective inhibition of PKC enzymatic activity does not influence subcellular localization of expressed PKC isoenzymes. Tetradecanoylphorbol Acetate 78-81 protein kinase C alpha Homo sapiens 117-120 9774148-7 1998 Down-modulation of PKC alpha and delta by 12-O-tetradecanoylphorbol-13-acetate (TPA) did not affect the drug accumulation by bryostatin 1. Tetradecanoylphorbol Acetate 80-83 protein kinase C alpha Homo sapiens 19-28 9832394-7 1998 On the other hand, the time-course of translocation/down-regulation of protein kinase C alpha and protein kinase C epsilon induced by PMA was in good correlation with the time-course of PMA-induced [methyl-3H]thymidine incorporation. Tetradecanoylphorbol Acetate 134-137 protein kinase C alpha Homo sapiens 71-93 9722545-8 1998 However, this "non-membrane" PKC activity was inhibited by the phorbol ester 4beta-12-O-tetradecanoylphorbol-13-acetate (TPA) and also by the fluorescent analog, SAPD, opposite to its effect on membrane-associated PKCalpha. Tetradecanoylphorbol Acetate 121-124 protein kinase C alpha Homo sapiens 29-32 9722545-8 1998 However, this "non-membrane" PKC activity was inhibited by the phorbol ester 4beta-12-O-tetradecanoylphorbol-13-acetate (TPA) and also by the fluorescent analog, SAPD, opposite to its effect on membrane-associated PKCalpha. Tetradecanoylphorbol Acetate 121-124 protein kinase C alpha Homo sapiens 214-222 9683525-19 1998 This arrest, in turn, is associated with a shift of PKC isozymes PKC alpha, PKC betaI, PKC betaII, PKC delta, PKC epsilon, and PKC mu to the membrane fraction which is induced by addition of TPA. Tetradecanoylphorbol Acetate 191-194 protein kinase C alpha Homo sapiens 52-55 9699515-5 1998 Down regulation of protein kinase C (PKC) by pretreatment for 24 hours with 500 nm PMA prevents induction by subsequent stimulation with either PMA or NGA. Tetradecanoylphorbol Acetate 83-86 protein kinase C alpha Homo sapiens 37-40 9699515-5 1998 Down regulation of protein kinase C (PKC) by pretreatment for 24 hours with 500 nm PMA prevents induction by subsequent stimulation with either PMA or NGA. Tetradecanoylphorbol Acetate 144-147 protein kinase C alpha Homo sapiens 37-40 9694709-1 1998 The expression of protein kinase C (PKC) isozymes in human basophils and the regulation of PKC isozymes during basophil activation by phorbol 12-myristate 13-acetate (PMA) +/- ionomycin, f-met-leu-phe (FMLP), and anti-IgE antibody were examined. Tetradecanoylphorbol Acetate 134-165 protein kinase C alpha Homo sapiens 91-94 9694709-1 1998 The expression of protein kinase C (PKC) isozymes in human basophils and the regulation of PKC isozymes during basophil activation by phorbol 12-myristate 13-acetate (PMA) +/- ionomycin, f-met-leu-phe (FMLP), and anti-IgE antibody were examined. Tetradecanoylphorbol Acetate 167-170 protein kinase C alpha Homo sapiens 91-94 9694709-6 1998 Within 1 minute of stimulation with PMA, 90% +/- 6% of PKC was found in the membrane fraction, however, no translocation of PKCdelta was apparent. Tetradecanoylphorbol Acetate 36-39 protein kinase C alpha Homo sapiens 55-58 9619293-4 1998 The potentiation by TPA of the MgATP-dependent priming was blocked by [Ser25]protein kinase C(19-31), a specific substrate of protein kinase C. Go 6976, an inhibitor selective for protein kinase C alpha and beta isoforms, also blocked the potentiation by TPA. Tetradecanoylphorbol Acetate 20-23 protein kinase C alpha Homo sapiens 180-202 9683525-14 1998 PKC alpha, betaI, betaII, delta, and epsilon isozymes were translocated to the membrane fraction from the cytosolic fraction when treated with TPA. Tetradecanoylphorbol Acetate 143-146 protein kinase C alpha Homo sapiens 0-9 9744516-4 1998 PMA also induced an increase in PKC beta and PKC alpha mRNA and protein. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 45-54 9714554-6 1998 PKC accumulation at the plasma membrane was detected 5 min after exposure to 12-O-tetradecanoyl phorbol-13-acetate and increased with time, thus demonstrating activation of these PKCs. Tetradecanoylphorbol Acetate 77-114 protein kinase C alpha Homo sapiens 0-3 9744516-5 1998 Simultaneous exposure to PMA and sphingosine blocked stimulation of CD11b and PKC expression without affecting growth arrest and VDR down regulation. Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 78-81 9639562-8 1998 Cellular fractionation and immunocytochemical staining results demonstrated that both 10 nM and 1 microM PMA treatments induced a marked translocation of PKC-alpha from cytosol to membrane or nuclear fraction within 5-30 min. Tetradecanoylphorbol Acetate 105-108 protein kinase C alpha Homo sapiens 154-163 9639562-10 1998 In addition, prolonged treatment with 1 microM PMA, but not with 10 nM PMA, selectively mediated the down-regulation of these three PKC isoenzymes. Tetradecanoylphorbol Acetate 47-50 protein kinase C alpha Homo sapiens 132-135 9517568-6 1998 Ca2+ ionophore-A23187 and PKC activator-TPA mimicked the effects of these three agonists to stimulate AA release. Tetradecanoylphorbol Acetate 40-43 protein kinase C alpha Homo sapiens 26-29 9593849-1 1998 The protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) stimulates both the synthesis and phospholipase D (PLD)-mediated hydrolysis of phosphatidylcholine (PtdCho). Tetradecanoylphorbol Acetate 37-68 protein kinase C alpha Homo sapiens 22-25 9593849-1 1998 The protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) stimulates both the synthesis and phospholipase D (PLD)-mediated hydrolysis of phosphatidylcholine (PtdCho). Tetradecanoylphorbol Acetate 70-73 protein kinase C alpha Homo sapiens 22-25 9588200-4 1998 Phorbol-myristate-acetate (PMA) induced a rapid PKC translocation to and activation in the particulate cell fraction as determined by PKC-activity measurements and Western blots for PKC alpha. Tetradecanoylphorbol Acetate 0-25 protein kinase C alpha Homo sapiens 48-51 9588200-4 1998 Phorbol-myristate-acetate (PMA) induced a rapid PKC translocation to and activation in the particulate cell fraction as determined by PKC-activity measurements and Western blots for PKC alpha. Tetradecanoylphorbol Acetate 0-25 protein kinase C alpha Homo sapiens 134-137 9588200-4 1998 Phorbol-myristate-acetate (PMA) induced a rapid PKC translocation to and activation in the particulate cell fraction as determined by PKC-activity measurements and Western blots for PKC alpha. Tetradecanoylphorbol Acetate 0-25 protein kinase C alpha Homo sapiens 182-191 9588200-4 1998 Phorbol-myristate-acetate (PMA) induced a rapid PKC translocation to and activation in the particulate cell fraction as determined by PKC-activity measurements and Western blots for PKC alpha. Tetradecanoylphorbol Acetate 27-30 protein kinase C alpha Homo sapiens 48-51 9588200-4 1998 Phorbol-myristate-acetate (PMA) induced a rapid PKC translocation to and activation in the particulate cell fraction as determined by PKC-activity measurements and Western blots for PKC alpha. Tetradecanoylphorbol Acetate 27-30 protein kinase C alpha Homo sapiens 134-137 9588200-4 1998 Phorbol-myristate-acetate (PMA) induced a rapid PKC translocation to and activation in the particulate cell fraction as determined by PKC-activity measurements and Western blots for PKC alpha. Tetradecanoylphorbol Acetate 27-30 protein kinase C alpha Homo sapiens 182-191 9601059-5 1998 PMA-stimulated PLD activity was blocked by the PKC inhibitor bisindolylmaleimide. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 47-50 9593849-4 1998 In multidrug resistant MCF-7/MDR1 cells, which highly express PKC-alpha but lack the PtdCho-specific PLD activity, 100-nM PMA had relatively small stimulatory effects on the uptake of [14C]choline (approximately 1.5-fold) and [14C]PtdCho synthesis (1.5- to 2-fold). Tetradecanoylphorbol Acetate 122-125 protein kinase C alpha Homo sapiens 62-71 9593849-5 1998 In NIH 3T3 fibroblasts and MCF-7/PKC-alpha cells, both expressing PKC-alpha and PLD activities at high levels, 10-100-nM PMA enhanced [14C]choline uptake only slightly (1.7- to 2.2-fold), while it had much greater (approximately 4-9-fold) stimulatory effects on PtdCho synthesis. Tetradecanoylphorbol Acetate 121-124 protein kinase C alpha Homo sapiens 33-42 9593849-5 1998 In NIH 3T3 fibroblasts and MCF-7/PKC-alpha cells, both expressing PKC-alpha and PLD activities at high levels, 10-100-nM PMA enhanced [14C]choline uptake only slightly (1.7- to 2.2-fold), while it had much greater (approximately 4-9-fold) stimulatory effects on PtdCho synthesis. Tetradecanoylphorbol Acetate 121-124 protein kinase C alpha Homo sapiens 66-75 9593849-6 1998 PMA significantly enhanced the formation of phosphatidic acid (PtdOH) in MCF-7/PKC-alpha cells (2.8-fold increase), but not in MCF-7/MDR1 cells (1.4-fold increase), while in both cell lines it had only small (1.3-1.5-fold) stimulatory effects on 1,2-diacylglycerol (1, 2-DAG) formation. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 79-88 9605775-2 1998 Recent investigations showed that activation of PKC alpha by 12-O-tetradecanoylphorbol 13-acetate (TPA) induced apoptosis in LNCaP prostate cancer cells. Tetradecanoylphorbol Acetate 61-97 protein kinase C alpha Homo sapiens 48-57 9605775-2 1998 Recent investigations showed that activation of PKC alpha by 12-O-tetradecanoylphorbol 13-acetate (TPA) induced apoptosis in LNCaP prostate cancer cells. Tetradecanoylphorbol Acetate 99-102 protein kinase C alpha Homo sapiens 48-57 9563854-1 1998 Phorbol ester-like protein kinase C (PKC) activators, such as 12-O-tetradecanoylphorbol-13-acetate, and perturbation of some growth factor receptors have been reported to alter the cytotoxicity of cis-diamminedichloroplatinum(II) (CDDP). Tetradecanoylphorbol Acetate 62-98 protein kinase C alpha Homo sapiens 37-40 9607141-2 1998 In the present study, we investigated the role of PKC and its isozymes in the synergistic induction of PI-3 kinase by TPA and insulin. Tetradecanoylphorbol Acetate 118-121 protein kinase C alpha Homo sapiens 50-53 9495244-8 1998 The opposed effects of TPA in ER+ and ER- cells could be due to the abnormal TPA regulation of PKCalpha observed in ER- cells. Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 95-103 9495244-8 1998 The opposed effects of TPA in ER+ and ER- cells could be due to the abnormal TPA regulation of PKCalpha observed in ER- cells. Tetradecanoylphorbol Acetate 77-80 protein kinase C alpha Homo sapiens 95-103 9442087-9 1998 The significance of these findings is shown with adenocarcinoma cells, which, when pretreated with 10 microM DECA and UV light, exhibited diminished 12-O-tetradecanoylphorbol-13-acetate-induced PKC alpha translocation. Tetradecanoylphorbol Acetate 149-185 protein kinase C alpha Homo sapiens 194-203 9514088-6 1998 12-O-Tetradecanoylphorbol-13-acetate (TPA) restored the membrane translocation of PKC-alpha and abrogated the synergistic cytotoxicity of tamoxifen. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 82-91 9514088-6 1998 12-O-Tetradecanoylphorbol-13-acetate (TPA) restored the membrane translocation of PKC-alpha and abrogated the synergistic cytotoxicity of tamoxifen. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 82-91 9475183-3 1998 Upon stimulation by three different activators, phorbol 12-myristate 13-acetate, fluoride and endothelin-1, a translocation of PKC activity from the cytosolic to the particulate fraction was observed. Tetradecanoylphorbol Acetate 48-79 protein kinase C alpha Homo sapiens 127-130 9666308-2 1998 In fact, epidermal growth factor was an excellent mitogen, even after prolonged pretreatment of cells with TPA, suggesting that the PKC isoform implicated in proliferation is not down-regulated by 12-O-tetradecanoyl phorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 107-110 protein kinase C alpha Homo sapiens 132-135 9666308-2 1998 In fact, epidermal growth factor was an excellent mitogen, even after prolonged pretreatment of cells with TPA, suggesting that the PKC isoform implicated in proliferation is not down-regulated by 12-O-tetradecanoyl phorbol-13-acetate (TPA). Tetradecanoylphorbol Acetate 236-239 protein kinase C alpha Homo sapiens 132-135 9666308-8 1998 PKC-alpha, -delta, and -epsilon were down-regulated by pretreatment of cells with TPA, while PKC-zeta was unaffected. Tetradecanoylphorbol Acetate 82-85 protein kinase C alpha Homo sapiens 0-31 9831302-7 1998 Our results indicate that i) glucosamine is a potent stimulator of PKC-translocation exhibiting an isoenzyme specific translocation kinetic which is different from PMA-induced PKC-isoenzyme translocation ii) the hexosamine pathway may be possibly involved in the high glucose-induced activation of PKC. Tetradecanoylphorbol Acetate 164-167 protein kinase C alpha Homo sapiens 67-70 9831302-7 1998 Our results indicate that i) glucosamine is a potent stimulator of PKC-translocation exhibiting an isoenzyme specific translocation kinetic which is different from PMA-induced PKC-isoenzyme translocation ii) the hexosamine pathway may be possibly involved in the high glucose-induced activation of PKC. Tetradecanoylphorbol Acetate 164-167 protein kinase C alpha Homo sapiens 176-179 9831302-7 1998 Our results indicate that i) glucosamine is a potent stimulator of PKC-translocation exhibiting an isoenzyme specific translocation kinetic which is different from PMA-induced PKC-isoenzyme translocation ii) the hexosamine pathway may be possibly involved in the high glucose-induced activation of PKC. Tetradecanoylphorbol Acetate 164-167 protein kinase C alpha Homo sapiens 176-179 9344462-1 1997 Stimulation of phosphatidylethanolamine (PtdEtn) synthesis by the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) has reportedly been found only in hepatocytes expressing the alpha-, betaII-, epsilon-, and zeta-PKC isozymes. Tetradecanoylphorbol Acetate 99-130 protein kinase C alpha Homo sapiens 84-87 10063971-7 1998 We also explored the PKC mechanism(s) responsible for the synergism of TPA and gemcitabine, and determined that treatment with 10 nM TPA for 24 h in BG-1 cells: 1) downregulated PKCdelta and PKCalpha, without affecting PKCepsilon, 2) did not affect cell cycle distribution into S phase. Tetradecanoylphorbol Acetate 133-136 protein kinase C alpha Homo sapiens 191-199 9344462-7 1997 In contrast, in MCF-7 cells overexpressing PKC-alpha, and as a consequence also expressing the betaI- and betaII-PKC isoforms, PMA effectively stimulated the synthesis of PtdEtn. Tetradecanoylphorbol Acetate 127-130 protein kinase C alpha Homo sapiens 43-52 9344462-8 1997 Finally, in HL60 human leukemia cells, which contains PKC-betaII as the major PKC isoform, PMA again stimulated PtdEtn synthesis. Tetradecanoylphorbol Acetate 91-94 protein kinase C alpha Homo sapiens 54-57 9372245-5 1997 Pretreatment of the cells with PKC inhibitors, CGP 41251 or tamoxifen, inhibited tyrosine phosphorylation of Erk1 and Erk2 MAP kinases induced by low concentrations of SP or TPA and significantly attenuated phosphorylation at high concentrations of SP or TPA. Tetradecanoylphorbol Acetate 174-177 protein kinase C alpha Homo sapiens 31-34 9367627-2 1997 A major phosphoprotein of 20 kDa in resting neutrophils was markedly dephosphorylated upon activation of cells with chemotactic peptide or phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC). Tetradecanoylphorbol Acetate 139-170 protein kinase C alpha Homo sapiens 212-215 9372245-5 1997 Pretreatment of the cells with PKC inhibitors, CGP 41251 or tamoxifen, inhibited tyrosine phosphorylation of Erk1 and Erk2 MAP kinases induced by low concentrations of SP or TPA and significantly attenuated phosphorylation at high concentrations of SP or TPA. Tetradecanoylphorbol Acetate 255-258 protein kinase C alpha Homo sapiens 31-34 9372245-9 1997 Prolonged treatment with TPA resulted in down-regulation of PKC and selective inhibition of TPA- and SP-induced Erk1 and Erk2 tyrosine phosphorylation in U-373 MG cells. Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 60-63 9356174-4 1997 To investigate the regulation of lens cell gap junctions by protein kinase C (PKC), differentiating lens cultures were treated with the PKC activator 12-O-tetradecanoylphorbol-13-acetate (beta-TPA). Tetradecanoylphorbol Acetate 150-186 protein kinase C alpha Homo sapiens 78-81 9392422-3 1997 The protein kinase C (PKC) inhibitors calphostin C and staurosporine prevented TPA-mediated LDL receptor mRNA induction. Tetradecanoylphorbol Acetate 79-82 protein kinase C alpha Homo sapiens 22-25 9367627-2 1997 A major phosphoprotein of 20 kDa in resting neutrophils was markedly dephosphorylated upon activation of cells with chemotactic peptide or phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC). Tetradecanoylphorbol Acetate 172-175 protein kinase C alpha Homo sapiens 212-215 9367627-8 1997 Ca(2+)-independent PKC isoforms, rather than PKC alpha or beta, may thus be involved in PMA-induced cofilin dephosphorylation. Tetradecanoylphorbol Acetate 88-91 protein kinase C alpha Homo sapiens 19-22 9367627-8 1997 Ca(2+)-independent PKC isoforms, rather than PKC alpha or beta, may thus be involved in PMA-induced cofilin dephosphorylation. Tetradecanoylphorbol Acetate 88-91 protein kinase C alpha Homo sapiens 45-54 9392422-6 1997 Treatment of HepG2 cells with 100 nM TPA resulted in translocation of cytosolic PKC alpha to the particulate fraction, with a maximum at 30 min-2 h of treatment, but was without effect on the subcellular distribution of the other isozymes. Tetradecanoylphorbol Acetate 37-40 protein kinase C alpha Homo sapiens 80-89 9392422-11 1997 Based on a close kinetic correlation between PKC alpha translocation and ERK activation, and the effects of specific inhibitors, these findings suggest that translocation/activation of PKC alpha, and subsequent activation of the Raf-1/MEK/ERK MAPK cascade, represent key events in the transcriptional induction of LDL receptor gene by TPA in HepG2 cells. Tetradecanoylphorbol Acetate 335-338 protein kinase C alpha Homo sapiens 185-194 9285638-12 1997 Specific antisense oligodesoxynucleotides (ODNs) against PKC alpha reduced the expression of the isoform, abolished the effects of glucose on endothelial cell permeability completely, and reduced the TPA effect significantly. Tetradecanoylphorbol Acetate 200-203 protein kinase C alpha Homo sapiens 57-66 9316415-5 1997 Treatment with PMA for 30 min increased PKC activity in subcellular fractions and induced a redistribution of PKC-beta II and -delta to a particulate fraction. Tetradecanoylphorbol Acetate 15-18 protein kinase C alpha Homo sapiens 40-43 9357764-1 1997 We have previously shown that a pretreatment with phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC), reduced deoxygenation-induced K+ loss and Ca2+ uptake and prevented cell dehydration in sickle anemia red blood cells (SS cells) (H. Fathallah, E. Coezy, R.-S. De Neef, M.-D. Hardy-Dessources, and F. Giraud. Tetradecanoylphorbol Acetate 50-81 protein kinase C alpha Homo sapiens 123-126 9357764-1 1997 We have previously shown that a pretreatment with phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C (PKC), reduced deoxygenation-induced K+ loss and Ca2+ uptake and prevented cell dehydration in sickle anemia red blood cells (SS cells) (H. Fathallah, E. Coezy, R.-S. De Neef, M.-D. Hardy-Dessources, and F. Giraud. Tetradecanoylphorbol Acetate 83-86 protein kinase C alpha Homo sapiens 123-126 9230140-3 1997 A similar enhancement was seen with PMA, a stimulus that acts on protein kinase C (PKC), or calcium ionophore (A23187), which increases intracellular calcium, suggesting that the effect of the fatty acids was post-surface receptor binding. Tetradecanoylphorbol Acetate 36-39 protein kinase C alpha Homo sapiens 83-86 9346296-5 1997 GDP and its analogue, guanosine 5"-O-[beta-thio]diphosphate, inhibited the stimulatory effect of GTP[S], whereas the PMA response was prevented by the nonselective PKC inhibitor, staurosporine, but not vice versa. Tetradecanoylphorbol Acetate 117-120 protein kinase C alpha Homo sapiens 164-167 9245795-5 1997 Induction of LAR processing by TPA in 293 cells did require overexpression of PKCalpha. Tetradecanoylphorbol Acetate 31-34 protein kinase C alpha Homo sapiens 78-86 9230140-9 1997 The synergistic response between fatty acids and A23187 was completely inhibited by pretreating the cells with a PKC inhibitor, GF-109203X, or by pretreatment of monocytes with PMA for 18 h, to deplete PKC levels. Tetradecanoylphorbol Acetate 177-180 protein kinase C alpha Homo sapiens 202-205 9246383-5 1997 Following prolonged pre-treatment with tetradecanoyl phorbol acetate (100 nmol L-1), which down-regulates PKC-alpha and delta, the angiotensin-induced PKC translocation was lost. Tetradecanoylphorbol Acetate 39-68 protein kinase C alpha Homo sapiens 106-115 9246383-5 1997 Following prolonged pre-treatment with tetradecanoyl phorbol acetate (100 nmol L-1), which down-regulates PKC-alpha and delta, the angiotensin-induced PKC translocation was lost. Tetradecanoylphorbol Acetate 39-68 protein kinase C alpha Homo sapiens 106-109 9045886-8 1997 This activation was PKC-dependent since phorbol 12-myristate 13-acetate (PMA) promoted down-regulation of PKC-eliminated MAP kinase activation by ATP or UTP. Tetradecanoylphorbol Acetate 40-71 protein kinase C alpha Homo sapiens 20-23 9176220-3 1997 The PKC inhibitors chelerythrine and Go-6976 reduced, whereas a PKC agonist, phorbol 12-myristate 13-acetate (PMA), increased glycochenodeoxycholate (GCDC)-induced hepatocyte apoptosis. Tetradecanoylphorbol Acetate 77-108 protein kinase C alpha Homo sapiens 64-67 9176220-3 1997 The PKC inhibitors chelerythrine and Go-6976 reduced, whereas a PKC agonist, phorbol 12-myristate 13-acetate (PMA), increased glycochenodeoxycholate (GCDC)-induced hepatocyte apoptosis. Tetradecanoylphorbol Acetate 110-113 protein kinase C alpha Homo sapiens 4-7 9099748-12 1997 Thus, the elevation of phospholipase D activity or activities induced by both TPA and vasopressin and the stimulation of translation by TPA involves PKC-alpha, -epsilon, and/or -delta. Tetradecanoylphorbol Acetate 136-139 protein kinase C alpha Homo sapiens 149-183 9038375-5 1997 Immunohistochemistry studies indicated that after treatment with TPA normal PKCalpha mainly translocated to the plasma membrane, but mutant PKCalpha translocated mainly to the perinuclear region and slightly to the nucleus. Tetradecanoylphorbol Acetate 65-68 protein kinase C alpha Homo sapiens 76-84 9045886-8 1997 This activation was PKC-dependent since phorbol 12-myristate 13-acetate (PMA) promoted down-regulation of PKC-eliminated MAP kinase activation by ATP or UTP. Tetradecanoylphorbol Acetate 40-71 protein kinase C alpha Homo sapiens 106-109 9045886-8 1997 This activation was PKC-dependent since phorbol 12-myristate 13-acetate (PMA) promoted down-regulation of PKC-eliminated MAP kinase activation by ATP or UTP. Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 20-23 9045886-8 1997 This activation was PKC-dependent since phorbol 12-myristate 13-acetate (PMA) promoted down-regulation of PKC-eliminated MAP kinase activation by ATP or UTP. Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 106-109 9045886-9 1997 Treatment of cells with the MAP kinase cascade inhibitor PD098059, the PKC inhibitor GF109203X, or down-regulation of PKC by PMA treatment, all suppressed AA release promoted by ATP or UTP, suggesting that both MAP kinase and PKC are involved in the regulation of cPLA2 by P2U receptors. Tetradecanoylphorbol Acetate 125-128 protein kinase C alpha Homo sapiens 118-121 9045886-9 1997 Treatment of cells with the MAP kinase cascade inhibitor PD098059, the PKC inhibitor GF109203X, or down-regulation of PKC by PMA treatment, all suppressed AA release promoted by ATP or UTP, suggesting that both MAP kinase and PKC are involved in the regulation of cPLA2 by P2U receptors. Tetradecanoylphorbol Acetate 125-128 protein kinase C alpha Homo sapiens 118-121 9045886-12 1997 This conclusion is further supported by data showing that PMA-promoted AA release, but not MAP kinase activation, was suppressed in cells in which PKCalpha expression was decreased by antisense transfection. Tetradecanoylphorbol Acetate 58-61 protein kinase C alpha Homo sapiens 147-155 9203625-3 1997 12-O-Tetradecanoylphorbol-13-acetate (TPA), a potent activator of PKC, is known to reduce the amplitude of agonist-induced calcium mobilization in various cell lines. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 66-69 9032469-1 1997 Activation of P388D1 macrophages by phorbol myristate acetate (PMA) resulted in the translocation of the protein kinase C (PKC) isoforms alpha, delta, and epsilon from the cytosol to membranes. Tetradecanoylphorbol Acetate 36-61 protein kinase C alpha Homo sapiens 105-162 9032469-1 1997 Activation of P388D1 macrophages by phorbol myristate acetate (PMA) resulted in the translocation of the protein kinase C (PKC) isoforms alpha, delta, and epsilon from the cytosol to membranes. Tetradecanoylphorbol Acetate 63-66 protein kinase C alpha Homo sapiens 105-162 9203625-8 1997 This reduction in PKC-alpha was sufficient to inhibit the reduction of bradykinin-induced calcium mobilization by TPA. Tetradecanoylphorbol Acetate 114-117 protein kinase C alpha Homo sapiens 18-27 9203625-3 1997 12-O-Tetradecanoylphorbol-13-acetate (TPA), a potent activator of PKC, is known to reduce the amplitude of agonist-induced calcium mobilization in various cell lines. Tetradecanoylphorbol Acetate 38-41 protein kinase C alpha Homo sapiens 66-69 9203625-9 1997 This finding is corroborated by the use of staurosporine, a nonselective PKC inhibitor, that prevented the effect of TPA. Tetradecanoylphorbol Acetate 117-120 protein kinase C alpha Homo sapiens 73-76 8910539-1 1996 Stimulation of phospholipase D (PLD)-mediated hydrolysis of phosphatidylcholine (PtdCho) by phorbol 12-myristate 13-acetate (PMA) has been shown to be mediated by the alpha- and betaI-isoforms of protein kinase C (PKC). Tetradecanoylphorbol Acetate 92-123 protein kinase C alpha Homo sapiens 214-217 9413940-3 1997 In addition, the PKC inhibitor Ro 31-8220 with predominant PKC-alpha isoform specificity almost completely inhibited PMA-induced up-regulation of p21WAF1 in HL-60 cells as well as in the myelomonocytic leukaemic U937 cells. Tetradecanoylphorbol Acetate 117-120 protein kinase C alpha Homo sapiens 17-20 9413940-3 1997 In addition, the PKC inhibitor Ro 31-8220 with predominant PKC-alpha isoform specificity almost completely inhibited PMA-induced up-regulation of p21WAF1 in HL-60 cells as well as in the myelomonocytic leukaemic U937 cells. Tetradecanoylphorbol Acetate 117-120 protein kinase C alpha Homo sapiens 59-68 9413940-4 1997 Pretreatment of HL-60 cells with Ro 31-8220 also inhibited PMA-induced activation of c-raf-1, a known PKC alpha target. Tetradecanoylphorbol Acetate 59-62 protein kinase C alpha Homo sapiens 102-105 8978751-8 1997 Selective down-regulation of PKC subtypes by prolonged exposure to phorbol 12,13-dibutyrate (100 nM) attenuated the TPA-induced enhancement of NA release and the translocation of MARCKS over an interval similar to that of down-regulation of PKC-alpha (but not -epsilon or -zeta). Tetradecanoylphorbol Acetate 116-119 protein kinase C alpha Homo sapiens 241-250 8978751-9 1997 Thus, we have demonstrated a strong correlation between the translocation of MARCKS and the enhancement of NA release from SH-SY5Y cells due to the TPA-induced activation of PKC-alpha. Tetradecanoylphorbol Acetate 148-151 protein kinase C alpha Homo sapiens 174-183 8997261-8 1996 The TPA-induced increase in H82 cell attachment was likely mediated by activation of EC protein kinase C (PKC). Tetradecanoylphorbol Acetate 4-7 protein kinase C alpha Homo sapiens 106-109 8997261-9 1996 Pretreatment of the EC with PKC inhibitors effectively blocked the TPA-mediated increase in H82 cell attachment. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 28-31 8997261-10 1996 In addition, prolonged exposure of EC to TPA resulted in decreased expression of the PKC-alpha and PKC-epsilon isoforms. Tetradecanoylphorbol Acetate 41-44 protein kinase C alpha Homo sapiens 85-94 8978751-2 1997 Subcellular fractionation and immunocytochemical studies demonstrated that an 8-min TPA treatment caused translocation of the alpha-subtype of protein kinase C (PKC) from the cytosol to the plasma membrane. Tetradecanoylphorbol Acetate 84-87 protein kinase C alpha Homo sapiens 161-164 8978751-7 1997 The ability of TPA to enhance NA release and to cause the translocation and phosphorylation of MARCKS was inhibited by the PKC inhibitor Ro 31-8220 (10 microM). Tetradecanoylphorbol Acetate 15-18 protein kinase C alpha Homo sapiens 123-126 8978751-8 1997 Selective down-regulation of PKC subtypes by prolonged exposure to phorbol 12,13-dibutyrate (100 nM) attenuated the TPA-induced enhancement of NA release and the translocation of MARCKS over an interval similar to that of down-regulation of PKC-alpha (but not -epsilon or -zeta). Tetradecanoylphorbol Acetate 116-119 protein kinase C alpha Homo sapiens 29-32 8910539-4 1996 Stable expression of PKC-alpha in MCF-7 cells, which was accompanied by increased levels of the betaI- and theta-isoforms as well, greatly enhanced both PMA-induced PLD-mediated formation of phosphatidylethanol (approximately 5-fold) and the hydrolysis of PtdEtn (2.5-2.9-fold) and PtdCho (5.5-7.2-fold). Tetradecanoylphorbol Acetate 153-156 protein kinase C alpha Homo sapiens 21-30 8910539-5 1996 The effects of PMA on the hydrolysis of PtdEtn (and PtdCho) in MCF-7/PKC-alpha cells were significantly inhibited by 0.5-3 microM concentrations of Go 6976, a selective inhibitor of the conventional PKC subfamily. Tetradecanoylphorbol Acetate 15-18 protein kinase C alpha Homo sapiens 69-78 8910539-5 1996 The effects of PMA on the hydrolysis of PtdEtn (and PtdCho) in MCF-7/PKC-alpha cells were significantly inhibited by 0.5-3 microM concentrations of Go 6976, a selective inhibitor of the conventional PKC subfamily. Tetradecanoylphorbol Acetate 15-18 protein kinase C alpha Homo sapiens 69-72 8910539-6 1996 Stable expression of PKC-alpha in R6 fibroblasts enhanced, at a shorter (10 min) incubation time, the effects of PMA on the hydrolysis of both PtdEtn and, to a lesser extent, PtdCho. Tetradecanoylphorbol Acetate 113-116 protein kinase C alpha Homo sapiens 21-30 8915773-11 1996 Acute pretreatment of cells with PMA reduced concomitantly the amounts of PKC alpha, but not of PKC epsilon, and the subsequent activation of PLD elicited by PKC activators. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 74-83 8972728-6 1996 Elevation of membrane PKC levels by 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment had no effect on cell survival after irradiation, while treatment with EGF during and after irradiation augmented cell survival. Tetradecanoylphorbol Acetate 36-72 protein kinase C alpha Homo sapiens 22-25 8972728-6 1996 Elevation of membrane PKC levels by 12-O-tetradecanoylphorbol 13-acetate (TPA) treatment had no effect on cell survival after irradiation, while treatment with EGF during and after irradiation augmented cell survival. Tetradecanoylphorbol Acetate 74-77 protein kinase C alpha Homo sapiens 22-25 8915773-11 1996 Acute pretreatment of cells with PMA reduced concomitantly the amounts of PKC alpha, but not of PKC epsilon, and the subsequent activation of PLD elicited by PKC activators. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 74-77 8912814-1 1996 The protein kinase C (PKC) signal transduction pathway is the prototype of a growth factor-responsive intracellular signaling system, which is activated by various cytokines, growth factors and tumor promoters, such as the phorbol ester 12-O-tetradecanoyl-phorbol acetate (TPA). Tetradecanoylphorbol Acetate 237-271 protein kinase C alpha Homo sapiens 22-25 8950233-8 1996 We also examined dPPA and PMA for their ability to activate and to downregulate expression of different PKC isoforms. Tetradecanoylphorbol Acetate 26-29 protein kinase C alpha Homo sapiens 104-107 8950233-9 1996 Fifteen-minute treatment with PMA resulted in the translocation of PKC isoforms alpha, epsilon, and theta from the cytosolic to the membrane fraction; twenty-four hour treatment resulted in the downregulation of these isoforms. Tetradecanoylphorbol Acetate 30-33 protein kinase C alpha Homo sapiens 67-105 8912814-1 1996 The protein kinase C (PKC) signal transduction pathway is the prototype of a growth factor-responsive intracellular signaling system, which is activated by various cytokines, growth factors and tumor promoters, such as the phorbol ester 12-O-tetradecanoyl-phorbol acetate (TPA). Tetradecanoylphorbol Acetate 273-276 protein kinase C alpha Homo sapiens 22-25 8912814-10 1996 Our data demonstrate that the proliferative response to TPA correlates with the expression levels of the majority of PKC isoforms in these cells. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 117-120 8798560-1 1996 Although the involvement of protein kinase C (PKC) in the activation of the mitogen-activated protein (MAP) kinase pathway has been implicated through experiments using 12-O-tetradecanoylphorbol-13-acetate (TPA), there has been no direct demonstration that PKC activates the MAP kinase pathway. Tetradecanoylphorbol Acetate 169-205 protein kinase C alpha Homo sapiens 46-49 8798560-1 1996 Although the involvement of protein kinase C (PKC) in the activation of the mitogen-activated protein (MAP) kinase pathway has been implicated through experiments using 12-O-tetradecanoylphorbol-13-acetate (TPA), there has been no direct demonstration that PKC activates the MAP kinase pathway. Tetradecanoylphorbol Acetate 207-210 protein kinase C alpha Homo sapiens 46-49 8774728-12 1996 Treatment with 30 nM TPA for 24 h completely depleted KB-3 cells of PKC alpha whereas 1 microM TPA was required to deplete KB-V1 cells of PKC alpha. Tetradecanoylphorbol Acetate 21-24 protein kinase C alpha Homo sapiens 68-77 8877100-5 1996 Compared with control clones, PKC-alpha- and -beta-overexpressing MCF-7 cells exhibited more drastic morphological changes in response to phorbol 12-myristate 13-acetate administration characterized by cellular flattening and vacuolization. Tetradecanoylphorbol Acetate 138-169 protein kinase C alpha Homo sapiens 30-39 8687492-4 1996 Complete down-regulation of PKC from MCF-7/Dox cells by 24-hr preincubation with PMA did not alter the degree of Dox resistance. Tetradecanoylphorbol Acetate 81-84 protein kinase C alpha Homo sapiens 28-31 8687492-13 1996 Differential effects of H7 on the PMA-induced changes suggest that different isoforms of PKC may be involved in cell growth and drug accumulation processes as well as P-glycoprotein expression. Tetradecanoylphorbol Acetate 34-37 protein kinase C alpha Homo sapiens 89-92 8754760-7 1996 Incubation of AsPc1 cells with the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate resulted in a time- and dose-dependent selective down-regulation of PKC alpha but not zeta. Tetradecanoylphorbol Acetate 49-86 protein kinase C alpha Homo sapiens 155-164 8774728-12 1996 Treatment with 30 nM TPA for 24 h completely depleted KB-3 cells of PKC alpha whereas 1 microM TPA was required to deplete KB-V1 cells of PKC alpha. Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 138-147 8774728-14 1996 Defective TPA-mediated down-regulation of PKC alpha was also observed in another PKC alpha-overexpressing MDR cell line. Tetradecanoylphorbol Acetate 10-13 protein kinase C alpha Homo sapiens 42-51 8774728-14 1996 Defective TPA-mediated down-regulation of PKC alpha was also observed in another PKC alpha-overexpressing MDR cell line. Tetradecanoylphorbol Acetate 10-13 protein kinase C alpha Homo sapiens 81-90 8856479-4 1996 Translocation and down-regulation of PKC alpha and epsilon but not zeta were detected by short-term and long-term treatment with TPA (12-O-tetradecanoylphorbol 13-acetate), respectively. Tetradecanoylphorbol Acetate 129-132 protein kinase C alpha Homo sapiens 37-46 8856479-4 1996 Translocation and down-regulation of PKC alpha and epsilon but not zeta were detected by short-term and long-term treatment with TPA (12-O-tetradecanoylphorbol 13-acetate), respectively. Tetradecanoylphorbol Acetate 134-170 protein kinase C alpha Homo sapiens 37-46 8712711-2 1996 The down-regulation of PKC-alpha and -beta in JCA-1 cells was correlated with the effects of TPA. Tetradecanoylphorbol Acetate 93-96 protein kinase C alpha Homo sapiens 23-42 8757771-7 1996 Immunocytochemical studies demonstrated that the isozymes are located in distinct cellular compartments and that following treatment with phorbol 12-myristate 13-acetate or with a collagen gel overlay, most isozymes (protein kinase C alpha, beta1, betaII, delta, epsilon, eta) translocated to different parts of the cell. Tetradecanoylphorbol Acetate 138-169 protein kinase C alpha Homo sapiens 217-239 8662781-3 1996 In Molt-4 cells, phorbol 12-myristate 13-acetate (PMA) induced retinoblastoma gene product (Rb) phosphorylation, and ceramide inhibited this effect, suggesting an inhibitory effect of ceramide on the protein kinase C (PKC) pathway, the primary target of PMA. Tetradecanoylphorbol Acetate 17-48 protein kinase C alpha Homo sapiens 218-221 8690086-2 1996 In T84 human epithelia] cells 12-O-tetradecanoyl phorbol 13-acetate (TPA) caused persistent translocation of PKC delta to the membrane compartment and a 400% increase of PKC delta-mRNA after 24 h. In contrast, PKC alpha protein was completely downregulated and its mRNA was decreased to 60% of control levels after 24 h. This is the first report of PKC delta-mRNA upregulation by TPA which was previously only shown for PKCbeta. Tetradecanoylphorbol Acetate 30-67 protein kinase C alpha Homo sapiens 210-219 8690086-2 1996 In T84 human epithelia] cells 12-O-tetradecanoyl phorbol 13-acetate (TPA) caused persistent translocation of PKC delta to the membrane compartment and a 400% increase of PKC delta-mRNA after 24 h. In contrast, PKC alpha protein was completely downregulated and its mRNA was decreased to 60% of control levels after 24 h. This is the first report of PKC delta-mRNA upregulation by TPA which was previously only shown for PKCbeta. Tetradecanoylphorbol Acetate 69-72 protein kinase C alpha Homo sapiens 210-219 8703801-4 1996 When differentiation of MEG-01 was induced by 100 nm 12-O-tetradecanoyl-phorbol-13-acetate (TPA), rapid translocation from cytosol to membrane fraction and down-regulation of PKC alpha, -epsilon and -theta was observed in 1-2h. Tetradecanoylphorbol Acetate 53-90 protein kinase C alpha Homo sapiens 175-205 8780891-8 1996 A high concentration of TPA (1.6 microM) down regulated PKC-alpha and PKC-beta I almost completely and PKC-epsilon partially in wild-type SH-SY5Y and SH-SY5Y/trk cells. Tetradecanoylphorbol Acetate 24-27 protein kinase C alpha Homo sapiens 56-65 8780891-9 1996 Cells with down-regulated PKC-alpha and PKC-beta I after 1.6 microM TPA treatment still differentiated with growth factors. Tetradecanoylphorbol Acetate 68-71 protein kinase C alpha Homo sapiens 26-35 8662781-13 1996 C6-ceramide inhibited basal and PMA-induced phosphorylation of PKCalpha. Tetradecanoylphorbol Acetate 32-35 protein kinase C alpha Homo sapiens 63-71 8662781-3 1996 In Molt-4 cells, phorbol 12-myristate 13-acetate (PMA) induced retinoblastoma gene product (Rb) phosphorylation, and ceramide inhibited this effect, suggesting an inhibitory effect of ceramide on the protein kinase C (PKC) pathway, the primary target of PMA. Tetradecanoylphorbol Acetate 50-53 protein kinase C alpha Homo sapiens 218-221 9052983-1 1996 Others have reported that the phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA), an activator and down-regulator of most protein kinase C (PKC) isozymes, can induce apoptotic cell death of androgen-sensitive LNCaP but not androgen-insensitive PC-3 or DU 145 human prostate cancer cells. Tetradecanoylphorbol Acetate 82-85 protein kinase C alpha Homo sapiens 146-149 8963726-10 1996 The phorbol ester TPA induced a rearrangement of PKC delta and a translocation of PKC alpha and epsilon to the nucleus. Tetradecanoylphorbol Acetate 18-21 protein kinase C alpha Homo sapiens 82-91 8963726-11 1996 Treatment of endothelial cells with TPA for 24 hours caused PKC alpha, delta, and epsilon to disappear, while PKC zeta was not influenced by TPA. Tetradecanoylphorbol Acetate 36-39 protein kinase C alpha Homo sapiens 60-69 8632160-6 1996 Moreover, the inhibition of TPA-enhanced secretion was also apparent after only 2-h exposure to either PDBu or bryostatin-1, conditions that caused down-regulation of PKC-alpha, but not PKC-epsilon or zeta. Tetradecanoylphorbol Acetate 28-31 protein kinase C alpha Homo sapiens 167-176 8632160-7 1996 The PKC inhibitor Go-6976 (2 microM), which has been shown to inhibit selectively PKC-alpha and beta in vitro, also inhibited the TPA enhancement of carbachol- and (K+)-evoked NA release by > 50%. Tetradecanoylphorbol Acetate 130-133 protein kinase C alpha Homo sapiens 4-7 8632160-8 1996 These data suggest that in SH-SY5Y cells, the ability of TPA to enhance carbachol- and (K+)-evoked NA secretion is due to activation of PKC-alpha. Tetradecanoylphorbol Acetate 57-60 protein kinase C alpha Homo sapiens 136-145 9052983-7 1996 TPA-resistant LNCaP cells in the continuous presence of TPA, or 24 h after removal of TPA, had down-regulated PKC alpha and remained resistant to re-addition of TPA. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 110-119 9052983-7 1996 TPA-resistant LNCaP cells in the continuous presence of TPA, or 24 h after removal of TPA, had down-regulated PKC alpha and remained resistant to re-addition of TPA. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 110-119 9052983-7 1996 TPA-resistant LNCaP cells in the continuous presence of TPA, or 24 h after removal of TPA, had down-regulated PKC alpha and remained resistant to re-addition of TPA. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 110-119 9052983-7 1996 TPA-resistant LNCaP cells in the continuous presence of TPA, or 24 h after removal of TPA, had down-regulated PKC alpha and remained resistant to re-addition of TPA. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 110-119 9052983-6 1996 Incubation with TPA for 6 h or more induced 95% inhibition of cell growth, a transient 12-fold increase and 5-fold decrease in PKC alpha and mu mRNA levels, respectively, and prolonged translocation of PKC alpha to non-nuclear membranes in unmodified LNCaP cells and in TPA-resistant LNCaP cells from which TPA had been removed for 10 days. Tetradecanoylphorbol Acetate 16-19 protein kinase C alpha Homo sapiens 127-136 9052983-6 1996 Incubation with TPA for 6 h or more induced 95% inhibition of cell growth, a transient 12-fold increase and 5-fold decrease in PKC alpha and mu mRNA levels, respectively, and prolonged translocation of PKC alpha to non-nuclear membranes in unmodified LNCaP cells and in TPA-resistant LNCaP cells from which TPA had been removed for 10 days. Tetradecanoylphorbol Acetate 16-19 protein kinase C alpha Homo sapiens 202-211 9052983-6 1996 Incubation with TPA for 6 h or more induced 95% inhibition of cell growth, a transient 12-fold increase and 5-fold decrease in PKC alpha and mu mRNA levels, respectively, and prolonged translocation of PKC alpha to non-nuclear membranes in unmodified LNCaP cells and in TPA-resistant LNCaP cells from which TPA had been removed for 10 days. Tetradecanoylphorbol Acetate 270-273 protein kinase C alpha Homo sapiens 202-211 9052983-6 1996 Incubation with TPA for 6 h or more induced 95% inhibition of cell growth, a transient 12-fold increase and 5-fold decrease in PKC alpha and mu mRNA levels, respectively, and prolonged translocation of PKC alpha to non-nuclear membranes in unmodified LNCaP cells and in TPA-resistant LNCaP cells from which TPA had been removed for 10 days. Tetradecanoylphorbol Acetate 270-273 protein kinase C alpha Homo sapiens 202-211 7560079-7 1995 In contrast, TPA treatment induced death of MCF-7-PKC-alpha cells. Tetradecanoylphorbol Acetate 13-16 protein kinase C alpha Homo sapiens 50-59 8616013-2 1996 PKC activity was analysed using a serine substituted specific peptide, which enabled us to evaluate the whole catalytic activity in the pluripotent haemopoietic HEL cell line treated with 10(-7)M phorbol myristate acetate (PMA) or haemin. Tetradecanoylphorbol Acetate 196-221 protein kinase C alpha Homo sapiens 0-3 8616013-2 1996 PKC activity was analysed using a serine substituted specific peptide, which enabled us to evaluate the whole catalytic activity in the pluripotent haemopoietic HEL cell line treated with 10(-7)M phorbol myristate acetate (PMA) or haemin. Tetradecanoylphorbol Acetate 223-226 protein kinase C alpha Homo sapiens 0-3 8616013-4 1996 PKC catalytic activity in the nuclei of HEL cells showed a peak after acute (30 min) treatment with PMA, followed by a significant (P < 0.05) decline after prolonged exposure (72 h) to the same agonist, when most HEL cells had acquired a differentiated megakaryocytic phenotype. Tetradecanoylphorbol Acetate 100-103 protein kinase C alpha Homo sapiens 0-3 8616013-5 1996 Western blot analysis of nuclear lysates consistently showed a significant increase of PKC-alpha, -beta I, -epsilon, theta and -zeta isoforms after 30 min of PMA treatment, followed by a drastic decline of all but PKC-zeta isoforms. Tetradecanoylphorbol Acetate 158-161 protein kinase C alpha Homo sapiens 87-96 8895200-7 1996 TPA initially induced translocation of PKCs alpha and delta, and to a lesser extent, PKC epsilon to the membrane fraction; 8 h after TPA treatment, differential effects on downregulation of PKCs alpha and delta were observed between cell lines, although PKC epsilon was not reduced in either cell line. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 39-59 8895200-7 1996 TPA initially induced translocation of PKCs alpha and delta, and to a lesser extent, PKC epsilon to the membrane fraction; 8 h after TPA treatment, differential effects on downregulation of PKCs alpha and delta were observed between cell lines, although PKC epsilon was not reduced in either cell line. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 190-210 9815959-7 1995 12-O-tetradecanoylphorbol-13-acetate caused translocation of PKC-alpha from the cytosol to the cell membrane after a 10-min treatment and its down-regulation after 24 h of treatment. Tetradecanoylphorbol Acetate 0-36 protein kinase C alpha Homo sapiens 61-70 8848016-2 1995 In C6 glioma cells, short term (10 min) treatment with 12-O-tetradecanoyl phorbol-13-acetate (TPA) results in a dose-dependent translocation of PKC alpha, PKC delta and PKC theta. Tetradecanoylphorbol Acetate 55-92 protein kinase C alpha Homo sapiens 144-153 8848016-2 1995 In C6 glioma cells, short term (10 min) treatment with 12-O-tetradecanoyl phorbol-13-acetate (TPA) results in a dose-dependent translocation of PKC alpha, PKC delta and PKC theta. Tetradecanoylphorbol Acetate 94-97 protein kinase C alpha Homo sapiens 144-153 8848016-3 1995 Long term (24 hr) treatment with appropriate doses of TPA results in the complete down-regulation of PKC delta but not of PKC alpha PKC theta. Tetradecanoylphorbol Acetate 54-57 protein kinase C alpha Homo sapiens 122-131 8848016-8 1995 We have shown that the Na(+)-H+ exchanger in C6 glioma cells can be stimulated by TPA-induced PKC activation and, for the first time, that PKC delta is involved in the activation of this antiporter. Tetradecanoylphorbol Acetate 82-85 protein kinase C alpha Homo sapiens 94-97 7589454-6 1995 Prolonged exposure of mesangial cells to phorbol myristate acetic acid (PMA) inhibited the enzymatic activity of PKC alpha but not PKC zeta. Tetradecanoylphorbol Acetate 72-75 protein kinase C alpha Homo sapiens 113-122 7560079-9 1995 TPA-treated MCF-7-PKC-alpha cells accumulated in G2/M, did not express p53, displayed decreased Cip1 expression, and demonstrated a reduction in retinoblastoma hypophosphorylation. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 18-27 7560079-10 1995 TPA-treated MCF-7-PKC-alpha cells expressed gadd-45 which occurred before the onset of apoptosis. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 18-27 7547506-2 1995 Prolonged treatment of RD cells with the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol-13-acetate (TPA) induces growth arrest and myogenic differentiation as shown by the accumulation of alpha-actin and myosin light and heavy chains, without affecting the expression of MyoD and myogenin. Tetradecanoylphorbol Acetate 112-115 protein kinase C alpha Homo sapiens 59-62 7568092-3 1995 alpha PKC is involved in phorbol 12-myristate 13-acetate-induced cytostasis and megakaryocytic differentiation, whereas beta II PKC is required for proliferation. Tetradecanoylphorbol Acetate 25-56 protein kinase C alpha Homo sapiens 6-9 7547506-0 1995 Rapid activation and down-regulation of protein kinase C alpha in 12-O-Tetradecanoylphorbol-13-acetate-induced differentiation of human rhabdomyosarcoma cells. Tetradecanoylphorbol Acetate 66-102 protein kinase C alpha Homo sapiens 40-62 7547506-2 1995 Prolonged treatment of RD cells with the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol-13-acetate (TPA) induces growth arrest and myogenic differentiation as shown by the accumulation of alpha-actin and myosin light and heavy chains, without affecting the expression of MyoD and myogenin. Tetradecanoylphorbol Acetate 74-110 protein kinase C alpha Homo sapiens 59-62 7653527-3 1995 After the activation of protein kinase C (PKC) by phorbol myristate acetate (PMA), NCE activity decreased exponentially by 75% in 48 h (half time approximately 19 h). Tetradecanoylphorbol Acetate 50-75 protein kinase C alpha Homo sapiens 42-45 7653527-3 1995 After the activation of protein kinase C (PKC) by phorbol myristate acetate (PMA), NCE activity decreased exponentially by 75% in 48 h (half time approximately 19 h). Tetradecanoylphorbol Acetate 77-80 protein kinase C alpha Homo sapiens 42-45 7653527-6 1995 PMA decreased the binding of 3H-labeled antibody to cell sonicates by 40% in 24 h. Immunoblots show that PMA produced a marked and extended increase in membrane-associated PKC-alpha, although PMA depleted total PKC-alpha by 65% in 24 h. In vivo 32P labeling of myristolated alanine-rich C kinase substrate, a specific PKC substrate, confirmed that PMA produced a rapid and extended activation of PKC. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 172-181 7653527-6 1995 PMA decreased the binding of 3H-labeled antibody to cell sonicates by 40% in 24 h. Immunoblots show that PMA produced a marked and extended increase in membrane-associated PKC-alpha, although PMA depleted total PKC-alpha by 65% in 24 h. In vivo 32P labeling of myristolated alanine-rich C kinase substrate, a specific PKC substrate, confirmed that PMA produced a rapid and extended activation of PKC. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 211-220 7653527-6 1995 PMA decreased the binding of 3H-labeled antibody to cell sonicates by 40% in 24 h. Immunoblots show that PMA produced a marked and extended increase in membrane-associated PKC-alpha, although PMA depleted total PKC-alpha by 65% in 24 h. In vivo 32P labeling of myristolated alanine-rich C kinase substrate, a specific PKC substrate, confirmed that PMA produced a rapid and extended activation of PKC. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 172-175 7653527-6 1995 PMA decreased the binding of 3H-labeled antibody to cell sonicates by 40% in 24 h. Immunoblots show that PMA produced a marked and extended increase in membrane-associated PKC-alpha, although PMA depleted total PKC-alpha by 65% in 24 h. In vivo 32P labeling of myristolated alanine-rich C kinase substrate, a specific PKC substrate, confirmed that PMA produced a rapid and extended activation of PKC. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 211-214 7547506-4 1995 Furthermore, PKC inhibitors, such as staurosporine or calphostin C, prevent TPA-induced differentiation but not cell growth arrest. Tetradecanoylphorbol Acetate 76-79 protein kinase C alpha Homo sapiens 13-16 7547506-9 1995 By immunofluorescence analysis, we show that the PKC alpha down-regulation is specific for those cells that respond to TPA by activating the muscle phenotype. Tetradecanoylphorbol Acetate 119-122 protein kinase C alpha Homo sapiens 49-58 7547506-10 1995 We propose that TPA-induced differentiation in RD cells is mediated by the transient activation of PKC alpha, which activates some of the intracellular events that are necessary for MyoD and myogenin transacting activity and for the induction of terminal differentiation of RD cells. Tetradecanoylphorbol Acetate 16-19 protein kinase C alpha Homo sapiens 99-108 7789317-3 1995 After prolonged treatment with high concentration of tumor promoter, 12-O-tetradecanoyl phorbol-13-acetate (TPA), the protein kinase C-alpha (PKC-alpha) level in the Hep3B cells was diminished and could not be detected by Western blot analysis. Tetradecanoylphorbol Acetate 69-106 protein kinase C alpha Homo sapiens 142-151 7628546-2 1995 All PKC isoenzymes except PKC zeta are down-regulated by TPA as well as by bryostatin. Tetradecanoylphorbol Acetate 57-60 protein kinase C alpha Homo sapiens 4-7 7923629-8 1994 To clarify the role of PKC in vasoconstrictor-stimulated VSMC production of bFGF and hypertrophy, PKC was down-regulated by prolonged exposure to PMA or was inhibited with calphostin C or staurosporine before the addition of TXA2 or Ang II. Tetradecanoylphorbol Acetate 146-149 protein kinase C alpha Homo sapiens 98-101 7544678-3 1995 The inhibitory effect of TPA on histamine-stimulated adenylate cyclase was enhanced by the presence of Ca2+, but decreased in a concentration-dependent manner by anti-peptide antibody to protein kinase C alpha, but not to protein kinase C epsilon. Tetradecanoylphorbol Acetate 25-28 protein kinase C alpha Homo sapiens 187-209 7830075-1 1995 Correlation between translocation and down-regulation of conventional protein kinase C alpha (cPKC alpha) and new PKC delta (nPKC delta) induced by 12-O-tetradecanoylphorbol 13-acetate (TPA) at different time courses (5 min, 30 min, 1 h, 3 h, 6 h, 10 h, 17 h, and 24 h) was studied in C6 glioma cells. Tetradecanoylphorbol Acetate 186-189 protein kinase C alpha Homo sapiens 70-92 7623773-5 1995 With TPA treatment of the cells for various times (10 min, 90 min, 3 hr, 6 hr, or 24 hr), translocation of PKC-alpha and PKC-delta from the cytosol to the membrane was seen after 10- or 90-min treatment and restoration to basal levels in the membrane fraction was seen after 3-hr treatment. Tetradecanoylphorbol Acetate 5-8 protein kinase C alpha Homo sapiens 107-116 7623773-10 1995 After 10- or 90-min TPA treatment, AIF4(-)--but not Ca2+ ionophore-induced PI hydrolysis was inhibited, whereas [3H]BK binding was unaffected, indicating that the site of action of PKC-alpha and PKC-delta in the BK receptor/G protein/PLC pathway is after the receptor and before PLC, i.e., the G protein. Tetradecanoylphorbol Acetate 20-23 protein kinase C alpha Homo sapiens 181-190 7623773-14 1995 The increase in AIF4(-)-induced PI hydrolysis after 24-hr TPA treatment was also inhibited by cycloheximide, indicating that new synthesis of BK receptors and G proteins was required after down-regulation of PKC-alpha and PKC-delta. Tetradecanoylphorbol Acetate 58-61 protein kinase C alpha Homo sapiens 208-217 7730383-5 1995 Activation of each isozyme"s kinase activity (with the exception of PKC-zeta) by treatment of these cells with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate results in isozyme-specific alterations of cell morphology, as well as in a rapid, selective redistribution of the different PKC isozymes to distinct subcellular structures. Tetradecanoylphorbol Acetate 129-165 protein kinase C alpha Homo sapiens 68-71 7730383-6 1995 Within minutes after 12-O-tetradecanoylphorbol-13-acetate treatment, PKC-alpha and -epsilon concentrate at cell margins. Tetradecanoylphorbol Acetate 21-57 protein kinase C alpha Homo sapiens 69-78 7538636-4 1995 The treatment of multidrug-resistant cells with 100 nM PMA for 2 hours resulted in the activation not of PKC-zeta but of PKC-alpha, with concomitant decrease in vincristine accumulation and increase in P-glycoprotein phosphorylation. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 121-130 7538636-5 1995 The exposure of multidrug-resistant cells to 100 nM PMA for 24 hours induced down-regulation not of PKC-zeta but of PKC-alpha, with concurrent decrease in vincristine accumulation, and reduced but still increased P-glycoprotein phosphorylation. Tetradecanoylphorbol Acetate 52-55 protein kinase C alpha Homo sapiens 116-125 7923629-4 1994 Western analysis confirmed the presence of these isoforms in cultured VSMC lines and demonstrated downregulation of PKC alpha, delta, and epsilon by phorbol 12-myristate 13-acetate (PMA) but not TXA2 or Ang II. Tetradecanoylphorbol Acetate 149-180 protein kinase C alpha Homo sapiens 116-125 7943245-3 1994 1,25(OH)2D3 and the PKC activator 12-O-tetradecanoylphorbol 13-acetate (TPA) each caused time-dependent translocations of PKC-alpha, but not PKC-zeta. Tetradecanoylphorbol Acetate 34-70 protein kinase C alpha Homo sapiens 122-131 7935389-1 1994 The cytoplasmic Raf-1 kinase is essential for mitogenic signalling by growth factors, which couple to tyrosine kinases, and by tumor-promoting phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate, which activate protein kinase C (PKC). Tetradecanoylphorbol Acetate 166-202 protein kinase C alpha Homo sapiens 237-240 7943245-3 1994 1,25(OH)2D3 and the PKC activator 12-O-tetradecanoylphorbol 13-acetate (TPA) each caused time-dependent translocations of PKC-alpha, but not PKC-zeta. Tetradecanoylphorbol Acetate 72-75 protein kinase C alpha Homo sapiens 122-131 7943245-4 1994 TPA treatment of these cells for 24 h induced a significant concentration-dependent downregulation of PKC-alpha, but not PKC-zeta. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 102-111 7943245-8 1994 Acute pretreatment with staurosporine or H-7 caused a significant stimulation, whereas acute TPA pretreatment caused a significant inhibition of the 1,25(OH)2D3-induced increase in the transient phase of [Ca2+]i. Preincubation of Caco-2 cells with 1,2-bis(2-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid-acetoxy-methyl ester (BAPTA-AM) abolished both the rise in [Ca2+]i and the increase in particulate-associated PKC-alpha stimulated by 1,25(OH)2D3. Tetradecanoylphorbol Acetate 93-96 protein kinase C alpha Homo sapiens 415-424 7943245-9 1994 Moreover, downregulation of PKC-alpha by chronic TPA treatment significantly augmented the transient phase of the 1,25(OH)2D3-stimulated rise in [Ca2+]i but had no effect on the 1,25(OH)2D3-induced change in Ins(1,4,5)P3 concentration. Tetradecanoylphorbol Acetate 49-52 protein kinase C alpha Homo sapiens 28-37 8031867-0 1994 TPA causes divergent responses of Ca(2+)-dependent and Ca(2+)-independent isoforms of PKC in the nuclei of Caco-2 cells. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 86-89 21559581-1 1994 The steady-state level and translocation of the protein kinase C (PKC) isozymes during the early stages of phorbol 12-myristate 13-acetate (PMA)-induced differentiation, was followed in AGF cells by Western blot analysis of various cell fractions, immunofluorescence staining and by confocal microscopy. Tetradecanoylphorbol Acetate 107-138 protein kinase C alpha Homo sapiens 66-69 21559581-1 1994 The steady-state level and translocation of the protein kinase C (PKC) isozymes during the early stages of phorbol 12-myristate 13-acetate (PMA)-induced differentiation, was followed in AGF cells by Western blot analysis of various cell fractions, immunofluorescence staining and by confocal microscopy. Tetradecanoylphorbol Acetate 140-143 protein kinase C alpha Homo sapiens 66-69 21559581-5 1994 Following stimulation with PMA from 15 min to 24 h, cytosolic PKC-alpha did not translocate to the membrane or nuclear fractions. Tetradecanoylphorbol Acetate 27-30 protein kinase C alpha Homo sapiens 62-71 8049080-6 1994 Exposure of FTEC with the PKC activator phorbol 12-myristate 13-acetate (PMA), failed to increase the release of mucin. Tetradecanoylphorbol Acetate 40-71 protein kinase C alpha Homo sapiens 26-29 8049080-8 1994 PMA also induced the translocation of PKC activity from the cytosol to the membrane fraction, which was still present after 15 min of exposure. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 38-41 8031867-3 1994 The phorbol ester, 12-O-tetradecanoyl phorbol 13-acetate (TPA) caused an acute redistribution of PKC-alpha to the nucleus, but did not change the distribution of PKC-zeta. Tetradecanoylphorbol Acetate 19-56 protein kinase C alpha Homo sapiens 97-106 8031867-3 1994 The phorbol ester, 12-O-tetradecanoyl phorbol 13-acetate (TPA) caused an acute redistribution of PKC-alpha to the nucleus, but did not change the distribution of PKC-zeta. Tetradecanoylphorbol Acetate 58-61 protein kinase C alpha Homo sapiens 97-106 8031867-4 1994 Chronic treatment with TPA down-regulated total PKC-alpha, but not -zeta. Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 48-57 8149484-1 1994 The involvement of protein kinase C (PKC), a 12-O-tetradecanoylphorbol-13-acetate (TPA) receptor, in the transcriptional regulation of TPA-inducible genes was determined. Tetradecanoylphorbol Acetate 83-86 protein kinase C alpha Homo sapiens 37-40 8031867-6 1994 These studies demonstrate for the first time the constitutive expression and divergent responses to TPA of the Ca(2+)-dependent and Ca(2+)-independent isoforms of PKC in the nuclei of Caco-2 cells and suggest that these specific isoforms may be involved in modulating gene expression. Tetradecanoylphorbol Acetate 100-103 protein kinase C alpha Homo sapiens 163-166 7911467-8 1994 When PKC-alpha protein levels are depleted by oligonucleotide treatment of A549 cells, the increase in ICAM-1 expression in response to phorbol 12-myristate 13-acetate is greatly reduced, demonstrating that PKC-alpha plays a major role in this process. Tetradecanoylphorbol Acetate 136-167 protein kinase C alpha Homo sapiens 5-14 7911467-8 1994 When PKC-alpha protein levels are depleted by oligonucleotide treatment of A549 cells, the increase in ICAM-1 expression in response to phorbol 12-myristate 13-acetate is greatly reduced, demonstrating that PKC-alpha plays a major role in this process. Tetradecanoylphorbol Acetate 136-167 protein kinase C alpha Homo sapiens 207-216 8149484-4 1994 To determine the effects of overexpression of PKC alpha K and PKC delta K on the AP-1-mediated TPA-inducible genes, we transfected into COS cells the PKC alpha K or PKC delta K expression plasmids with collagenase chloramphenicol acetyltransferase (CAT) reporter construct containing one TPA responsive element (TRE), or a construct containing five synthetic TRE linked to a thymidine kinase promoter. Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 46-55 8149484-10 1994 Cotransfection of PKC alpha K or PKC delta K expression plasmids with a TPA-inducible ODC luc construct (-72/+130-ODC-luc) into HeLa cells resulted in an increased luc activity. Tetradecanoylphorbol Acetate 72-75 protein kinase C alpha Homo sapiens 18-27 8149484-11 1994 These results indicate that both PKC alpha (calcium dependent) and PKC delta (calcium independent) may mediate the transcription of TPA-inducible genes through both AP-1 and non-AP-1 sequences. Tetradecanoylphorbol Acetate 132-135 protein kinase C alpha Homo sapiens 33-42 8314307-1 1994 In vitro growth of 6 human melanoma-derived cell lines was inhibited markedly by the phorbol-ester tumor promoter 12-O-tetradecanoyl phorbol 13-acetate (TPA), a potent activator of several isoforms of protein kinase C (PKC). Tetradecanoylphorbol Acetate 114-151 protein kinase C alpha Homo sapiens 219-222 8112895-2 1994 Like the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) it activates protein kinase C (PKC). Tetradecanoylphorbol Acetate 39-75 protein kinase C alpha Homo sapiens 113-116 8112895-2 1994 Like the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) it activates protein kinase C (PKC). Tetradecanoylphorbol Acetate 77-80 protein kinase C alpha Homo sapiens 113-116 8286746-1 1994 Treatment of human HL-60 leukemic cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with activation of protein kinase C (PKC) and induction of monocytic differentiation. Tetradecanoylphorbol Acetate 45-81 protein kinase C alpha Homo sapiens 139-142 8286746-1 1994 Treatment of human HL-60 leukemic cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with activation of protein kinase C (PKC) and induction of monocytic differentiation. Tetradecanoylphorbol Acetate 83-86 protein kinase C alpha Homo sapiens 139-142 8286746-5 1994 In order to measure PKC expression associated with the reversal of TPA resistance by ATRA, we exposed HL-525 cells to ATRA and analyzed PKC-mRNA and protein levels. Tetradecanoylphorbol Acetate 67-70 protein kinase C alpha Homo sapiens 20-23 8286746-8 1994 These findings are consistent with the hypothesis that ATRA reverses TPA resistance in HL-525 cells by enhancing the expression of PKC. Tetradecanoylphorbol Acetate 69-72 protein kinase C alpha Homo sapiens 131-134 8112895-8 1994 Exposure of cells to bryostatin I or TPA for 30 min caused the redistribution of PKCs-alpha and -epsilon from the cytosol to the particulate and nuclear fractions in a concentration-dependent fashion. Tetradecanoylphorbol Acetate 37-40 protein kinase C alpha Homo sapiens 81-104 8297348-6 1994 Prolonged (48 h) exposure of cells to the phorbol ester phorbol 12-myristate 13-acetate (PMA; 100 nM) resulted in a marked decrease in the amounts of PKC-alpha and PKC-epsilon, with no change in levels of PKC-zeta. Tetradecanoylphorbol Acetate 56-87 protein kinase C alpha Homo sapiens 150-159 8297348-6 1994 Prolonged (48 h) exposure of cells to the phorbol ester phorbol 12-myristate 13-acetate (PMA; 100 nM) resulted in a marked decrease in the amounts of PKC-alpha and PKC-epsilon, with no change in levels of PKC-zeta. Tetradecanoylphorbol Acetate 89-92 protein kinase C alpha Homo sapiens 150-159 8314307-5 1994 On the other hand, treatment of parental and TPA-resistant SK-Mel 173 cells with TPA led to partial down-regulation of PKC alpha in both cell lines. Tetradecanoylphorbol Acetate 81-84 protein kinase C alpha Homo sapiens 119-128 8314307-6 1994 Total PKC enzyme activity was also greater in TPA-resistant cells than in parental SK-Mel 173 cells. Tetradecanoylphorbol Acetate 46-49 protein kinase C alpha Homo sapiens 6-9 8314307-7 1994 Our results show that TPA might inhibit the growth of melanoma cells by causing down-regulation of specific isoforms of PKC that are required to maintain the growth of these cells. Tetradecanoylphorbol Acetate 22-25 protein kinase C alpha Homo sapiens 120-123 8314307-1 1994 In vitro growth of 6 human melanoma-derived cell lines was inhibited markedly by the phorbol-ester tumor promoter 12-O-tetradecanoyl phorbol 13-acetate (TPA), a potent activator of several isoforms of protein kinase C (PKC). Tetradecanoylphorbol Acetate 153-156 protein kinase C alpha Homo sapiens 219-222 8314307-5 1994 On the other hand, treatment of parental and TPA-resistant SK-Mel 173 cells with TPA led to partial down-regulation of PKC alpha in both cell lines. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 119-128 7942278-2 1994 Expression of Ha-ras by dexamethasone leads to a transcriptional activation of the fos-CAT construct which was found to be sensitive to the PKC inhibitor ilmofosine (BM41440) and abrogated by PKC depletion following long-term exposure to TPA. Tetradecanoylphorbol Acetate 238-241 protein kinase C alpha Homo sapiens 140-143 7942278-2 1994 Expression of Ha-ras by dexamethasone leads to a transcriptional activation of the fos-CAT construct which was found to be sensitive to the PKC inhibitor ilmofosine (BM41440) and abrogated by PKC depletion following long-term exposure to TPA. Tetradecanoylphorbol Acetate 238-241 protein kinase C alpha Homo sapiens 192-195 7942278-5 1994 Transcriptional activation of the SRE-FAP-TK-CAT as well as the SRE-TK-CAT constructs by Ha-ras is sensitive to the PKC-inhibitor ilmofosine (BM41440) and blocked by long-term exposure to TPA. Tetradecanoylphorbol Acetate 188-191 protein kinase C alpha Homo sapiens 116-119 7942278-6 1994 Long-term exposure to TPA depletes cells of PKC alpha and significantly reduces the PKC epsilon levels. Tetradecanoylphorbol Acetate 22-25 protein kinase C alpha Homo sapiens 44-53 8288312-6 1993 Following the treatment of monocytes with PMA, the physical translocation of PKC alpha from the cytosol to the membrane occurred over 60 min. Tetradecanoylphorbol Acetate 42-45 protein kinase C alpha Homo sapiens 77-86 8145770-4 1993 We show that selective inhibition of protein kinase C (PKC) and its depletion by prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate lead to the loss of ligand-dependent transcription of an RA-inducible promoter. Tetradecanoylphorbol Acetate 106-142 protein kinase C alpha Homo sapiens 55-58 8224186-6 1993 While PMA-induced growth arrest occurs in L-2 cells which possess PKC alpha and zeta, PMA-induced growth arrest does not occur in L-2/PMA which is deficient in these isoforms. Tetradecanoylphorbol Acetate 6-9 protein kinase C alpha Homo sapiens 66-75 8405436-1 1993 TPA induces translocation and down-regulation of conventional and new PKC isoforms but not atypical PKC zeta. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 70-73 8405436-4 1993 Exposure of the cells to 100 nM TPA for 10 min resulted in the translocation of conventional PKC alpha (cPKC alpha) and new PKC delta (nPKC delta) and -epsilon from the cytosolic to the membrane fraction, while left atypical PKC zeta (aPKC zeta) unaffected. Tetradecanoylphorbol Acetate 32-35 protein kinase C alpha Homo sapiens 93-102 8473351-2 1993 We have established an assay system where overexpression of a specific protein kinase C (PKC) type caused by introduction of the respective cDNA results in the enhancement of a cell response: the transcriptional activation of a set of genes in response to PKC activators such as 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 279-315 protein kinase C alpha Homo sapiens 89-92 8239270-3 1993 The effect of PMA was inhibited by the PKC antagonist H-7 in control cells, but not in cells that overexpressed PKC alpha. Tetradecanoylphorbol Acetate 14-17 protein kinase C alpha Homo sapiens 39-42 8473351-2 1993 We have established an assay system where overexpression of a specific protein kinase C (PKC) type caused by introduction of the respective cDNA results in the enhancement of a cell response: the transcriptional activation of a set of genes in response to PKC activators such as 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 279-315 protein kinase C alpha Homo sapiens 256-259 8473351-2 1993 We have established an assay system where overexpression of a specific protein kinase C (PKC) type caused by introduction of the respective cDNA results in the enhancement of a cell response: the transcriptional activation of a set of genes in response to PKC activators such as 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 317-320 protein kinase C alpha Homo sapiens 89-92 8473351-2 1993 We have established an assay system where overexpression of a specific protein kinase C (PKC) type caused by introduction of the respective cDNA results in the enhancement of a cell response: the transcriptional activation of a set of genes in response to PKC activators such as 12-O-tetradecanoylphorbol 13-acetate (TPA). Tetradecanoylphorbol Acetate 317-320 protein kinase C alpha Homo sapiens 256-259 8444883-5 1993 On the other hand, PMA and thrombin induced translocation of all four isoenzymes of PKC. Tetradecanoylphorbol Acetate 19-22 protein kinase C alpha Homo sapiens 84-87 8454058-1 1993 Phorbol esters such as phorbol 12-myristate,13-acetate (PMA) are potent activators of protein kinase C (PKC), and activate all PKC isozymes except zeta and lambda. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 104-107 8454058-1 1993 Phorbol esters such as phorbol 12-myristate,13-acetate (PMA) are potent activators of protein kinase C (PKC), and activate all PKC isozymes except zeta and lambda. Tetradecanoylphorbol Acetate 56-59 protein kinase C alpha Homo sapiens 127-130 8461005-3 1993 Both TPA and bryostatin 1 at 10 nM induced a rapid increase in membrane-associated PKC-alpha immunoreactivity which was sustained for 72 hours in TPA-treated cells, but was down-regulated within 24 hours in bryostatin-treated cells. Tetradecanoylphorbol Acetate 5-8 protein kinase C alpha Homo sapiens 83-92 8461005-3 1993 Both TPA and bryostatin 1 at 10 nM induced a rapid increase in membrane-associated PKC-alpha immunoreactivity which was sustained for 72 hours in TPA-treated cells, but was down-regulated within 24 hours in bryostatin-treated cells. Tetradecanoylphorbol Acetate 146-149 protein kinase C alpha Homo sapiens 83-92 8461005-4 1993 TPA likewise induced a sustained phosphorylation of an 80 kDa PKC substrate whereas in bryostatin-treated cells the 80 kDa substrate was rapidly phosphorylated reaching a maximum at 6 hours followed by a decline to basal level within 48 hours. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 62-65 8461005-5 1993 A higher concentration of TPA (300 nM), which results in a less differentiated phenotype, induced down-regulation of PKC-alpha within 24 hours. Tetradecanoylphorbol Acetate 26-29 protein kinase C alpha Homo sapiens 117-126 8461005-7 1993 These results suggest that the divergent actions of bryostatin 1 and TPA in SH-SY5Y cells are at least partially due to differential modulation of PKC-alpha but not PKC-epsilon by these two agents. Tetradecanoylphorbol Acetate 69-72 protein kinase C alpha Homo sapiens 147-156 7682303-4 1993 The data obtained with TPA were tentatively correlated with the amounts of immunoreactive PKC alpha. Tetradecanoylphorbol Acetate 23-26 protein kinase C alpha Homo sapiens 90-99 8432975-4 1993 After a longer, 20-h treatment with PMA (20 nM), a considerable portion of PKC was still membrane-associated, and the total amount of immunoreactive PKC was not reduced considerably. Tetradecanoylphorbol Acetate 36-39 protein kinase C alpha Homo sapiens 75-78 8432975-4 1993 After a longer, 20-h treatment with PMA (20 nM), a considerable portion of PKC was still membrane-associated, and the total amount of immunoreactive PKC was not reduced considerably. Tetradecanoylphorbol Acetate 36-39 protein kinase C alpha Homo sapiens 149-152 8432975-9 1993 We propose that Bryo inhibits PMA-induced T cell proliferation by causing rapid degradation of PKC, reflecting a requirement of persistent PKC stimulation (lasting approximately 48 h) for the activation of human T cells and progression through the cell cycle. Tetradecanoylphorbol Acetate 30-33 protein kinase C alpha Homo sapiens 95-98 8453997-3 1993 Since phorbol 12-myristate 13-acetate, which directly binds and activates protein kinase C (PKC), induced cox expression, we examined the role of PKC as an intracellular mediator of IL-1 activity in human endothelial cells. Tetradecanoylphorbol Acetate 6-37 protein kinase C alpha Homo sapiens 92-95 8436813-5 1993 PKC alpha and beta existed primarily in the cytosol, translocated to the membrane fraction after 10 minutes of treatment with PMA, and almost completely disappeared within 16 h. A larger fraction of PKC delta and epsilon existed in the membrane fraction compared to PKC alpha or beta, and PKC epsilon translocated to the membrane fraction rapidly. Tetradecanoylphorbol Acetate 126-129 protein kinase C alpha Homo sapiens 0-9 8352882-7 1993 When MEK and HEK cultures were treated with TPA for 3 h, less than 30% of the control level of PKC activity was detected, indicating that TPA-induced downregulation of PKC was similar in MEKs and HEKs. Tetradecanoylphorbol Acetate 44-47 protein kinase C alpha Homo sapiens 95-98 8352882-7 1993 When MEK and HEK cultures were treated with TPA for 3 h, less than 30% of the control level of PKC activity was detected, indicating that TPA-induced downregulation of PKC was similar in MEKs and HEKs. Tetradecanoylphorbol Acetate 138-141 protein kinase C alpha Homo sapiens 168-171 8352882-1 1993 The goal of this study was to compare the response of mouse epidermal keratinocytes (MEKs) and human epidermal keratinocytes (HEKs) to 12-O-tetradecanoylphorbol-13-acetate (TPA) with respect to the activation and downregulation of protein kinase C (PKC), the expression of c-jun and c-fos, and the expression and induction of ornithine decarboxylase (ODC) activity. Tetradecanoylphorbol Acetate 135-171 protein kinase C alpha Homo sapiens 249-252 8352882-6 1993 Activation of partially purified total PKC by TPA was similar in freshly isolated and cultured MEKs and HEKs, indicating that the two species were similar in this regard and that 2 wk of culture did not alter this characteristic. Tetradecanoylphorbol Acetate 46-49 protein kinase C alpha Homo sapiens 39-42 1445803-1 1992 To study the signal transduction pathway leading to phorbol 12-myristate 13-acetate (PMA)-induced differentiation in human promyelocytic HL-60 leukemia cells, we examined the expression of protein kinase C (PKC) isozyme genes in HL-60 cells that are susceptible or resistant to PMA-induced differentiation. Tetradecanoylphorbol Acetate 52-83 protein kinase C alpha Homo sapiens 207-210 1444457-5 1992 The effects of the inhibitors on some suggested critical steps of the differentiation, a rapid phosphorylation of specific proteins, a rapid membrane association of PKC, and down-regulation of PKC at 18 h after addition of TPA, were not correlated with those on the differentiation marker induction. Tetradecanoylphorbol Acetate 223-226 protein kinase C alpha Homo sapiens 193-196 1444457-6 1992 Only the effect of the inhibitors on up-regulation of PKC-alpha was closely correlated with TPA-induced annexin I expression; staurosporine inhibited up-regulation of PKC-alpha but other inhibitors did not similarly affect the induction of annexin I expression. Tetradecanoylphorbol Acetate 92-95 protein kinase C alpha Homo sapiens 54-63 1444457-6 1992 Only the effect of the inhibitors on up-regulation of PKC-alpha was closely correlated with TPA-induced annexin I expression; staurosporine inhibited up-regulation of PKC-alpha but other inhibitors did not similarly affect the induction of annexin I expression. Tetradecanoylphorbol Acetate 92-95 protein kinase C alpha Homo sapiens 167-176 1444457-7 1992 These results suggest that PKC-alpha is intimately related to macrophage-like differentiation of HL-60 cells by TPA. Tetradecanoylphorbol Acetate 112-115 protein kinase C alpha Homo sapiens 27-36 1400474-1 1992 Activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) was compared with calcium/phosphatidylserine (Ca/PS). Tetradecanoylphorbol Acetate 40-71 protein kinase C alpha Homo sapiens 32-35 1400474-1 1992 Activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) was compared with calcium/phosphatidylserine (Ca/PS). Tetradecanoylphorbol Acetate 73-76 protein kinase C alpha Homo sapiens 32-35 1400474-7 1992 Differential substrate phosphorylation by PS/PMA also occurred for PKC isozymes resolved by hydroxylapatite chromatography and was most dramatic for PKC-alpha, which could no longer phosphorylate histone or GS1-12. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 67-70 1400474-7 1992 Differential substrate phosphorylation by PS/PMA also occurred for PKC isozymes resolved by hydroxylapatite chromatography and was most dramatic for PKC-alpha, which could no longer phosphorylate histone or GS1-12. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 149-158 1400474-8 1992 Differential activities of PKC were also observed in synaptosol and in intact synaptosomes where PMA stimulated phosphorylation of MARCKS, but not dephosphin. Tetradecanoylphorbol Acetate 97-100 protein kinase C alpha Homo sapiens 27-30 1445803-1 1992 To study the signal transduction pathway leading to phorbol 12-myristate 13-acetate (PMA)-induced differentiation in human promyelocytic HL-60 leukemia cells, we examined the expression of protein kinase C (PKC) isozyme genes in HL-60 cells that are susceptible or resistant to PMA-induced differentiation. Tetradecanoylphorbol Acetate 85-88 protein kinase C alpha Homo sapiens 207-210 1445803-1 1992 To study the signal transduction pathway leading to phorbol 12-myristate 13-acetate (PMA)-induced differentiation in human promyelocytic HL-60 leukemia cells, we examined the expression of protein kinase C (PKC) isozyme genes in HL-60 cells that are susceptible or resistant to PMA-induced differentiation. Tetradecanoylphorbol Acetate 278-281 protein kinase C alpha Homo sapiens 207-210 1506412-3 1992 However, we now report that TPA-treated and non-treated SH-SY5Y cells express PKC-alpha, but not PKC-beta and PKC-gamma, mRNA. Tetradecanoylphorbol Acetate 28-31 protein kinase C alpha Homo sapiens 78-87 1506412-4 1992 Furthermore, only a slight down-regulation of the PKC-alpha protein could be seen during prolonged treatment with 16 nM TPA, the concentration giving optimal differentiation. Tetradecanoylphorbol Acetate 120-123 protein kinase C alpha Homo sapiens 50-59 1506412-5 1992 In contrast, a higher concentration of TPA (1.6 microM) results in a poor neuronal differentiation and a complete down-regulation of PKC-alpha. Tetradecanoylphorbol Acetate 39-42 protein kinase C alpha Homo sapiens 133-142 1506412-6 1992 PKC-alpha was rapidly translocated to the particulate fraction and remained membrane bound for at least 4 days during treatment with 16 nM TPA. Tetradecanoylphorbol Acetate 139-142 protein kinase C alpha Homo sapiens 0-9 1643643-1 1992 To investigate the role of protein kinase C (PKC) in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-dependent growth of human melanocytes, we analyzed the effects of phorbol ester treatment on both PKC expression and growth control in these cells. Tetradecanoylphorbol Acetate 57-93 protein kinase C alpha Homo sapiens 45-48 1643643-1 1992 To investigate the role of protein kinase C (PKC) in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-dependent growth of human melanocytes, we analyzed the effects of phorbol ester treatment on both PKC expression and growth control in these cells. Tetradecanoylphorbol Acetate 95-98 protein kinase C alpha Homo sapiens 45-48 1643643-4 1992 Dose-response studies revealed that the most effective TPA concentration for stimulation of DNA synthesis and growth of melanocytes (10 ng/ml TPA) also supported a relatively high level of PKC enzyme activity, increased membrane association of the PKC alpha and PKC epsilon isoforms, and led to a high level of phosphorylation of a major PKC substrate, the myristoylated alanine-rich C kinase substrate (MARCKS) protein. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 189-192 1643643-4 1992 Dose-response studies revealed that the most effective TPA concentration for stimulation of DNA synthesis and growth of melanocytes (10 ng/ml TPA) also supported a relatively high level of PKC enzyme activity, increased membrane association of the PKC alpha and PKC epsilon isoforms, and led to a high level of phosphorylation of a major PKC substrate, the myristoylated alanine-rich C kinase substrate (MARCKS) protein. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 248-257 1643643-4 1992 Dose-response studies revealed that the most effective TPA concentration for stimulation of DNA synthesis and growth of melanocytes (10 ng/ml TPA) also supported a relatively high level of PKC enzyme activity, increased membrane association of the PKC alpha and PKC epsilon isoforms, and led to a high level of phosphorylation of a major PKC substrate, the myristoylated alanine-rich C kinase substrate (MARCKS) protein. Tetradecanoylphorbol Acetate 55-58 protein kinase C alpha Homo sapiens 248-251 1643643-4 1992 Dose-response studies revealed that the most effective TPA concentration for stimulation of DNA synthesis and growth of melanocytes (10 ng/ml TPA) also supported a relatively high level of PKC enzyme activity, increased membrane association of the PKC alpha and PKC epsilon isoforms, and led to a high level of phosphorylation of a major PKC substrate, the myristoylated alanine-rich C kinase substrate (MARCKS) protein. Tetradecanoylphorbol Acetate 142-145 protein kinase C alpha Homo sapiens 189-192 1643643-4 1992 Dose-response studies revealed that the most effective TPA concentration for stimulation of DNA synthesis and growth of melanocytes (10 ng/ml TPA) also supported a relatively high level of PKC enzyme activity, increased membrane association of the PKC alpha and PKC epsilon isoforms, and led to a high level of phosphorylation of a major PKC substrate, the myristoylated alanine-rich C kinase substrate (MARCKS) protein. Tetradecanoylphorbol Acetate 142-145 protein kinase C alpha Homo sapiens 248-257 1643643-4 1992 Dose-response studies revealed that the most effective TPA concentration for stimulation of DNA synthesis and growth of melanocytes (10 ng/ml TPA) also supported a relatively high level of PKC enzyme activity, increased membrane association of the PKC alpha and PKC epsilon isoforms, and led to a high level of phosphorylation of a major PKC substrate, the myristoylated alanine-rich C kinase substrate (MARCKS) protein. Tetradecanoylphorbol Acetate 142-145 protein kinase C alpha Homo sapiens 248-251 1643643-6 1992 Furthermore, treatment of melanocytes with 100 ng/ml TPA for 48 h resulted in a marked decrease in total PKC enzyme activity and the loss of expression of the PKC alpha and PKC epsilon isoforms in both the cytosol and membrane-bound fractions, when examined by immunoblot analysis. Tetradecanoylphorbol Acetate 53-56 protein kinase C alpha Homo sapiens 105-108 1643643-6 1992 Furthermore, treatment of melanocytes with 100 ng/ml TPA for 48 h resulted in a marked decrease in total PKC enzyme activity and the loss of expression of the PKC alpha and PKC epsilon isoforms in both the cytosol and membrane-bound fractions, when examined by immunoblot analysis. Tetradecanoylphorbol Acetate 53-56 protein kinase C alpha Homo sapiens 159-168 1643643-7 1992 These results, taken together, suggest that continuous activation of PKC by TPA, rather than the loss of PKC due to TPA-induced down-regulation, is responsible for the growth-stimulatory effects of phorbol esters on normal human melanocytes. Tetradecanoylphorbol Acetate 76-79 protein kinase C alpha Homo sapiens 69-72 1643643-8 1992 Additionally, the conditioned medium from TPA-treated human melanocytes stimulated DNA synthesis in quiescent melanocytes and human melanoma cells, thus suggesting that activation of the PKC signaling pathway in melanocytes leads to the production of an autocrine growth factor. Tetradecanoylphorbol Acetate 42-45 protein kinase C alpha Homo sapiens 187-190 1637359-4 1992 The carbachol-, PDB- and 8-Br-cAMP-induced ISC responses were inhibited by pretreatment of the cells with PMA (0.5 microM) for 2 h, a time period in which PKC alpha, beta 1 and gamma levels were not changed. Tetradecanoylphorbol Acetate 106-109 protein kinase C alpha Homo sapiens 155-164 1388136-3 1992 TPA-induced T-cell proliferation, expression of interleukin-2 receptor-alpha subunit (IL-2R alpha) and transferrin receptor, CD3 down-regulation and, lastly, the cytosol-to-membrane PKC translocation (determined by an enzymatic assay or by immunoblotting with a cross-reactive anti-PKC peptide antibody) were all facilitated by ionomycin. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 182-185 1388136-3 1992 TPA-induced T-cell proliferation, expression of interleukin-2 receptor-alpha subunit (IL-2R alpha) and transferrin receptor, CD3 down-regulation and, lastly, the cytosol-to-membrane PKC translocation (determined by an enzymatic assay or by immunoblotting with a cross-reactive anti-PKC peptide antibody) were all facilitated by ionomycin. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 282-285 1388136-4 1992 Immunoblots with isoenzyme-specific anti-PKC monoclonal antibodies demonstrated expression of immunoreactive PKC alpha, PKC beta and PKC gamma proteins that were translocated to the membrane upon TPA plus ionomycin stimulation. Tetradecanoylphorbol Acetate 196-199 protein kinase C alpha Homo sapiens 41-44 1388136-4 1992 Immunoblots with isoenzyme-specific anti-PKC monoclonal antibodies demonstrated expression of immunoreactive PKC alpha, PKC beta and PKC gamma proteins that were translocated to the membrane upon TPA plus ionomycin stimulation. Tetradecanoylphorbol Acetate 196-199 protein kinase C alpha Homo sapiens 109-118 1388136-7 1992 Ionomycin synergized with TPA in increasing the expression of PKC alpha and PKC beta mRNA. Tetradecanoylphorbol Acetate 26-29 protein kinase C alpha Homo sapiens 62-71 1388136-11 1992 Moreover, the combined effects of TPA and ionomycin on T-cell function and cell-surface antigen expression appear to be due, at least in part, to their synergistic activation of distinct PKC isoenzyme(s). Tetradecanoylphorbol Acetate 34-37 protein kinase C alpha Homo sapiens 187-190 1537859-7 1992 To examine whether PKC-zeta was activated by TPA, PKC activity was evaluated in COS cells transiently over-expressing this isoform. Tetradecanoylphorbol Acetate 45-48 protein kinase C alpha Homo sapiens 19-22 1567838-4 1992 Lyngbyatoxin A (0.1 microM) like TPA induced a rapid translocation of PKC from the cytosol to the membrane and subsequently led to a sustained decrease in both cytosolic and membrane PKC activity. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 70-73 1567838-4 1992 Lyngbyatoxin A (0.1 microM) like TPA induced a rapid translocation of PKC from the cytosol to the membrane and subsequently led to a sustained decrease in both cytosolic and membrane PKC activity. Tetradecanoylphorbol Acetate 33-36 protein kinase C alpha Homo sapiens 183-186 1567838-7 1992 Western blot analyses with monoclonal antibodies to PKC isoforms indicated that reduction in PKC activity by chronic exposure to TPA or lyngbyatoxin A analogues could be explained by downregulation of PKC alpha. Tetradecanoylphorbol Acetate 129-132 protein kinase C alpha Homo sapiens 52-55 1567838-7 1992 Western blot analyses with monoclonal antibodies to PKC isoforms indicated that reduction in PKC activity by chronic exposure to TPA or lyngbyatoxin A analogues could be explained by downregulation of PKC alpha. Tetradecanoylphorbol Acetate 129-132 protein kinase C alpha Homo sapiens 93-96 1567838-7 1992 Western blot analyses with monoclonal antibodies to PKC isoforms indicated that reduction in PKC activity by chronic exposure to TPA or lyngbyatoxin A analogues could be explained by downregulation of PKC alpha. Tetradecanoylphorbol Acetate 129-132 protein kinase C alpha Homo sapiens 201-210 1335968-5 1992 The half-life for PKC alpha mRNA was approximately 16 h and levels of the mRNA were increased slightly following addition of phorbol myristate acetate (PMA) or transforming growth factor-beta (TGF beta). Tetradecanoylphorbol Acetate 125-150 protein kinase C alpha Homo sapiens 18-27 1737390-6 1992 TPA induced rapid translocation of the PKC-alpha isozyme and PKC activity to the membrane fraction of MCF-7 cells. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 39-48 1737390-6 1992 TPA induced rapid translocation of the PKC-alpha isozyme and PKC activity to the membrane fraction of MCF-7 cells. Tetradecanoylphorbol Acetate 0-3 protein kinase C alpha Homo sapiens 39-42 1737390-9 1992 Similar effects on PKC-alpha isozyme and PKC activity were seen in a second cell line whose growth was inhibited by TPA but not by bryostatin 1, MDA-MB-468. Tetradecanoylphorbol Acetate 116-119 protein kinase C alpha Homo sapiens 19-28 1737390-9 1992 Similar effects on PKC-alpha isozyme and PKC activity were seen in a second cell line whose growth was inhibited by TPA but not by bryostatin 1, MDA-MB-468. Tetradecanoylphorbol Acetate 116-119 protein kinase C alpha Homo sapiens 19-22 1737390-12 1992 Thus, differential actions of bryostatin 1 and TPA on PKC activity and alpha-isoform level in the membrane-associated fraction of MCF-7 and MDA-MB-468 cells may account for the divergent effects of these two agents on cell growth and morphology. Tetradecanoylphorbol Acetate 47-50 protein kinase C alpha Homo sapiens 54-57 1616823-7 1992 The hPKC alpha overexpressing cells were able to grow in soft agarose after treatment with phorbol ester such as TPA (12-O-tetradecanoylphorbol 13-acetate). Tetradecanoylphorbol Acetate 113-116 protein kinase C alpha Homo sapiens 4-14 1616823-7 1992 The hPKC alpha overexpressing cells were able to grow in soft agarose after treatment with phorbol ester such as TPA (12-O-tetradecanoylphorbol 13-acetate). Tetradecanoylphorbol Acetate 118-154 protein kinase C alpha Homo sapiens 4-14 1335968-5 1992 The half-life for PKC alpha mRNA was approximately 16 h and levels of the mRNA were increased slightly following addition of phorbol myristate acetate (PMA) or transforming growth factor-beta (TGF beta). Tetradecanoylphorbol Acetate 152-155 protein kinase C alpha Homo sapiens 18-27 1335968-11 1992 In a more detailed study, translocation of PKC-alpha in the presence of PMA was complete by 10 min, and a major decrease in the PKC translocated to the plasma-membrane fraction occurred some time between 2 and 4 h after PMA addition, while a major decrease in the translocated nuclear fraction occurred some time after 6 h. cAMP alone had no effect on the PKC alpha protein level or distribution, nor did it alter the translocation and down-regulation due to PMA exposure. Tetradecanoylphorbol Acetate 72-75 protein kinase C alpha Homo sapiens 43-52 1335968-11 1992 In a more detailed study, translocation of PKC-alpha in the presence of PMA was complete by 10 min, and a major decrease in the PKC translocated to the plasma-membrane fraction occurred some time between 2 and 4 h after PMA addition, while a major decrease in the translocated nuclear fraction occurred some time after 6 h. cAMP alone had no effect on the PKC alpha protein level or distribution, nor did it alter the translocation and down-regulation due to PMA exposure. Tetradecanoylphorbol Acetate 72-75 protein kinase C alpha Homo sapiens 43-46 1335968-11 1992 In a more detailed study, translocation of PKC-alpha in the presence of PMA was complete by 10 min, and a major decrease in the PKC translocated to the plasma-membrane fraction occurred some time between 2 and 4 h after PMA addition, while a major decrease in the translocated nuclear fraction occurred some time after 6 h. cAMP alone had no effect on the PKC alpha protein level or distribution, nor did it alter the translocation and down-regulation due to PMA exposure. Tetradecanoylphorbol Acetate 220-223 protein kinase C alpha Homo sapiens 43-52 1988168-4 1991 In contrast, PKC alpha and epsilon RNA transcripts were detected in melanocytes cultivated in medium without serum and TPA, but were repressed in melanocytes cultivated in medium with serum and TPA. Tetradecanoylphorbol Acetate 119-122 protein kinase C alpha Homo sapiens 13-22 1988168-4 1991 In contrast, PKC alpha and epsilon RNA transcripts were detected in melanocytes cultivated in medium without serum and TPA, but were repressed in melanocytes cultivated in medium with serum and TPA. Tetradecanoylphorbol Acetate 194-197 protein kinase C alpha Homo sapiens 13-22 33535882-6 2021 Further evidence showed that PKCepsilon knockdown by siRNA antagonized the AngII-induced chronic inhibition on the I Ks current, whereas knockdown of cPKC (PKCalpha and PKCbeta) attenuated the inhibition effect of PMA on the current. Tetradecanoylphorbol Acetate 214-217 protein kinase C alpha Homo sapiens 156-164 33535882-6 2021 Further evidence showed that PKCepsilon knockdown by siRNA antagonized the AngII-induced chronic inhibition on the I Ks current, whereas knockdown of cPKC (PKCalpha and PKCbeta) attenuated the inhibition effect of PMA on the current. Tetradecanoylphorbol Acetate 214-217 protein kinase C alpha Homo sapiens 169-176 1834742-4 1991 Bryostatin (Bryo) and phorbol esters (e.g., 12-O-tetradecanoylphorbol 13-acetate (TPA] are PKC activators with somewhat different immunologic effects. Tetradecanoylphorbol Acetate 44-80 protein kinase C alpha Homo sapiens 91-94 1834742-4 1991 Bryostatin (Bryo) and phorbol esters (e.g., 12-O-tetradecanoylphorbol 13-acetate (TPA] are PKC activators with somewhat different immunologic effects. Tetradecanoylphorbol Acetate 82-85 protein kinase C alpha Homo sapiens 91-94 1656952-4 1991 Treatment with phorbol 12-myristate 13-acetate (PMA) for 24 h dose-dependently inhibited Epo formation, thus suggesting that down-regulation of PKC might be responsible for this inhibition. Tetradecanoylphorbol Acetate 15-46 protein kinase C alpha Homo sapiens 144-147 1656952-4 1991 Treatment with phorbol 12-myristate 13-acetate (PMA) for 24 h dose-dependently inhibited Epo formation, thus suggesting that down-regulation of PKC might be responsible for this inhibition. Tetradecanoylphorbol Acetate 48-51 protein kinase C alpha Homo sapiens 144-147 1656952-5 1991 Immunoblotting experiments showed that incubation of HepG2 cells with PMA for 24 h resulted in a selective and almost complete down-regulation of PKC-alpha. Tetradecanoylphorbol Acetate 70-73 protein kinase C alpha Homo sapiens 146-155