PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23786520-3 2013 Herein, it was investigated whether 1 and three other flavonoids [chrysin (2), apigenin (3), and tricetin (4)] blocked 12-O-tetradecanoylphorbol 13-acetate (TPA)-triggered induction of CD families, which were induced through the activation of protein kinase C (PKC), mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK), and NADPH oxidase (NOX)-derived reactive oxygen species (ROS). Tetradecanoylphorbol Acetate 119-155 mitogen-activated protein kinase kinase 7 Homo sapiens 267-299 23833248-8 2013 However, while pharmacological inhibition of PKC suppressed PMA-induced activation of MEK-ERK-IKK signaling, activation by palmitate was upheld, suggesting that DAG-sensitive PKC and RKIP were dispensable for palmitate"s proinflammatory action. Tetradecanoylphorbol Acetate 60-63 mitogen-activated protein kinase kinase 7 Homo sapiens 86-89 23775084-5 2013 We show that both chemical suppression and siRNA silencing of PP2Ac in T-cells resulted in sustained phosphorylation of MEK and ERK following stimulation with phorbol 12-myristate 13-acetate and ionomycin. Tetradecanoylphorbol Acetate 159-190 mitogen-activated protein kinase kinase 7 Homo sapiens 120-123 25915860-10 2015 Taken together, these results suggest that TPA is able to induce VIL2 V1 over-expression in ESCC cells by activating MEK/ERK1/2 signaling and increasing binding of Sp1 and c-Jun to the TRE of the VIL2 V1 promoter, and that VIL2 is an important TPA-induced effector. Tetradecanoylphorbol Acetate 43-46 mitogen-activated protein kinase kinase 7 Homo sapiens 117-120 23786520-3 2013 Herein, it was investigated whether 1 and three other flavonoids [chrysin (2), apigenin (3), and tricetin (4)] blocked 12-O-tetradecanoylphorbol 13-acetate (TPA)-triggered induction of CD families, which were induced through the activation of protein kinase C (PKC), mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK), and NADPH oxidase (NOX)-derived reactive oxygen species (ROS). Tetradecanoylphorbol Acetate 119-155 mitogen-activated protein kinase kinase 7 Homo sapiens 301-304 23175175-0 2013 Induction of differentiation-specific miRNAs in TPA-induced myeloid leukemia cells through MEK/ERK activation. Tetradecanoylphorbol Acetate 48-51 mitogen-activated protein kinase kinase 7 Homo sapiens 103-106 23175175-4 2013 The upregulation of these miRNAs was further verified by quantitative RT-PCR, and, markedly, a subset of the miRNAs was found to be induced via the MEK/ERK signaling pathway using TPA and specific pharmacological inhibitors. Tetradecanoylphorbol Acetate 204-207 mitogen-activated protein kinase kinase 7 Homo sapiens 172-175 23353996-6 2013 In addition, TPA-induced phosphorylation of MEK and ERK was also inhibited by silibinin. Tetradecanoylphorbol Acetate 13-16 mitogen-activated protein kinase kinase 7 Homo sapiens 44-47 23353996-7 2013 Taken together, we suggest that silibinin suppresses TPA-induced cell migration and MMP-9 expression through the MEK/ERK-dependent pathway in thyroid and breast cancer cells. Tetradecanoylphorbol Acetate 53-56 mitogen-activated protein kinase kinase 7 Homo sapiens 125-128 22313459-0 2012 TPA induces the expression of EC-SOD in human monocytic THP-1 cells: involvement of PKC, MEK/ERK and NOX-derived ROS. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase kinase 7 Homo sapiens 89-92 23175175-6 2013 Therefore, we identified the unique miRNAs that respond to TPA treatment in leukemia cells and demonstrated the essential role of the MEK/ERK signaling pathway in the induction of these miRNA transcripts. Tetradecanoylphorbol Acetate 71-74 mitogen-activated protein kinase kinase 7 Homo sapiens 158-161 21730054-12 2011 U0126, an MEK inhibitor, and DPQ, a poly(ADP-ribose) polymerase-1 inhibitor, suppressed PMA-induced up-regulation of H1R gene expression. Tetradecanoylphorbol Acetate 88-91 mitogen-activated protein kinase kinase 7 Homo sapiens 10-13 22052014-8 2012 In addition, blockade of PKCdelta by rottlerin, a PKCdelta-specific inhibitor, and ERK1/2 by U0126, a MEK-ERK inhibitor, abrogated PMA-induced Egr-1 expression. Tetradecanoylphorbol Acetate 131-134 mitogen-activated protein kinase kinase 7 Homo sapiens 102-105 22052014-5 2012 We show that, in response to PMA, PKCdelta, a member of novel PKC isozymes, and MEK-ERK1/2 pathway of mitogen-activated protein kinases stimulate the NHE2 expression in C2BBe1 intestinal epithelial cells. Tetradecanoylphorbol Acetate 29-32 mitogen-activated protein kinase kinase 7 Homo sapiens 80-83 22020547-11 2012 Taken together, we suggest that TPA reciprocally regulates the level of p21 and p53 expression via a MEK/ERK-dependent pathway. Tetradecanoylphorbol Acetate 44-47 mitogen-activated protein kinase kinase 7 Homo sapiens 125-128 21297032-11 2011 These results suggest that the MEK/ERK1/2 pathway is necessary but not sufficient to regulate the PMA-dependent activation of Nox5. Tetradecanoylphorbol Acetate 98-101 mitogen-activated protein kinase kinase 7 Homo sapiens 31-34 21659537-6 2011 Previous work indicated that mTORC1 activation by the phorbol ester PMA (phorbol 12-myristate 13-acetate) depends upon PKCs and may involve MEK. Tetradecanoylphorbol Acetate 73-104 mitogen-activated protein kinase kinase 7 Homo sapiens 140-143 21077177-10 2011 Overall, our results suggest that the expression of EC-SOD is decreased by TPA through intracellular signaling consisting of PKC, NOX-derived ROS and MEK/ERK, but not of NF-kappaB signaling. Tetradecanoylphorbol Acetate 75-78 mitogen-activated protein kinase kinase 7 Homo sapiens 150-153 19715751-2 2009 In a previous study, we reported that silibinin suppresses TPA-induced MMP-9 expression through the Raf/MEK/ERK pathway. Tetradecanoylphorbol Acetate 59-62 mitogen-activated protein kinase kinase 7 Homo sapiens 104-107 20299489-9 2010 Taken together, the results show that PMA activates the MEK-ERK pathway and strongly induces miRNA-34a expression, which in turn inhibits cell proliferation by repressing the expression of MEK1. Tetradecanoylphorbol Acetate 38-41 mitogen-activated protein kinase kinase 7 Homo sapiens 56-59 20592496-8 2010 Additionally, treatment with As(2)O(3) in combination with inhibitors specific for MEK (U0126) in HOS and MNNG cells resulted in a marked inhibition of cell invasion and As(2)O(3) could significantly reduce PMA-induced invasion. Tetradecanoylphorbol Acetate 207-210 mitogen-activated protein kinase kinase 7 Homo sapiens 83-86 19181503-7 2009 TPA-induced MEK and ERK phosphorylation was significantly decreased by silibinin in MCF7 cells. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase kinase 7 Homo sapiens 12-15 19181503-10 2009 Taken together, we suggest that the inhibition of TPA-induced MMP-9 and VEGF expression by silibinin is mediated by the suppression of the Raf/MEK/ERK pathway in MCF-7 breast cancer cells. Tetradecanoylphorbol Acetate 50-53 mitogen-activated protein kinase kinase 7 Homo sapiens 143-146 18519570-7 2008 The TPA-induced phosphorylation of MEK, extracellular signal-regulated kinase, and p90 ribosomal s6 kinase was suppressed by CPF or procyanidin B2. Tetradecanoylphorbol Acetate 4-7 mitogen-activated protein kinase kinase 7 Homo sapiens 35-38 19181503-0 2009 Silibinin prevents TPA-induced MMP-9 expression and VEGF secretion by inactivation of the Raf/MEK/ERK pathway in MCF-7 human breast cancer cells. Tetradecanoylphorbol Acetate 19-22 mitogen-activated protein kinase kinase 7 Homo sapiens 94-97 18282472-4 2008 However, caspase-9/-3-mediated cytotoxicity can be induced in TPA-differentiated cells if they are pretreated with a protein kinase C (PKC) or a mitogen activated protein kinase (MEK) inhibitor. Tetradecanoylphorbol Acetate 62-65 mitogen-activated protein kinase kinase 7 Homo sapiens 145-177 18282472-4 2008 However, caspase-9/-3-mediated cytotoxicity can be induced in TPA-differentiated cells if they are pretreated with a protein kinase C (PKC) or a mitogen activated protein kinase (MEK) inhibitor. Tetradecanoylphorbol Acetate 62-65 mitogen-activated protein kinase kinase 7 Homo sapiens 179-182 18282472-5 2008 Taken together, this study demonstrates that TPA-differentiated HL-60 cells inhibit caspases-9/-3-mediated cytotoxicity through the PKC and MEK signaling pathways. Tetradecanoylphorbol Acetate 45-48 mitogen-activated protein kinase kinase 7 Homo sapiens 140-143 17114644-0 2007 Ascofuranone suppresses PMA-mediated matrix metalloproteinase-9 gene activation through the Ras/Raf/MEK/ERK- and Ap1-dependent mechanisms. Tetradecanoylphorbol Acetate 24-27 mitogen-activated protein kinase kinase 7 Homo sapiens 100-103 18053806-6 2008 MEK kinase assay using myelin basic protein (MBP) revealed that TPA-augmented MEK activity in HT-1080 cells and that the augmented MEK activity was diminished by nobiletin treatment. Tetradecanoylphorbol Acetate 64-67 mitogen-activated protein kinase kinase 7 Homo sapiens 0-3 18053806-6 2008 MEK kinase assay using myelin basic protein (MBP) revealed that TPA-augmented MEK activity in HT-1080 cells and that the augmented MEK activity was diminished by nobiletin treatment. Tetradecanoylphorbol Acetate 64-67 mitogen-activated protein kinase kinase 7 Homo sapiens 78-81 18053806-6 2008 MEK kinase assay using myelin basic protein (MBP) revealed that TPA-augmented MEK activity in HT-1080 cells and that the augmented MEK activity was diminished by nobiletin treatment. Tetradecanoylphorbol Acetate 64-67 mitogen-activated protein kinase kinase 7 Homo sapiens 78-81 17114644-6 2007 In addition, ascofuranone suppressed PMA-induced phosphorylation of Ras, Raf, MEK and extracellular signal-regulated kinase (ERK), upstream factors involved in AP-1activation, whereas the phosphorylation of p38 and JNK/mitogen-activated protein kinase was not affected by ascofuranone, suggesting that the primary target of ascofuranone for suppression of the AP-1 induction is present in upstream of ERK signaling pathway. Tetradecanoylphorbol Acetate 37-40 mitogen-activated protein kinase kinase 7 Homo sapiens 78-81 16868480-10 2006 TPA induced extracellular signal-regulated kinase1/2 phosphorylation, whereas the MEK inhibitor, PD98059, blocked the TPA-induced p21 expression. Tetradecanoylphorbol Acetate 118-121 mitogen-activated protein kinase kinase 7 Homo sapiens 82-85 17131377-5 2007 ICAM-1 expression in response to TPA was inhibited by pretreatment with GF109203X [a specific inhibitor of protein kinase C (PKC)], or with PD98059 and U0126 (specific inhibitors of MEK), suggesting the importance of PKC, and Erk1/2 signaling cascades in this response. Tetradecanoylphorbol Acetate 33-36 mitogen-activated protein kinase kinase 7 Homo sapiens 182-185 17101779-4 2007 Here we show that stimulation by tetradecanoyl phorbol acetate (TPA) attenuates PPARgamma"s activity in a MEK-dependent manner, even when Ser84 is mutated to Ala. To elucidate the mechanism of attenuation, we found that PPARgamma directly interacts with MEKs, which are the activators of ERKs, but not with ERKs themselves, both in vivo and in vitro. Tetradecanoylphorbol Acetate 33-62 mitogen-activated protein kinase kinase 7 Homo sapiens 106-109 17101779-4 2007 Here we show that stimulation by tetradecanoyl phorbol acetate (TPA) attenuates PPARgamma"s activity in a MEK-dependent manner, even when Ser84 is mutated to Ala. To elucidate the mechanism of attenuation, we found that PPARgamma directly interacts with MEKs, which are the activators of ERKs, but not with ERKs themselves, both in vivo and in vitro. Tetradecanoylphorbol Acetate 64-67 mitogen-activated protein kinase kinase 7 Homo sapiens 106-109 17394769-3 2007 Though no apparent elevation of ERK activity was observed during the apoptosis in NB4 cells caused by 20 microM sodium selenite treatment, PD98059 and U0126, specific chemical inhibitors of the MEK/ERK signaling pathway, were shown to strongly prevent the apoptosis process, while ERK activator TPA enhanced the process. Tetradecanoylphorbol Acetate 295-298 mitogen-activated protein kinase kinase 7 Homo sapiens 194-197 16868480-12 2006 CONCLUSIONS: TPA-induced p21 expression is mediated by the MEK/ERK pathway but is not involved in TPA-induced growth inhibition. Tetradecanoylphorbol Acetate 13-16 mitogen-activated protein kinase kinase 7 Homo sapiens 59-62 17329956-4 2006 Induction of cyclin D1 expression in TPA-treated HL60 cells was inhibited with protein kinase C (PKC) inhibitor bisindolylmaleimide I and mitogen activated protein kinase kinase (MEK) inhibitor PD98059. Tetradecanoylphorbol Acetate 37-40 mitogen-activated protein kinase kinase 7 Homo sapiens 179-182 16773182-7 2006 Inhibitors of mitogen-activated protein/extracellular signal regulated kinase (MEK), such as ERK inhibitor PD98059 and JNK inhibitors dicumarol and SP60015, but not p38 inhibitor SB203580, inhibited PMA-induced MUC5AC reporter activity. Tetradecanoylphorbol Acetate 199-202 mitogen-activated protein kinase kinase 7 Homo sapiens 79-82 17329956-4 2006 Induction of cyclin D1 expression in TPA-treated HL60 cells was inhibited with protein kinase C (PKC) inhibitor bisindolylmaleimide I and mitogen activated protein kinase kinase (MEK) inhibitor PD98059. Tetradecanoylphorbol Acetate 37-40 mitogen-activated protein kinase kinase 7 Homo sapiens 138-177 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 mitogen-activated protein kinase kinase 7 Homo sapiens 55-58 16169661-9 2006 Consistently, Western blot of Phospho(ser-218/222)-MEK demonstrated that phosphorylation of MEK-1 was greatly induced by 50nM TPA, which can be prevented by the PKC inhibitor Bisindolylmaleimides II. Tetradecanoylphorbol Acetate 126-129 mitogen-activated protein kinase kinase 7 Homo sapiens 51-54 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 mitogen-activated protein kinase kinase 7 Homo sapiens 55-58 16571380-7 2006 In mechanistic terms, the transcriptional upregulation of SK-1 is dependent on PKC and the extracellular signal-regulated protein kinase (ERK) cascade since staurosporine and the MEK inhibitor U0126 abolish the TPA-induced SK-1 induction. Tetradecanoylphorbol Acetate 211-214 mitogen-activated protein kinase kinase 7 Homo sapiens 179-182 17329956-5 2006 Induction of p21Waf1 expression in TPA-treated HL60 cells was inhibited with PKC inhibitor bisindolylmaleimide I and Go6976, MEK inhibitor PD98059, and p38 mitogen-actibated protein kinase (MAPK) inhibitor SB202190. Tetradecanoylphorbol Acetate 35-38 mitogen-activated protein kinase kinase 7 Homo sapiens 125-128 15721302-0 2005 Phorbol ester phorbol-12-myristate-13-acetate promotes anchorage-independent growth and survival of melanomas through MEK-independent activation of ERK1/2. Tetradecanoylphorbol Acetate 14-45 mitogen-activated protein kinase kinase 7 Homo sapiens 118-121 16267831-7 2006 Inhibition of MAPK kinase (MEK), an upstream kinase, by U0126, blocked TPA-induced activation of ERK1/2 in wild-type p53 cells and in mutant p53 cells. Tetradecanoylphorbol Acetate 71-74 mitogen-activated protein kinase kinase 7 Homo sapiens 27-30 16351709-7 2005 Furthermore, the TPA-mediated post-transcriptional mechanism of p21WAF1-enhanced expression in RD cells is due to activation of the MEK/ERK pathway, as shown by transfections with constitutively active MEK1 or MEK2, which induces p21WAF1 expression, and with ERK1 and ERK2 siRNA, which prevents p21WAF1 expression. Tetradecanoylphorbol Acetate 17-20 mitogen-activated protein kinase kinase 7 Homo sapiens 132-135 15757899-4 2005 Pretreatment with protein kinase C (PKC) inhibitor blocked the TPA-induced increase in NAG-1 protein levels and NF-kappa B binding/transcriptional activity, whereas an inhibition of p38, JNK, MEK activity had no effect on TPA-induced NAG-1 levels and NF-kappa B transcriptional activity. Tetradecanoylphorbol Acetate 63-66 mitogen-activated protein kinase kinase 7 Homo sapiens 192-195 15147830-3 2004 The MEK inhibitor U0126 (0.1 to 10 microM) enhanced the TPA-induced ICAM-1 expression but not the IFN-gamma-induced one. Tetradecanoylphorbol Acetate 56-59 mitogen-activated protein kinase kinase 7 Homo sapiens 4-7 15567061-2 2005 PMA-induced COX-2 expression was attenuated by PKC inhibitors (Go 6976 and Ro 31-8220), a Ras inhibitor (manumycin A), a Raf-1 inhibitor (GW 5074), a MEK inhibitor (PD 098059), and an NF-kappaB inhibitor (PDTC), but not by a tyrosine kinase inhibitor (genistein) or a p38 MAPK inhibitor (SB 203580). Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase kinase 7 Homo sapiens 150-153 15147830-5 2004 Furthermore, PD98059 (0.5 to 50 microM), another MEK inhibitor, enhanced the TPA-induced ICAM-1 expression as well. Tetradecanoylphorbol Acetate 77-80 mitogen-activated protein kinase kinase 7 Homo sapiens 49-52 12244094-4 2002 Conversely, the TPA-stimulated MEK binding and kinase activity are diminished when this region is deleted or Ser(338) and Ser(339) are mutated to alanines. Tetradecanoylphorbol Acetate 16-19 mitogen-activated protein kinase kinase 7 Homo sapiens 31-34 14981539-6 2004 In addition, the MEK/ERK inhibitors, PD98059 and UO126, suppressed PMA-stimulated TRAF1 promoter activity indicating a role for ERK in TRAF1 induction. Tetradecanoylphorbol Acetate 67-70 mitogen-activated protein kinase kinase 7 Homo sapiens 17-20 12472895-10 2002 More importantly, both neurite outgrowth and phosphorylation of ERK by TPA were blocked by PD 098059, a specific inhibitor of MEK (MAP kinase/ERK kinase-1), but not by SB203580, a specific inhibitor of p38 MAP kinase. Tetradecanoylphorbol Acetate 71-74 mitogen-activated protein kinase kinase 7 Homo sapiens 126-129 12472895-10 2002 More importantly, both neurite outgrowth and phosphorylation of ERK by TPA were blocked by PD 098059, a specific inhibitor of MEK (MAP kinase/ERK kinase-1), but not by SB203580, a specific inhibitor of p38 MAP kinase. Tetradecanoylphorbol Acetate 71-74 mitogen-activated protein kinase kinase 7 Homo sapiens 131-154 12867426-7 2003 Phosphorylation of tuberin by phorbol 12-myristate 13-acetate was reduced by treatment of cells with either bisindolylmaleimide I or UO126, inhibitors of PKC and MAPK/MEK (MAPK/ERK kinase), respectively, but not by wortmannin (an inhibitor of PI3K). Tetradecanoylphorbol Acetate 30-61 mitogen-activated protein kinase kinase 7 Homo sapiens 167-170 12851698-0 2003 NAMI-A inhibits the PMA-induced ODC gene expression in ECV304 cells: involvement of PKC/Raf/Mek/ERK signalling pathway. Tetradecanoylphorbol Acetate 20-23 mitogen-activated protein kinase kinase 7 Homo sapiens 92-95 12592382-5 2003 Pretreatment of 20 microg/ml PD98059, an inhibitor of MEK which is the upstream kinase of ERK, prevents the TPA- and Saikosaponin a-triggered HepG2 growth inhibition by 50 and 30%, respectively, accompanied by a 50 - 85% decrease of the p15(INK4b)/p16(INK4a) RNAs and proteins induced by both drugs. Tetradecanoylphorbol Acetate 108-111 mitogen-activated protein kinase kinase 7 Homo sapiens 54-57 12444974-7 2002 NAMI-A was also able to inhibit the phosphorylation of MEK, the upstream activator of ERK, and, similar to both the protein kinase C (PKC) inhibitor GF109203X and the MAPK/ERK (MEK) inhibitor PD98059, it completely counteracted PMA-induced ERK phosphorylation. Tetradecanoylphorbol Acetate 228-231 mitogen-activated protein kinase kinase 7 Homo sapiens 55-58 12181747-5 2002 The inhibitory effect of TPA was mostly abrogated by pretreatment of a specific MEK inhibitor PD98059, indicating that the effect depends upon MEK/ERK-mediated signals. Tetradecanoylphorbol Acetate 25-28 mitogen-activated protein kinase kinase 7 Homo sapiens 80-83 12181747-5 2002 The inhibitory effect of TPA was mostly abrogated by pretreatment of a specific MEK inhibitor PD98059, indicating that the effect depends upon MEK/ERK-mediated signals. Tetradecanoylphorbol Acetate 25-28 mitogen-activated protein kinase kinase 7 Homo sapiens 143-146 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 mitogen-activated protein kinase kinase 7 Homo sapiens 34-37 12009309-3 2002 METHODS: Using the JB6 cell model, we determined the involvement of PKC isoforms, mitogen-activated protein kinase kinase (MAPK kinase/MEK) and MAPK in TPA-induced OPN expression using inhibitors specific to PKC isoforms and MEK and performing Northern blot analyses. Tetradecanoylphorbol Acetate 152-155 mitogen-activated protein kinase kinase 7 Homo sapiens 135-138 12009309-3 2002 METHODS: Using the JB6 cell model, we determined the involvement of PKC isoforms, mitogen-activated protein kinase kinase (MAPK kinase/MEK) and MAPK in TPA-induced OPN expression using inhibitors specific to PKC isoforms and MEK and performing Northern blot analyses. Tetradecanoylphorbol Acetate 152-155 mitogen-activated protein kinase kinase 7 Homo sapiens 225-228 12009309-7 2002 Additionally, inhibition of MEK activity, which activates MAPK, attenuated TPA-induced OPN expression. Tetradecanoylphorbol Acetate 75-78 mitogen-activated protein kinase kinase 7 Homo sapiens 28-31 12048182-5 2002 Phorbol 12-myristate 13-acetate, a differentiation-inducing stimulus, potently activates the Ras-Raf-MEK-ERK pathway but only weakly activates PI3K/Akt and does not trigger the cross-talk. Tetradecanoylphorbol Acetate 0-31 mitogen-activated protein kinase kinase 7 Homo sapiens 101-104 12137745-6 2002 On immunoblot analysis, PMA enhanced NEP/CD10 expression in a dose- and time-dependent manner, which was completely abolished by Bis I and a mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor, PD98059. Tetradecanoylphorbol Acetate 24-27 mitogen-activated protein kinase kinase 7 Homo sapiens 189-192 11799119-5 2002 The TPA-stimulated phosphorylation of all these sites is sensitive to inhibitors of MEK and to the inhibitor of mTOR, rapamycin, indicating that inputs from both mTOR and MEK are required for the regulation of 4E-BP1 phosphorylation by TPA. Tetradecanoylphorbol Acetate 4-7 mitogen-activated protein kinase kinase 7 Homo sapiens 84-87 12191496-6 2002 Accordingly, PMA induced rapid phosphorylation of MEK substrate, i.e. Erk1/2 (p42/44 MAPK). Tetradecanoylphorbol Acetate 13-16 mitogen-activated protein kinase kinase 7 Homo sapiens 50-53 11940578-3 2002 To explore the importance of the c-Raf/MAPK kinase (MEK)/MAPK pathway, we stimulated adult feline cardiomyocytes with 12-O-tetradecanoylphorbol-13-acetate (TPA), insulin, or forskolin to activate PKC, phosphatidylinositol-3-OH kinase, or protein kinase A (PKA), respectively. Tetradecanoylphorbol Acetate 118-154 mitogen-activated protein kinase kinase 7 Homo sapiens 52-55 11959794-15 2002 MEK inhibitor U0126 inhibited TPA/ionomycin induced IL-13 synthesis very effectively, whereas alpha-CD3/alpha-CD28 stimulated IL-13 induction was resistant to this drug. Tetradecanoylphorbol Acetate 30-33 mitogen-activated protein kinase kinase 7 Homo sapiens 0-3 11799119-5 2002 The TPA-stimulated phosphorylation of all these sites is sensitive to inhibitors of MEK and to the inhibitor of mTOR, rapamycin, indicating that inputs from both mTOR and MEK are required for the regulation of 4E-BP1 phosphorylation by TPA. Tetradecanoylphorbol Acetate 4-7 mitogen-activated protein kinase kinase 7 Homo sapiens 171-174 11914583-3 2002 Treatment of cells with PD98059, which is an inhibitor of mitogen-activated protein kinase kinase (MEK), decreased the PMA-induced expression of 12(S)-lipoxygenase. Tetradecanoylphorbol Acetate 119-122 mitogen-activated protein kinase kinase 7 Homo sapiens 58-97 11914583-3 2002 Treatment of cells with PD98059, which is an inhibitor of mitogen-activated protein kinase kinase (MEK), decreased the PMA-induced expression of 12(S)-lipoxygenase. Tetradecanoylphorbol Acetate 119-122 mitogen-activated protein kinase kinase 7 Homo sapiens 99-102 11278385-6 2001 PMA-stimulated activation of ERK/MAPK, RSK1, and NF-kappaB and the PMA-induced megakaryocytic differentiation were prevented by pretreatment with PD98059, a specific inhibitor of the mitogen-activated ERK kinase (MEK). Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase kinase 7 Homo sapiens 183-211 11719466-10 2001 Taken together, this study shows that a PKC-epsilon-Raf-1-MEK-ERK-AP1 signaling cascade acts on a 12-O-tetradecanoylphorbol-13-acetate response element-like element to mediate hypoxia-induced GRP78 expression in human gastric cancer cells. Tetradecanoylphorbol Acetate 98-134 mitogen-activated protein kinase kinase 7 Homo sapiens 58-61 11583819-4 2001 Moreover, Bge cell treatment with inhibitors of protein kinase C (PKC), Ras and MAPK kinase (Mek) suppressed PMA-induced expression of activated MAPK, suggesting that PKC-, Ras- and Mek-like molecules may be acting upstream of MAPK. Tetradecanoylphorbol Acetate 109-112 mitogen-activated protein kinase kinase 7 Homo sapiens 93-96 11583819-4 2001 Moreover, Bge cell treatment with inhibitors of protein kinase C (PKC), Ras and MAPK kinase (Mek) suppressed PMA-induced expression of activated MAPK, suggesting that PKC-, Ras- and Mek-like molecules may be acting upstream of MAPK. Tetradecanoylphorbol Acetate 109-112 mitogen-activated protein kinase kinase 7 Homo sapiens 182-185 11734574-3 2001 We stimulated the MAP kinase pathway with anti-CD3 antibodies and phorbol 12-myristate 13-acetate (PMA), which act upstream of the MAP kinase (MAPK)/ERK kinase (MEK) as U0126, an MEK inhibitor, abolished the actions of these two agents on MAP kinase activation. Tetradecanoylphorbol Acetate 66-97 mitogen-activated protein kinase kinase 7 Homo sapiens 161-164 11734574-3 2001 We stimulated the MAP kinase pathway with anti-CD3 antibodies and phorbol 12-myristate 13-acetate (PMA), which act upstream of the MAP kinase (MAPK)/ERK kinase (MEK) as U0126, an MEK inhibitor, abolished the actions of these two agents on MAP kinase activation. Tetradecanoylphorbol Acetate 66-97 mitogen-activated protein kinase kinase 7 Homo sapiens 179-182 11734574-3 2001 We stimulated the MAP kinase pathway with anti-CD3 antibodies and phorbol 12-myristate 13-acetate (PMA), which act upstream of the MAP kinase (MAPK)/ERK kinase (MEK) as U0126, an MEK inhibitor, abolished the actions of these two agents on MAP kinase activation. Tetradecanoylphorbol Acetate 99-102 mitogen-activated protein kinase kinase 7 Homo sapiens 161-164 11734574-3 2001 We stimulated the MAP kinase pathway with anti-CD3 antibodies and phorbol 12-myristate 13-acetate (PMA), which act upstream of the MAP kinase (MAPK)/ERK kinase (MEK) as U0126, an MEK inhibitor, abolished the actions of these two agents on MAP kinase activation. Tetradecanoylphorbol Acetate 99-102 mitogen-activated protein kinase kinase 7 Homo sapiens 179-182 11707282-5 2001 The TPA-induced increase in neuropeptide Y expression was also inhibited by the MEK inhibitor PD98059. Tetradecanoylphorbol Acetate 4-7 mitogen-activated protein kinase kinase 7 Homo sapiens 80-83 11400863-6 2001 Activation by EGF and TPA and the early response induced by FBS were strongly reduced by the MEK inhibitor PD98059. Tetradecanoylphorbol Acetate 22-25 mitogen-activated protein kinase kinase 7 Homo sapiens 93-96 11278385-6 2001 PMA-stimulated activation of ERK/MAPK, RSK1, and NF-kappaB and the PMA-induced megakaryocytic differentiation were prevented by pretreatment with PD98059, a specific inhibitor of the mitogen-activated ERK kinase (MEK). Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase kinase 7 Homo sapiens 213-216 11278385-6 2001 PMA-stimulated activation of ERK/MAPK, RSK1, and NF-kappaB and the PMA-induced megakaryocytic differentiation were prevented by pretreatment with PD98059, a specific inhibitor of the mitogen-activated ERK kinase (MEK). Tetradecanoylphorbol Acetate 67-70 mitogen-activated protein kinase kinase 7 Homo sapiens 183-211 11278385-6 2001 PMA-stimulated activation of ERK/MAPK, RSK1, and NF-kappaB and the PMA-induced megakaryocytic differentiation were prevented by pretreatment with PD98059, a specific inhibitor of the mitogen-activated ERK kinase (MEK). Tetradecanoylphorbol Acetate 67-70 mitogen-activated protein kinase kinase 7 Homo sapiens 213-216 11359422-13 2001 The mechanism of IL-5 priming after PMA stimulation of oxygen radical production is MEK independent. Tetradecanoylphorbol Acetate 36-39 mitogen-activated protein kinase kinase 7 Homo sapiens 84-87 11310793-8 2001 Studies using inhibitors for protein kinases involved in cell signaling pathways suggested that stress-activated kinase p38 and mitogen-activated protein kinase kinase MEK are involved in TPA-independent regulation of TYRP2 expression in melanocytes. Tetradecanoylphorbol Acetate 188-191 mitogen-activated protein kinase kinase 7 Homo sapiens 168-171 11124968-4 2001 In addition, reduction in CD45 expression caused the duration of peak PMA-induced MEK and extracellular signal-regulated kinase (ERK) 1/2 activity to increase from 5 min to 30 min while leading to a 4-fold increase in PMA-dependent PKCdelta activation. Tetradecanoylphorbol Acetate 70-73 mitogen-activated protein kinase kinase 7 Homo sapiens 82-85 11124968-6 2001 Finally, inhibitors of MEK (PD98059) and PKCdelta (rottlerin) completely blocked PMA-induced monocytic cell differentiation. Tetradecanoylphorbol Acetate 81-84 mitogen-activated protein kinase kinase 7 Homo sapiens 23-26 10871841-5 2000 Morphological changes induced by TPA were reduced by annexin V overexpression as well as by the pan-PKC inhibitor, bisindolylmaleimide I, and by the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK) inhibitor, PD98059. Tetradecanoylphorbol Acetate 33-36 mitogen-activated protein kinase kinase 7 Homo sapiens 228-231 10926560-3 2000 An inhibitor of the dual-specificity ERK kinase (MEK), PD-98059, completely abolished PMA-induced ERK activation. Tetradecanoylphorbol Acetate 86-89 mitogen-activated protein kinase kinase 7 Homo sapiens 49-52 10871841-12 2000 PD98059 inhibited this increase, suggesting that TPA upregulation of p21WAF/CIP1 occurs via the MEK pathway, and that annexin V overexpression blunts it. Tetradecanoylphorbol Acetate 49-52 mitogen-activated protein kinase kinase 7 Homo sapiens 96-99 10446156-8 1999 Inhibition of MEK blocked both bombesin- and phorbol 12-myristate 13-acetate-induced secretion. Tetradecanoylphorbol Acetate 45-76 mitogen-activated protein kinase kinase 7 Homo sapiens 14-17 10775036-5 2000 PMA treatment rapidly (10 min) induced phosphorylation of MAPK kinase (MEK and p44/42 MAPK), which persisted for at least 24 h. p44/42 MAPK immunoprecipitates from lysates of PMA-treated cells had increased ability to phosphorylate the transcription factor Elk-1. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase kinase 7 Homo sapiens 71-74 10775036-5 2000 PMA treatment rapidly (10 min) induced phosphorylation of MAPK kinase (MEK and p44/42 MAPK), which persisted for at least 24 h. p44/42 MAPK immunoprecipitates from lysates of PMA-treated cells had increased ability to phosphorylate the transcription factor Elk-1. Tetradecanoylphorbol Acetate 175-178 mitogen-activated protein kinase kinase 7 Homo sapiens 71-74 10775036-10 2000 Furthermore, transient transfection with an inactive, dominant-negative MEK mutant also inhibited PMA-induced differentiation, whereas transient transfection with a plasmid coding for constitutively activated MEK led to macrophage-like differentiation in the absence of PMA. Tetradecanoylphorbol Acetate 98-101 mitogen-activated protein kinase kinase 7 Homo sapiens 72-75 10737257-1 2000 The purpose of this study was to evaluate whether the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) signaling pathway contributes to 12-O-tertadecanoyl phorbol 13-acetate (TPA)-mediated protection from taxol-induced apoptosis of human leukemia HL-60 cells. Tetradecanoylphorbol Acetate 203-206 mitogen-activated protein kinase kinase 7 Homo sapiens 54-124 10737257-1 2000 The purpose of this study was to evaluate whether the mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) signaling pathway contributes to 12-O-tertadecanoyl phorbol 13-acetate (TPA)-mediated protection from taxol-induced apoptosis of human leukemia HL-60 cells. Tetradecanoylphorbol Acetate 203-206 mitogen-activated protein kinase kinase 7 Homo sapiens 126-129 10737257-4 2000 Since TPA stimulates MEK signal transduction pathway in HL-60 cells, we postulated that MEK pathway may be playing a role in the ability of TPA to inhibit taxol-induced apoptosis. Tetradecanoylphorbol Acetate 6-9 mitogen-activated protein kinase kinase 7 Homo sapiens 21-24 10737257-4 2000 Since TPA stimulates MEK signal transduction pathway in HL-60 cells, we postulated that MEK pathway may be playing a role in the ability of TPA to inhibit taxol-induced apoptosis. Tetradecanoylphorbol Acetate 6-9 mitogen-activated protein kinase kinase 7 Homo sapiens 88-91 10737257-4 2000 Since TPA stimulates MEK signal transduction pathway in HL-60 cells, we postulated that MEK pathway may be playing a role in the ability of TPA to inhibit taxol-induced apoptosis. Tetradecanoylphorbol Acetate 140-143 mitogen-activated protein kinase kinase 7 Homo sapiens 88-91 10737257-5 2000 PD098059, a specific MEK kinase inhibitor, abolished the ability of TPA to inhibit taxol-induced apoptosis. Tetradecanoylphorbol Acetate 68-71 mitogen-activated protein kinase kinase 7 Homo sapiens 21-24 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 mitogen-activated protein kinase kinase 7 Homo sapiens 89-92 10523856-8 1999 TPA also activated the Raf1/MEK/ERK cascade and activated another MAPK member, p38, but not JNK. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase kinase 7 Homo sapiens 28-31 10523856-10 1999 The MEK inhibitor PD 098059, as well as the PKC inhibitors, completely blocked TPA-mediated ERK activation. Tetradecanoylphorbol Acetate 79-82 mitogen-activated protein kinase kinase 7 Homo sapiens 4-7 10733524-3 2000 We show that induction of the circadian oscillation of gene expression is triggered by TPA treatment of NIH-3T3 fibroblasts, which is inhibited by a MEK inhibitor, and that prolonged activation of the MAPK cascade is sufficient to trigger circadian gene expression. Tetradecanoylphorbol Acetate 87-90 mitogen-activated protein kinase kinase 7 Homo sapiens 149-152 10359012-4 1999 Treatment of cells with PD98059, a specific inhibitor of mitogen-activated protein kinase kinase (MEK), inhibited TPA-induced ERK2 activity. Tetradecanoylphorbol Acetate 114-117 mitogen-activated protein kinase kinase 7 Homo sapiens 98-101 10359012-6 1999 We conclude that activation of the MEK/ERK signaling pathway is necessary for TPA-induced mononuclear cell differentiation. Tetradecanoylphorbol Acetate 78-81 mitogen-activated protein kinase kinase 7 Homo sapiens 35-38 10319997-2 1999 This is shown to be due to the inability of TPA to maintain activation of MAP/extracellular signal-regulated kinase kinase (MEK) and cRaf1. Tetradecanoylphorbol Acetate 44-47 mitogen-activated protein kinase kinase 7 Homo sapiens 124-127 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 mitogen-activated protein kinase kinase 7 Homo sapiens 235-238 10102471-11 1999 PD 098059 and U0126, both highly specific MEK inhibitors, efficiently prevented PMA-induced PAI-1 synthesis (mRNA and protein levels) and cell adhesion whereas SB203580, a specific inhibitor of stress-activated MAPK p38, did not. Tetradecanoylphorbol Acetate 80-83 mitogen-activated protein kinase kinase 7 Homo sapiens 42-45 10102471-13 1999 In conclusion, we propose that the pathway PKCbeta-MEK-MAPK p42 is a potential linear route for PAI-1 synthesis leading to morphological changes and adherence linked to PMA-induced differentiation in HL-60 cells. Tetradecanoylphorbol Acetate 169-172 mitogen-activated protein kinase kinase 7 Homo sapiens 51-54 9797142-3 1998 Similarly, PD98059, a specific inhibitor of MEK, abolished p21(WAF1/CIP1) induction and PMA-induced growth arrest. Tetradecanoylphorbol Acetate 88-91 mitogen-activated protein kinase kinase 7 Homo sapiens 44-47 9686602-8 1998 Strikingly, the inhibition of MEK with PD98059 altered the phenotype of C2-ceramide- and PMA-stimulated U937 cells to that of cells treated with C2-ceramide alone. Tetradecanoylphorbol Acetate 89-92 mitogen-activated protein kinase kinase 7 Homo sapiens 30-33 9473349-0 1998 A role for the MEK/MAPK pathway in PMA-induced cell cycle arrest: modulation of megakaryocytic differentiation of K562 cells. Tetradecanoylphorbol Acetate 35-38 mitogen-activated protein kinase kinase 7 Homo sapiens 15-18 9473349-3 1998 These PMA-induced changes in K562 cells are preceded by a rapid rise in the activity of MEK (MAP kinase/extracellular regulated kinases) that leads to a sustained activation of ERK2 (extracellular regulated kinase; MAPK). Tetradecanoylphorbol Acetate 6-9 mitogen-activated protein kinase kinase 7 Homo sapiens 88-91 9473349-3 1998 These PMA-induced changes in K562 cells are preceded by a rapid rise in the activity of MEK (MAP kinase/extracellular regulated kinases) that leads to a sustained activation of ERK2 (extracellular regulated kinase; MAPK). Tetradecanoylphorbol Acetate 6-9 mitogen-activated protein kinase kinase 7 Homo sapiens 93-135 10319997-3 1999 A direct relationship between sustained p42MAPK activation and differentiation is provided by the demonstration that blockade of MEK activation by PD098059 prevents TPA-induced morphological differentiation of wild type U937 cells. Tetradecanoylphorbol Acetate 165-168 mitogen-activated protein kinase kinase 7 Homo sapiens 129-132 9844925-4 1998 We have previously established that PMA-induced megakaryocyte differentiation of K562 cells requires the activity of the MEK/MAPK pathway (Herrera et al Exp Cell Res 1998; 238: 407-414). Tetradecanoylphorbol Acetate 36-39 mitogen-activated protein kinase kinase 7 Homo sapiens 121-124 10397459-5 1998 However, PMA-induced differentiation was blocked by pretreatment with PD98059, a specific inhibitor of MEK, in both parental and NF-kappaB-transfected cells. Tetradecanoylphorbol Acetate 9-12 mitogen-activated protein kinase kinase 7 Homo sapiens 103-106 9804192-4 1998 Pretreatment of cells with MEK inhibitor, PD98059, inhibited TPA-induced phosphorylation of ERK1/2 and the cytoprotective ability of TPA. Tetradecanoylphorbol Acetate 61-64 mitogen-activated protein kinase kinase 7 Homo sapiens 27-30 9804192-4 1998 Pretreatment of cells with MEK inhibitor, PD98059, inhibited TPA-induced phosphorylation of ERK1/2 and the cytoprotective ability of TPA. Tetradecanoylphorbol Acetate 133-136 mitogen-activated protein kinase kinase 7 Homo sapiens 27-30 9733728-8 1998 Co-transfection of the hINV promoter with dominant negative forms of Ras, MEKK1, MEK1, MEK7, MEK3, p38/RK, and c-Jun inhibit the TPA-dependent increase. Tetradecanoylphorbol Acetate 129-132 mitogen-activated protein kinase kinase 7 Homo sapiens 87-91 9553058-2 1998 We have identified a distal IL-2 enhancer regulated by the Raf-MEK-ERK signaling pathway, which can be induced by TPA/ionomycin treatment. Tetradecanoylphorbol Acetate 114-117 mitogen-activated protein kinase kinase 7 Homo sapiens 63-66 9553058-7 1998 Furthermore, the JNK/SAPK signaling pathway cooperates with the Raf-MEK-ERK cascade in TPA/ionomycin-induced DSE activity. Tetradecanoylphorbol Acetate 87-90 mitogen-activated protein kinase kinase 7 Homo sapiens 68-71 7936644-0 1994 Signalling from TPA to MAP kinase requires protein kinase C, raf and MEK: reconstitution of the signalling pathway in vitro. Tetradecanoylphorbol Acetate 16-19 mitogen-activated protein kinase kinase 7 Homo sapiens 69-72 9183012-5 1997 Similarly, the expression of MEK- and of [Asn17]Ras mutants decreased the 12-O-tetradecanoyl-phorbol 13-acetate (TPA)-mediated p21(waf1/cip1) induction. Tetradecanoylphorbol Acetate 74-111 mitogen-activated protein kinase kinase 7 Homo sapiens 29-32 9183012-5 1997 Similarly, the expression of MEK- and of [Asn17]Ras mutants decreased the 12-O-tetradecanoyl-phorbol 13-acetate (TPA)-mediated p21(waf1/cip1) induction. Tetradecanoylphorbol Acetate 113-116 mitogen-activated protein kinase kinase 7 Homo sapiens 29-32 8798560-3 1996 Treatment of cells with TPA or epidermal growth factor resulted in the activation of MEK and ERK. Tetradecanoylphorbol Acetate 24-27 mitogen-activated protein kinase kinase 7 Homo sapiens 85-88 8663100-7 1996 The MAPK and NHE activities induced by PMA were inhibited by staurosporine, a potent inhibitor for protein kinase C (PKC), and by MAPK kinase (MEK) inhibitor, PD98059, but were not affected by the tyrosine kinase inhibitor genistein. Tetradecanoylphorbol Acetate 39-42 mitogen-activated protein kinase kinase 7 Homo sapiens 143-146 7936644-4 1994 Using recombinant proteins and in vitro phosphorylation reactions we identified the components in the signal transduction pathway from TPA to MAPkinase and we show that the activation of MAPkinase by TPA requires the presence of protein kinase C, c-raf and the MAPkinase activator MEK. Tetradecanoylphorbol Acetate 135-138 mitogen-activated protein kinase kinase 7 Homo sapiens 281-284 7936644-4 1994 Using recombinant proteins and in vitro phosphorylation reactions we identified the components in the signal transduction pathway from TPA to MAPkinase and we show that the activation of MAPkinase by TPA requires the presence of protein kinase C, c-raf and the MAPkinase activator MEK. Tetradecanoylphorbol Acetate 200-203 mitogen-activated protein kinase kinase 7 Homo sapiens 281-284 12446683-5 2003 This PMA induction was blocked with the MEK inhibitor UO126, suggesting that the PMA-induced activation of the hTFPI-2 promoter is mediated through MEK. Tetradecanoylphorbol Acetate 5-8 mitogen-activated protein kinase kinase 7 Homo sapiens 40-43 8352882-8 1993 After treatment with TPA, MEK cultures produced a large induction of both c-jun and c-fos mRNA by 60 min, as determined by northern blot analysis, and a large induction of ODC mRNA and enzyme activity by 6 h. TPA treatment of cultured HEKs, however, did not induce ODC activity; in fact, less activity, compared with that of control cultures, was observed. Tetradecanoylphorbol Acetate 21-24 mitogen-activated protein kinase kinase 7 Homo sapiens 26-29 8352882-8 1993 After treatment with TPA, MEK cultures produced a large induction of both c-jun and c-fos mRNA by 60 min, as determined by northern blot analysis, and a large induction of ODC mRNA and enzyme activity by 6 h. TPA treatment of cultured HEKs, however, did not induce ODC activity; in fact, less activity, compared with that of control cultures, was observed. Tetradecanoylphorbol Acetate 209-212 mitogen-activated protein kinase kinase 7 Homo sapiens 26-29 8175693-1 1994 Treatment of adipocytes with insulin or phorbol 12-myristate 13-acetate (PMA) results in transient activation of mitogen-activated protein kinase kinase (MEK) (Tmax = 90 s) and mitogen-activated protein kinase (MAPK) (Tmax = 300 s). Tetradecanoylphorbol Acetate 40-71 mitogen-activated protein kinase kinase 7 Homo sapiens 154-157 8175693-1 1994 Treatment of adipocytes with insulin or phorbol 12-myristate 13-acetate (PMA) results in transient activation of mitogen-activated protein kinase kinase (MEK) (Tmax = 90 s) and mitogen-activated protein kinase (MAPK) (Tmax = 300 s). Tetradecanoylphorbol Acetate 73-76 mitogen-activated protein kinase kinase 7 Homo sapiens 154-157 8125975-2 1994 Following anti-IgM antibody and phorbol 12-myristate 13-acetate (PMA) stimulation, we demonstrate the activation of Ras, Raf-1, and MAPK/ERK kinase (MEK), all of which are thought to participate in an important signaling cascade that leads to MAPK activation. Tetradecanoylphorbol Acetate 32-63 mitogen-activated protein kinase kinase 7 Homo sapiens 149-152 8125975-2 1994 Following anti-IgM antibody and phorbol 12-myristate 13-acetate (PMA) stimulation, we demonstrate the activation of Ras, Raf-1, and MAPK/ERK kinase (MEK), all of which are thought to participate in an important signaling cascade that leads to MAPK activation. Tetradecanoylphorbol Acetate 65-68 mitogen-activated protein kinase kinase 7 Homo sapiens 149-152 8125975-5 1994 Similarly, MEK activity toward kinase-active or -inactive recombinant MAPK also increased upon anti-IgM or PMA treatment. Tetradecanoylphorbol Acetate 107-110 mitogen-activated protein kinase kinase 7 Homo sapiens 11-14 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 mitogen-activated protein kinase kinase 7 Homo sapiens 5-8 12446683-5 2003 This PMA induction was blocked with the MEK inhibitor UO126, suggesting that the PMA-induced activation of the hTFPI-2 promoter is mediated through MEK. Tetradecanoylphorbol Acetate 5-8 mitogen-activated protein kinase kinase 7 Homo sapiens 148-151 28286738-4 2017 Treatment with phorbol-12-myristate-13-acetate (PMA), a potent agonist of protein kinase C (PKC) and its downstream effector in the MEK/ERK-dependent pathway, resulted in the activation of mTORC1 signaling and phosphorylation of the upstream regulator tuberous sclerosis 2 (TSC2) in C2C12 myoblasts. Tetradecanoylphorbol Acetate 15-46 mitogen-activated protein kinase kinase 7 Homo sapiens 132-135 33290316-8 2021 The inhibition of MEK and ERK was confirmed by using MEK stimulators, GM-CSF and phorbol 12-myristate 13-acetate, and MEK-specific inhibitor, PD98059. Tetradecanoylphorbol Acetate 81-112 mitogen-activated protein kinase kinase 7 Homo sapiens 18-21 30073169-10 2018 In agreement, 80 nM PMA (a PKC activator) mimicked the effect of LPS on the activation of the MEK/ERK/TSC2/mTORC1/S6K pathway, monocyte adhesion to ECV cells and actin cytoskeleton rearrangement. Tetradecanoylphorbol Acetate 20-23 mitogen-activated protein kinase kinase 7 Homo sapiens 94-97 29959857-10 2018 Taken together, our findings suggest that the PMA-stimulated PKC and MEK/ERK signaling pathways induce Sp1-mediated transcription of the GC-A encoding gene in human monocytic THP-1 cells. Tetradecanoylphorbol Acetate 46-49 mitogen-activated protein kinase kinase 7 Homo sapiens 69-72 28286738-4 2017 Treatment with phorbol-12-myristate-13-acetate (PMA), a potent agonist of protein kinase C (PKC) and its downstream effector in the MEK/ERK-dependent pathway, resulted in the activation of mTORC1 signaling and phosphorylation of the upstream regulator tuberous sclerosis 2 (TSC2) in C2C12 myoblasts. Tetradecanoylphorbol Acetate 48-51 mitogen-activated protein kinase kinase 7 Homo sapiens 132-135 26786102-5 2016 We show that androgen signaling suppresses TPA-induced c-Fos expression through repressing a PKC/MEK/ERK/ELK-1 signaling pathway. Tetradecanoylphorbol Acetate 43-46 mitogen-activated protein kinase kinase 7 Homo sapiens 97-100