PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29710490-0 2018 Anti-metastatic potential of a proton beam is regulated by p38 MAPK/c-Fos signaling pathway in TPA-treated HepG2 human hepatocellular carcinoma. Tetradecanoylphorbol Acetate 95-98 mitogen-activated protein kinase 14 Homo sapiens 59-62 29170390-4 2017 Stimulation with CD3/CD28, PMA/ionomycin, or latency reversing agents prostratin and SAHA, yielded increased phosphorylation of IkappaBalpha, ERK, p38, and JNK in HIV-infected cells across two in vitro latency models. Tetradecanoylphorbol Acetate 27-30 mitogen-activated protein kinase 14 Homo sapiens 147-150 29710490-8 2018 Therefore, the result demonstrates that the anti-metastatic effects of a proton beam in TPA-treated HepG2 cells are associated with the inhibition of MMP-9 activity and the down-regulations of MMP-9, uPA, uPAR, Snail-1 and VEGF gene expression via the p38 MAPK/c-Fos signaling pathway. Tetradecanoylphorbol Acetate 88-91 mitogen-activated protein kinase 14 Homo sapiens 252-255 28970848-10 2017 CONCLUSION: The results indicated that the inhibitory effects of CFE against TPA-induced MMP-9 expression and MCF-7 cell invasion were dependent on the protein kinase C delta/p38/c-Jun N-terminal kinase/AP-1 pathway. Tetradecanoylphorbol Acetate 77-80 mitogen-activated protein kinase 14 Homo sapiens 175-178 27240473-13 2016 In THP-1 cells transfected with miRNA-128 mimic, TNF-alpha production was lower, and phosphorylation of p38 was inhibited when challenged with PMA or PFA-fixed E. coli. Tetradecanoylphorbol Acetate 143-146 mitogen-activated protein kinase 14 Homo sapiens 104-107 25787879-6 2016 TPA-induced phosphorylation of p38, JNK1/2 and Akt was also suppressed by DGC. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 31-34 27476935-7 2016 Furthermore, p-cymene was found to suppress the constitutive and/or TPA-augmented phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase (MAPK) in HT-1080 cells. Tetradecanoylphorbol Acetate 68-71 mitogen-activated protein kinase 14 Homo sapiens 152-188 26852212-5 2016 Additionally, the effect of GMHGYGT on the phorbol-12-myristate-13-acetate plus calcium ionophore A23187-induced phosphorylation of extracellular signal-regulated kinase, C-Jun N-terminal kinase and p38 in HMC-1 cells was investigated. Tetradecanoylphorbol Acetate 43-74 mitogen-activated protein kinase 14 Homo sapiens 199-202 27043542-7 2016 Furthermore, C2 ceramide significantly inhibited PMA-induced reactive oxygen species (ROS) production and NADPH oxidase 4 (NOX4) expression, and inhibition of ROS by diphenylene iodonium (DPI, NADPH oxidase inhibitor) mimicked the effects of C2 ceramide on MMP expression and NF-kappaB/AP-1 via inhibition of p38 MAPK. Tetradecanoylphorbol Acetate 49-52 mitogen-activated protein kinase 14 Homo sapiens 309-312 26116564-12 2015 TPA-induced induction of MMP-7 expression was suppressed by AP-1, NF-kappaB, and MAPK (ERK, p38, and JNK) inhibitors, whereas TPA-induced expression of NOX2 and its regulators, p47phox and p67phox, was blocked by p38 and NF-kappaB inhibitors. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 92-95 26116564-12 2015 TPA-induced induction of MMP-7 expression was suppressed by AP-1, NF-kappaB, and MAPK (ERK, p38, and JNK) inhibitors, whereas TPA-induced expression of NOX2 and its regulators, p47phox and p67phox, was blocked by p38 and NF-kappaB inhibitors. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 213-216 26116564-12 2015 TPA-induced induction of MMP-7 expression was suppressed by AP-1, NF-kappaB, and MAPK (ERK, p38, and JNK) inhibitors, whereas TPA-induced expression of NOX2 and its regulators, p47phox and p67phox, was blocked by p38 and NF-kappaB inhibitors. Tetradecanoylphorbol Acetate 126-129 mitogen-activated protein kinase 14 Homo sapiens 213-216 22310390-6 2012 When cells were treated with p38 kinase inducer, hydrogen peroxide or phorbol 12-myristate 13-acetate (PMA), U6 promoter activity was down regulated and this inhibition was reversed by p38 kinase inhibitors. Tetradecanoylphorbol Acetate 70-101 mitogen-activated protein kinase 14 Homo sapiens 29-32 25908095-2 2015 Interestingly, a massive increase of REGgamma in skin tissues or cells resulting from TPA induces activation of p38 mitogen-activated protein kinase (MAPK/p38). Tetradecanoylphorbol Acetate 86-89 mitogen-activated protein kinase 14 Homo sapiens 112-115 25908095-2 2015 Interestingly, a massive increase of REGgamma in skin tissues or cells resulting from TPA induces activation of p38 mitogen-activated protein kinase (MAPK/p38). Tetradecanoylphorbol Acetate 86-89 mitogen-activated protein kinase 14 Homo sapiens 155-158 25908095-3 2015 Blocking p38 MAPK activation prevents REGgamma elevation in HaCaT cells with TPA treatment. Tetradecanoylphorbol Acetate 77-80 mitogen-activated protein kinase 14 Homo sapiens 9-12 25908095-4 2015 AP-1, the downstream effector of MAPK/p38, directly binds to the REGgamma promoter and activates its transcription in response to TPA stimulation. Tetradecanoylphorbol Acetate 130-133 mitogen-activated protein kinase 14 Homo sapiens 38-41 25908095-6 2015 Conversely, MAPK/p38 inactivation or REGgamma deletion prevents the increase of cyclinD1 and c-Myc by TPA. Tetradecanoylphorbol Acetate 102-105 mitogen-activated protein kinase 14 Homo sapiens 17-20 24622777-7 2014 Treatment with rutin resulted in a decrease of PMA-stimulated phosphorylation of p38, extracellular regulated kinases 1/2, and c-Jun N-terminal kinase. Tetradecanoylphorbol Acetate 47-50 mitogen-activated protein kinase 14 Homo sapiens 81-84 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 mitogen-activated protein kinase 14 Homo sapiens 71-74 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 36-39 mitogen-activated protein kinase 14 Homo sapiens 67-70 23671446-11 2013 In addition, this sedative drug inhibited PMA-induced levels of phos-ERK (1.243 +-0.12, 1.108 +-0.16 and 0.903 +-0.19, respectively) and phos-p38 (1.146 +-0.10, 1.063 +-0.13 and 0.946 +-0.18, at concentrations of (5, 10 and 20 microM), respectively. Tetradecanoylphorbol Acetate 42-45 mitogen-activated protein kinase 14 Homo sapiens 142-145 23671446-12 2013 CONCLUSIONS: These results are important for understanding the mechanism of midazolam in inhibiting PMA-induced MMP expression through the signaling pathways of either NF-kappaB or ERK/p38 MAPKs down-regulation. Tetradecanoylphorbol Acetate 100-103 mitogen-activated protein kinase 14 Homo sapiens 185-188 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 38-41 mitogen-activated protein kinase 14 Homo sapiens 69-72 22310390-6 2012 When cells were treated with p38 kinase inducer, hydrogen peroxide or phorbol 12-myristate 13-acetate (PMA), U6 promoter activity was down regulated and this inhibition was reversed by p38 kinase inhibitors. Tetradecanoylphorbol Acetate 70-101 mitogen-activated protein kinase 14 Homo sapiens 185-188 22310390-6 2012 When cells were treated with p38 kinase inducer, hydrogen peroxide or phorbol 12-myristate 13-acetate (PMA), U6 promoter activity was down regulated and this inhibition was reversed by p38 kinase inhibitors. Tetradecanoylphorbol Acetate 103-106 mitogen-activated protein kinase 14 Homo sapiens 29-32 22310390-6 2012 When cells were treated with p38 kinase inducer, hydrogen peroxide or phorbol 12-myristate 13-acetate (PMA), U6 promoter activity was down regulated and this inhibition was reversed by p38 kinase inhibitors. Tetradecanoylphorbol Acetate 103-106 mitogen-activated protein kinase 14 Homo sapiens 185-188 22020547-7 2012 Our results showed that the TPA-induced up-regulation of p21 and down-regulation of p53 was reversed by UO126 (a MEK1/2 inhibitor), but not by SP600125 (a JNK inhibitor) or SB203580 (a p38 inhibitor), although TPA increased the phosphorylation of ERK and JNK in MCF-7 cells. Tetradecanoylphorbol Acetate 28-31 mitogen-activated protein kinase 14 Homo sapiens 209-212 22232712-0 2011 The Effect of Doxycycline on PMA-Induced MUC5B Expression via MMP-9 and p38 in NCI-H292 Cells. Tetradecanoylphorbol Acetate 29-32 mitogen-activated protein kinase 14 Homo sapiens 72-75 22232712-11 2011 CONCLUSION: The results of this study suggest that doxycycline inhibited PMA-induced MUC5B mRNA expression and protein production through the MMP-9 and p38 pathways in human NCI-H292 airway epithelial cells. Tetradecanoylphorbol Acetate 73-76 mitogen-activated protein kinase 14 Homo sapiens 152-155 20131957-5 2010 In addition, PMA-stimulated phosphorylation of extracellular signal regulated kinase 1/2 (ERK 1/2) was suppressed by HM treatment, whereas the phosphorylation of either c-Jun N-terminal kinase (JNK) or p38 mitogen-activated protein kinase (MAPK) was not affected. Tetradecanoylphorbol Acetate 13-16 mitogen-activated protein kinase 14 Homo sapiens 202-238 19576641-0 2011 Berberine reduces both MMP-9 and EMMPRIN expression through prevention of p38 pathway activation in PMA-induced macrophages. Tetradecanoylphorbol Acetate 100-103 mitogen-activated protein kinase 14 Homo sapiens 74-77 20869211-6 2010 TPA-induced the phosphorylation of p38 MAPK and the elongation of dendrite length, suggesting that MKK6 may be involved in this process. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 35-38 19656660-14 2009 CONCLUSIONS: GS-HCl differentially down-regulates COX-2 and MMP-13 expression in the IL-1beta- or PMA-treated human skin fibroblasts via the p38 MAPK-independent COX-2 translational inhibition and the p38 MAPK-dependent MMP-13 transcriptional suppression, respectively. Tetradecanoylphorbol Acetate 98-101 mitogen-activated protein kinase 14 Homo sapiens 141-144 20590612-7 2010 In addition, metformin strongly repressed the PMA-induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and protein kinase C(PKC)alpha, whereas the phosphorylation of p38 mitogen-activated protein kinase was not affected by metformin. Tetradecanoylphorbol Acetate 46-49 mitogen-activated protein kinase 14 Homo sapiens 215-251 19943262-0 2010 Suppression of phorbol-12-myristate-13-acetate-induced tumor cell invasion by bergamottin via the inhibition of protein kinase Cdelta/p38 mitogen-activated protein kinase and JNK/nuclear factor-kappaB-dependent matrix metalloproteinase-9 expression. Tetradecanoylphorbol Acetate 15-46 mitogen-activated protein kinase 14 Homo sapiens 134-137 19943262-7 2010 Furthermore, bergamottin strongly repressed the PMA-induced phosphorylation of p38 mitogen-activated protein kinase and c-Jun N-terminal kinase (JNK), which are dependent on the protein kinase C-delta pathway. Tetradecanoylphorbol Acetate 48-51 mitogen-activated protein kinase 14 Homo sapiens 79-82 20514473-0 2010 Suppression of phorbol-12-myristate-13-acetate-induced tumor cell invasion by apigenin via the inhibition of p38 mitogen-activated protein kinase-dependent matrix metalloproteinase-9 expression. Tetradecanoylphorbol Acetate 15-46 mitogen-activated protein kinase 14 Homo sapiens 109-112 20514473-6 2010 We found that apigenin could inhibit PMA-induced phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), which was involved in the down-regulation of the expression of matrix metalloproteinase-9 (MMP-9) at mRNA levels. Tetradecanoylphorbol Acetate 37-40 mitogen-activated protein kinase 14 Homo sapiens 68-104 20514473-6 2010 We found that apigenin could inhibit PMA-induced phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), which was involved in the down-regulation of the expression of matrix metalloproteinase-9 (MMP-9) at mRNA levels. Tetradecanoylphorbol Acetate 37-40 mitogen-activated protein kinase 14 Homo sapiens 106-114 20331435-4 2010 By using PMA and the phosphatase inhibitors cantharidin and calyculin A, we could selectively activate PKC or p38 MAPK respectively to promote TACE-dependent shedding of L-selectin. Tetradecanoylphorbol Acetate 9-12 mitogen-activated protein kinase 14 Homo sapiens 110-113 20138977-3 2010 First, we suggest that the expression of MMP-9 by TPA involves phosphorylation of IKK, p38, and PKC in hepG2. Tetradecanoylphorbol Acetate 50-53 mitogen-activated protein kinase 14 Homo sapiens 87-90 20138977-7 2010 Hesperidin suppressed TPA-stimulated NF-kappaB translocation into the nucleus through IkappaB inhibitory signaling pathways and also inhibited TPA-induced AP-1 activity by the inhibitory phosphorylation of p38 kinase and c-Jun N-terminal kinase (JNK) signaling pathways. Tetradecanoylphorbol Acetate 143-146 mitogen-activated protein kinase 14 Homo sapiens 206-209 20106976-3 2010 The level of nSMase2 phosphorylation can be modulated by treatment with anisomycin or phorbol 12-myristate 13-acetate (PMA/12-O-tetradecanoylphorbol-13-acetate), suggesting that p38 mitogen-activated protein kinase (MAPK) and protein kinases Cs are upstream of nSMase2 phosphorylation. Tetradecanoylphorbol Acetate 86-117 mitogen-activated protein kinase 14 Homo sapiens 178-214 20106976-3 2010 The level of nSMase2 phosphorylation can be modulated by treatment with anisomycin or phorbol 12-myristate 13-acetate (PMA/12-O-tetradecanoylphorbol-13-acetate), suggesting that p38 mitogen-activated protein kinase (MAPK) and protein kinases Cs are upstream of nSMase2 phosphorylation. Tetradecanoylphorbol Acetate 119-122 mitogen-activated protein kinase 14 Homo sapiens 178-214 20106976-3 2010 The level of nSMase2 phosphorylation can be modulated by treatment with anisomycin or phorbol 12-myristate 13-acetate (PMA/12-O-tetradecanoylphorbol-13-acetate), suggesting that p38 mitogen-activated protein kinase (MAPK) and protein kinases Cs are upstream of nSMase2 phosphorylation. Tetradecanoylphorbol Acetate 123-159 mitogen-activated protein kinase 14 Homo sapiens 178-214 20053683-2 2010 Here, we demonstrate that during the phorbol 12-myristate 13-acetate (PMA)-induced differentiation of HL-60 cells toward macrophages, beta-actin translocates from the cytoplasm to the nucleus and that this process is dramatically inhibited by pretreatment with p38 mitogen-activated protein kinase inhibitors. Tetradecanoylphorbol Acetate 37-68 mitogen-activated protein kinase 14 Homo sapiens 261-264 20053683-2 2010 Here, we demonstrate that during the phorbol 12-myristate 13-acetate (PMA)-induced differentiation of HL-60 cells toward macrophages, beta-actin translocates from the cytoplasm to the nucleus and that this process is dramatically inhibited by pretreatment with p38 mitogen-activated protein kinase inhibitors. Tetradecanoylphorbol Acetate 70-73 mitogen-activated protein kinase 14 Homo sapiens 261-264 19766325-8 2009 Patients with HAM/TSP had a higher p38/ERK ratio (p<0.05) associated with a reduced response to mitogens (phytohaemagglutinin or PMA+ionomycin) (p<0.001) and higher sensitivity to dexamethasone (p<0.05). Tetradecanoylphorbol Acetate 132-135 mitogen-activated protein kinase 14 Homo sapiens 35-38 19447859-7 2009 Moreover, pterostilbene can suppress TPA-induced activation of extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase, c-Jun N-terminal kinases 1/2 and phosphatidylinositol 3-kinase/Akt and protein kinase C that are upstream of NF-kappaB and AP-1. Tetradecanoylphorbol Acetate 37-40 mitogen-activated protein kinase 14 Homo sapiens 106-109 18088599-4 2008 Capillarisin has been found to suppress PMA-induced MMP-9 expression through inhibition of the NF-kappaB-dependent transcriptional activity of MMP-9 gene via p38 MAPK and JNK signaling pathways. Tetradecanoylphorbol Acetate 40-43 mitogen-activated protein kinase 14 Homo sapiens 158-161 19276187-6 2009 Interestingly, pretreatment with phorbol 12-myristate 13-acetate or transfection of MAPK/ERK kinase/ERK resulting in ERK activation completely attenuated sphingosine-induced p38 MAPK activation. Tetradecanoylphorbol Acetate 33-64 mitogen-activated protein kinase 14 Homo sapiens 174-177 19375915-5 2009 Apparently, phorbol myristate acetate (PMA) stimulated expressions of ERK, JNK and p38 were altered in the presence of potent tumour inducer, phorbol myristate acetate QAGlc, suggesting their suppression also contributes to QAGlc-mediated inhibition of MMP-9 and MMP-2. Tetradecanoylphorbol Acetate 12-37 mitogen-activated protein kinase 14 Homo sapiens 83-86 19375915-5 2009 Apparently, phorbol myristate acetate (PMA) stimulated expressions of ERK, JNK and p38 were altered in the presence of potent tumour inducer, phorbol myristate acetate QAGlc, suggesting their suppression also contributes to QAGlc-mediated inhibition of MMP-9 and MMP-2. Tetradecanoylphorbol Acetate 39-42 mitogen-activated protein kinase 14 Homo sapiens 83-86 19375915-5 2009 Apparently, phorbol myristate acetate (PMA) stimulated expressions of ERK, JNK and p38 were altered in the presence of potent tumour inducer, phorbol myristate acetate QAGlc, suggesting their suppression also contributes to QAGlc-mediated inhibition of MMP-9 and MMP-2. Tetradecanoylphorbol Acetate 142-167 mitogen-activated protein kinase 14 Homo sapiens 83-86 19279008-3 2009 Inhibition of ceramide formation by fumonisin B1 or down-regulation of PKCdelta potentiated PMA-induced activation of p38 in human breast cancer MCF-7 cells. Tetradecanoylphorbol Acetate 92-95 mitogen-activated protein kinase 14 Homo sapiens 118-121 18575777-6 2008 It also inhibited p38 phosphorylation in transfected K562 cells treated with TPA. Tetradecanoylphorbol Acetate 77-80 mitogen-activated protein kinase 14 Homo sapiens 18-21 18090122-5 2007 Sulforaphane upregulates p38 in MCF-7 cells and prevented TPA-reduced phosphorylation of p38 in M13SV1 cells, but activated caspase-7 associated with apoptosis in MCF-7 cells. Tetradecanoylphorbol Acetate 58-61 mitogen-activated protein kinase 14 Homo sapiens 89-92 17964626-6 2008 Here, we report that, besides the MEK/ERK pathway, the JNK and p38 MAPK pathways also mediate TPA-induced KSHV reactivation from latency. Tetradecanoylphorbol Acetate 94-97 mitogen-activated protein kinase 14 Homo sapiens 63-66 17964626-8 2008 TPA treatment enhanced the levels of activated ERK and p38 but not those of activated JNK. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 55-58 17982670-9 2007 These results suggest that TPA induces the expression of B7-DC, -H1, -H2, and -H3 mRNA in K562 cells via activation of PKC, ERK, p38 MAPK, and NF-kappaB. Tetradecanoylphorbol Acetate 27-30 mitogen-activated protein kinase 14 Homo sapiens 129-132 17600309-1 2007 We previously showed that the MUC5B gene expression was elevated by phorbol 12-myristate 13-acetate (PMA) through an epidermal growth factor receptor-independent Ras/MEKK1/JNK and P38 signaling-based transcriptional mechanism. Tetradecanoylphorbol Acetate 68-99 mitogen-activated protein kinase 14 Homo sapiens 180-183 17982698-5 2007 MAP kinase p38 was shown to be activated in HNSCC by phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 53-84 mitogen-activated protein kinase 14 Homo sapiens 11-14 17600309-1 2007 We previously showed that the MUC5B gene expression was elevated by phorbol 12-myristate 13-acetate (PMA) through an epidermal growth factor receptor-independent Ras/MEKK1/JNK and P38 signaling-based transcriptional mechanism. Tetradecanoylphorbol Acetate 101-104 mitogen-activated protein kinase 14 Homo sapiens 180-183 17468105-7 2007 In addition, we have found that the p38 mitogen-activated protein kinase is required for BRG1 recruitment in TPA-mediated myogenin induction. Tetradecanoylphorbol Acetate 109-112 mitogen-activated protein kinase 14 Homo sapiens 36-39 17640620-1 2007 We investigated the mechanism of phorbol 12-myristate 13-acetate (PMA)-induced migration of glioblastoma cells focusing on the p38 mitogen-activated protein kinase (MAPK)/heat shock protein 27 (Hsp27) pathway. Tetradecanoylphorbol Acetate 33-64 mitogen-activated protein kinase 14 Homo sapiens 127-163 17640620-1 2007 We investigated the mechanism of phorbol 12-myristate 13-acetate (PMA)-induced migration of glioblastoma cells focusing on the p38 mitogen-activated protein kinase (MAPK)/heat shock protein 27 (Hsp27) pathway. Tetradecanoylphorbol Acetate 66-69 mitogen-activated protein kinase 14 Homo sapiens 127-163 17982670-3 2007 TPA also induced activation of ERK, p38 mitogen-activated protein kinase (MAPK), JNK, phosphatidylinositol-3-kinase (PI-3K), or nuclear factor (NF)-kappaB. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 36-72 17982670-4 2007 Pre-treatments with protein kinase C (PKC) inhibitors significantly inhibited TPA-induced expression of B7-DC, -H1, -H2, and -H3 mRNA as well as TPA-induced phosphorylation of ERK, p38 MAPK, JNK, and PI-3K. Tetradecanoylphorbol Acetate 78-81 mitogen-activated protein kinase 14 Homo sapiens 181-184 17982670-4 2007 Pre-treatments with protein kinase C (PKC) inhibitors significantly inhibited TPA-induced expression of B7-DC, -H1, -H2, and -H3 mRNA as well as TPA-induced phosphorylation of ERK, p38 MAPK, JNK, and PI-3K. Tetradecanoylphorbol Acetate 145-148 mitogen-activated protein kinase 14 Homo sapiens 181-184 17982670-5 2007 TPA-induced expression of B7-DC, -H1, -H2, and -H3 mRNA was abrogated by pre-treatments with inhibitors of ERK and p38 MAPK. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 115-118 17468105-8 2007 We propose that there are two distinct activation steps for the induction of myogenin in TPA-induced early differentiation of RD cells: 1) an early step that requires PCAF activity to acetylate core histones and MyoD to initiate myogenin gene expression, and 2) a later step that requires p38-dependent activity of the SWI/SNF remodeling complex to provide an open conformation for the induction of myogenin. Tetradecanoylphorbol Acetate 89-92 mitogen-activated protein kinase 14 Homo sapiens 289-292 17200179-5 2007 Regarding downstream transduction, PMA-induced MUC5B expression was sensitive to inhibitors and dominant-negative expression of signaling molecules involved in Ras/mitogen-activated protein kinase/extracellular signal-regulated kinase kinase kinase1-mediated c-Jun N-terminal kinase and p38 pathways. Tetradecanoylphorbol Acetate 35-38 mitogen-activated protein kinase 14 Homo sapiens 287-290 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 14 Homo sapiens 207-210 17013757-6 2006 TPA addition induces the phosphorylation of JNKs and ERKs, but not p38, protein in HL-60 cells, and incubation of HL-60 cells with JNKs inhibitor SP600125, but not ERKs inhibitor, PD98059 or the p38 inhibitor SB203580, suppressed the protective effect of TPA against BE-induced apoptotic events including DNA ladders, apoptotic bodies, caspase 3 and D4-GDI protein cleavage in according with blocking JNKs protein phosphorylation. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 195-198 14984736-9 2004 When HEK-293 cells expressed either PLD1 or PLD2, we observed elevated p38 phosphorylation in response to TPA stimulation. Tetradecanoylphorbol Acetate 106-109 mitogen-activated protein kinase 14 Homo sapiens 71-74 15936242-5 2005 Blockade of the p38 mitogen-activated protein kinase pathway by SB203580 also suppressed 12-O-tetradecanoylphorbol-13-acetate-induced aldose reductase expression. Tetradecanoylphorbol Acetate 89-125 mitogen-activated protein kinase 14 Homo sapiens 16-19 15936242-10 2005 A p38 mitogen-activated protein kinase pathway, distinct from the tyrosine kinase pathway, may also take part in 12-O-tetradecanoylphorbol-13-acetate-induced increase in aldose reductase gene expression. Tetradecanoylphorbol Acetate 113-149 mitogen-activated protein kinase 14 Homo sapiens 2-5 16044407-9 2005 Chemical inhibitors of MEK (PD98059), p38 (SB202190), but not JNK (SP600125) blocked TPA induction of COX-2 although apigenin did not inhibit TPA-mediated COX-2 expression through these pathways. Tetradecanoylphorbol Acetate 85-88 mitogen-activated protein kinase 14 Homo sapiens 38-41 15944151-7 2005 At low concentrations, chlorogenic acid decreased the phosphorylation of c-Jun NH2-terminal kinases, p38 kinase, and MAPK kinase 4 induced by UVB/12-O-tetradecanoylphorbol-13-acetate, yet higher doses were required to inhibit extracellular signal-regulated kinases. Tetradecanoylphorbol Acetate 146-182 mitogen-activated protein kinase 14 Homo sapiens 101-104 15611126-8 2005 Investigation of PMA-induced events required for LNCaP and C4-2 apoptosis revealed that p38 activation is dependent on PKCdelta, whereas induction of retinoblastoma protein hypophosphorylation requires both PKC signaling pathways and is downstream of p38 activation in the PKCdelta pathway. Tetradecanoylphorbol Acetate 17-20 mitogen-activated protein kinase 14 Homo sapiens 88-91 15479821-9 2004 Our present study demonstrates for the first time that either p38 or c-myc siRNA can efficiently inhibit TPA-induced EBV reactivation in GT38 cells, indicating that p38- and/or c-myc-associated signaling pathways may play critical roles in the disruption of EBV latency by TPA. Tetradecanoylphorbol Acetate 105-108 mitogen-activated protein kinase 14 Homo sapiens 165-168 15479821-9 2004 Our present study demonstrates for the first time that either p38 or c-myc siRNA can efficiently inhibit TPA-induced EBV reactivation in GT38 cells, indicating that p38- and/or c-myc-associated signaling pathways may play critical roles in the disruption of EBV latency by TPA. Tetradecanoylphorbol Acetate 273-276 mitogen-activated protein kinase 14 Homo sapiens 165-168 15324351-8 2004 Tyrosine kinase inhibitor herbimycin A reduced MMP-1 production induced by PMA, whereas the p38 MAPK-inhibitor SB 203580 synergistically increased the stimulatory effect of PMA on both MMP-1 and TIMP-1 production. Tetradecanoylphorbol Acetate 173-176 mitogen-activated protein kinase 14 Homo sapiens 92-95 15232218-6 2004 Rottlerin also inhibited PMA-induced phosphorylation of p38 mitogen-activated protein kinase (p38MAPK), and the p38 MAPK inhibitor SB203580 inhibited induction of RANK. Tetradecanoylphorbol Acetate 25-28 mitogen-activated protein kinase 14 Homo sapiens 56-92 15232218-6 2004 Rottlerin also inhibited PMA-induced phosphorylation of p38 mitogen-activated protein kinase (p38MAPK), and the p38 MAPK inhibitor SB203580 inhibited induction of RANK. Tetradecanoylphorbol Acetate 25-28 mitogen-activated protein kinase 14 Homo sapiens 94-101 15232218-6 2004 Rottlerin also inhibited PMA-induced phosphorylation of p38 mitogen-activated protein kinase (p38MAPK), and the p38 MAPK inhibitor SB203580 inhibited induction of RANK. Tetradecanoylphorbol Acetate 25-28 mitogen-activated protein kinase 14 Homo sapiens 56-59 15041541-4 2004 PMA treatment caused an increase in extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) activities. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 116-152 15041541-4 2004 PMA treatment caused an increase in extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) activities. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 154-162 16149074-8 2005 The pretreatment with SB202190, an inhibitor for p38 mitogen-activated protein kinase pathway (p38-MAPK), but not other signaling inhibitors, reversed the PMA-induced repression. Tetradecanoylphorbol Acetate 155-158 mitogen-activated protein kinase 14 Homo sapiens 49-85 16149074-8 2005 The pretreatment with SB202190, an inhibitor for p38 mitogen-activated protein kinase pathway (p38-MAPK), but not other signaling inhibitors, reversed the PMA-induced repression. Tetradecanoylphorbol Acetate 155-158 mitogen-activated protein kinase 14 Homo sapiens 95-103 16102725-6 2005 Furthermore, curcumin strongly repressed the PMA-induced phosphorylation of ERK, JNK, and p38 MAP kinase, which were dependent on the PKC pathway. Tetradecanoylphorbol Acetate 45-48 mitogen-activated protein kinase 14 Homo sapiens 90-93 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 14 Homo sapiens 182-185 15707584-4 2005 We report that three distinct MAPKs, ERK, JNK, and p38, are activated during the TPA-induced megakaryocytic differentiation. Tetradecanoylphorbol Acetate 81-84 mitogen-activated protein kinase 14 Homo sapiens 51-54 15611126-8 2005 Investigation of PMA-induced events required for LNCaP and C4-2 apoptosis revealed that p38 activation is dependent on PKCdelta, whereas induction of retinoblastoma protein hypophosphorylation requires both PKC signaling pathways and is downstream of p38 activation in the PKCdelta pathway. Tetradecanoylphorbol Acetate 17-20 mitogen-activated protein kinase 14 Homo sapiens 251-254 15543559-7 2005 Moreover, forskolin reduced the p38 MAP kinase phosphorylation induced by the 12-O-tetradecanoylphorbol-13-acetate (TPA), a PKC-activating phorbol ester, and significantly suppressed the TPA-stimulated accumulation of HSP27. Tetradecanoylphorbol Acetate 78-114 mitogen-activated protein kinase 14 Homo sapiens 32-35 15543559-7 2005 Moreover, forskolin reduced the p38 MAP kinase phosphorylation induced by the 12-O-tetradecanoylphorbol-13-acetate (TPA), a PKC-activating phorbol ester, and significantly suppressed the TPA-stimulated accumulation of HSP27. Tetradecanoylphorbol Acetate 116-119 mitogen-activated protein kinase 14 Homo sapiens 32-35 15263067-6 2004 CD3/CD28- or phorbol 12-myristate 13-acetate (PMA)/ionomycin-induced p38 and extracellular signal-regulated kinase 1/2 phosphorylation or c-jun NH2-terminal kinase (JNK) 1/2 kinase activity was significantly diminished by pentobarbital, thiamylal, secobarbital, or methohexital treatment. Tetradecanoylphorbol Acetate 13-44 mitogen-activated protein kinase 14 Homo sapiens 69-72 15263067-6 2004 CD3/CD28- or phorbol 12-myristate 13-acetate (PMA)/ionomycin-induced p38 and extracellular signal-regulated kinase 1/2 phosphorylation or c-jun NH2-terminal kinase (JNK) 1/2 kinase activity was significantly diminished by pentobarbital, thiamylal, secobarbital, or methohexital treatment. Tetradecanoylphorbol Acetate 46-49 mitogen-activated protein kinase 14 Homo sapiens 69-72 15479821-2 2004 In this study, we found that TPA up-regulated phosphorylation of p38, a mitogen-activated protein kinase, and activated c-myc mRNA in EBV-positive epithelial GT38 cells. Tetradecanoylphorbol Acetate 29-32 mitogen-activated protein kinase 14 Homo sapiens 65-68 15479821-5 2004 The p38 inhibitor SB203580 blocked both p38 phosphorylation and ZEBRA expression by TPA. Tetradecanoylphorbol Acetate 84-87 mitogen-activated protein kinase 14 Homo sapiens 4-7 15479821-9 2004 Our present study demonstrates for the first time that either p38 or c-myc siRNA can efficiently inhibit TPA-induced EBV reactivation in GT38 cells, indicating that p38- and/or c-myc-associated signaling pathways may play critical roles in the disruption of EBV latency by TPA. Tetradecanoylphorbol Acetate 105-108 mitogen-activated protein kinase 14 Homo sapiens 62-65 15329596-0 2004 Sevoflurane inhibits phorbol-myristate-acetate-induced activator protein-1 activation in human T lymphocytes in vitro: potential role of the p38-stress kinase pathway. Tetradecanoylphorbol Acetate 21-46 mitogen-activated protein kinase 14 Homo sapiens 141-144 14610070-4 2004 In addition TPA decreased the intracellular GSH content, caused ERK activation, and potentiated the As(2)O(3)-provoked activation of p38 and JNK. Tetradecanoylphorbol Acetate 12-15 mitogen-activated protein kinase 14 Homo sapiens 133-136 14757441-5 2004 Furthermore, when HL-60 myeloid leukemic cells were differentiated with phorbol ester (TPA), PBK/TOPK protein expression was strongly down-regulated by 24 h. Under these same conditions, phosphorylated c-Myc was rapidly down-regulated (by 4 h), while the levels of cyclin D1 and phosphorylated p38 were constant. Tetradecanoylphorbol Acetate 87-90 mitogen-activated protein kinase 14 Homo sapiens 294-297 12801911-6 2003 Also, nuclear translocation of ERK induced by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was inhibited by SB 239063, which does not associate with c-Raf and is highly selective for p38 MAP kinase. Tetradecanoylphorbol Acetate 46-83 mitogen-activated protein kinase 14 Homo sapiens 182-185 12758252-6 2003 Using human primary lymphocytes and Jurkat CD4(+) T cells stimulated with PMA/ionomycin, we demonstrate activation (phosphorylation) of JNK and p38, which is further confirmed by two additional established techniques (WB and confocal microscopy). Tetradecanoylphorbol Acetate 74-77 mitogen-activated protein kinase 14 Homo sapiens 144-147 12919900-1 2003 OBJECTIVE: To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathways in regulating the in vitro invasion of JAR human choriocarcinoma cells induced by phorbol 12-myristate 13-acetate (PMA). Tetradecanoylphorbol Acetate 193-224 mitogen-activated protein kinase 14 Homo sapiens 38-41 12801911-6 2003 Also, nuclear translocation of ERK induced by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was inhibited by SB 239063, which does not associate with c-Raf and is highly selective for p38 MAP kinase. Tetradecanoylphorbol Acetate 85-88 mitogen-activated protein kinase 14 Homo sapiens 182-185 12801911-7 2003 In addition, the forced expression of the dominant negative mutant of p38 MAP kinase suppressed serum responsive element-dependent transactivation induced by TPA. Tetradecanoylphorbol Acetate 158-161 mitogen-activated protein kinase 14 Homo sapiens 70-73 12039887-13 2002 PMA phosphorylated both p38 and p44/42 MAPK. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 24-27 12592382-2 2003 Western blot of three activated forms of mitogen-activated protein kinase (MAPK) (p-ERK, p-JNK and p-p38) demonstrated that phosphorylation of ERK is dramatically induced (11.6-fold ) by TPA during 15 min to 1 h and significantly induced (2.5-fold) by Saikosaponin alpha at 30 min, whereas phosphorylation of JNK was induced only by TPA during 30 min to 1 h. Phosphorylation of p38 was not induced by either drug. Tetradecanoylphorbol Acetate 187-190 mitogen-activated protein kinase 14 Homo sapiens 101-104 12592382-2 2003 Western blot of three activated forms of mitogen-activated protein kinase (MAPK) (p-ERK, p-JNK and p-p38) demonstrated that phosphorylation of ERK is dramatically induced (11.6-fold ) by TPA during 15 min to 1 h and significantly induced (2.5-fold) by Saikosaponin alpha at 30 min, whereas phosphorylation of JNK was induced only by TPA during 30 min to 1 h. Phosphorylation of p38 was not induced by either drug. Tetradecanoylphorbol Acetate 187-190 mitogen-activated protein kinase 14 Homo sapiens 378-381 11312276-4 2001 TPA treatment leads to the rapid activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK), the inactivation of p38 mitogen-activated protein kinase (MAPK), and the downregulation of PKCdelta. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 148-184 11756226-8 2002 PMA-induced COX-2 expression in both transformed and CYP2E1-expressing cells resulted from an induction in COX-2 mRNA, and was dependent on extracellular signal-regulated kinase, p38 mitogen-activated protein kinase and phosphatidylinositol 3-kinase. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 179-182 11532081-19 2001 Phorbol ester (PMA) treatment stimulated a twofold increase in p38 MAPK activity. Tetradecanoylphorbol Acetate 15-18 mitogen-activated protein kinase 14 Homo sapiens 63-66 11489969-7 2001 Stimulatory activity of TPA on HCMV replication was suppressed by protein kinase C inhibitors and inhibitors of p42/44 and p38 mitogen-activated protein kinases but not by NF-kappaB inhibitors. Tetradecanoylphorbol Acetate 24-27 mitogen-activated protein kinase 14 Homo sapiens 123-126 11716547-4 2001 We have previously demonstrated that the tumor promoter TPA can induce MMP-9 expression via a third signaling cascade, the p38 pathway. Tetradecanoylphorbol Acetate 56-59 mitogen-activated protein kinase 14 Homo sapiens 123-126 11716547-5 2001 Considering that TPA is a potent activator of AP-1, we hypothesized that this transcription factor might also be required for p38 pathway-dependent MMP-9 regulation. Tetradecanoylphorbol Acetate 17-20 mitogen-activated protein kinase 14 Homo sapiens 126-129 11461775-8 2001 Further, the vitamin was able to amplify the PMA-dependent induction of p38 and pJNK. Tetradecanoylphorbol Acetate 45-48 mitogen-activated protein kinase 14 Homo sapiens 72-75 11312276-6 2001 Both p38 MAPK inactivation and JNK activation appear to be downstream of ERK because an agent that blocks ERK activation also blocks the modulation of these other MAP kinase family members by TPA treatment. Tetradecanoylphorbol Acetate 192-195 mitogen-activated protein kinase 14 Homo sapiens 5-8 11388701-7 2001 GF109203X, a protein kinase C inhibitor, and prolonged treatment with phorbol 12-myristate 13-acetate partially inhibited p38 MAPK activation. Tetradecanoylphorbol Acetate 70-101 mitogen-activated protein kinase 14 Homo sapiens 122-125 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 14 Homo sapiens 79-82 10811116-6 2000 Ursolic acid inhibited PMA-mediated activation of protein kinase C, extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase, and p38 mitogen-activated protein kinases. Tetradecanoylphorbol Acetate 23-26 mitogen-activated protein kinase 14 Homo sapiens 140-143 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 mitogen-activated protein kinase 14 Homo sapiens 123-126 9933633-8 1999 Selective inhibition of one or more MAPK pathways impairs TNF-alpha induction by TPA/ionomycin, indicating a cooperation between these signal transduction pathways. Tetradecanoylphorbol Acetate 81-84 mitogen-activated protein kinase 14 Homo sapiens 36-40 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 14 Homo sapiens 216-219 10362531-1 1999 Activation of the neutrophil NADPH oxidase by either the bacterial peptide fMLP or phorbol myristate acetate (PMA) is partially suppressed by SB 203580, a specific inhibitor of the MAP kinase family member, SAPK2/p38. Tetradecanoylphorbol Acetate 83-108 mitogen-activated protein kinase 14 Homo sapiens 213-216 10362531-1 1999 Activation of the neutrophil NADPH oxidase by either the bacterial peptide fMLP or phorbol myristate acetate (PMA) is partially suppressed by SB 203580, a specific inhibitor of the MAP kinase family member, SAPK2/p38. Tetradecanoylphorbol Acetate 110-113 mitogen-activated protein kinase 14 Homo sapiens 213-216 10051531-5 1999 Marked or slight activation, respectively, of p44/42 MAPK or p38 was also seen after 10-min treatment with 12-O-tetradecanoylphorbol-13-acetate, but c-Jun NH2-terminal kinase activation did not occur. Tetradecanoylphorbol Acetate 107-143 mitogen-activated protein kinase 14 Homo sapiens 61-64 9515796-4 1998 We found that inhibition of p38 by SB 203580 resulted in the almost complete reduction of phorbol myristate acetate-induced MMP-9 secretion but not of urokinase-type plasminogen activator secretion. Tetradecanoylphorbol Acetate 90-115 mitogen-activated protein kinase 14 Homo sapiens 28-31 9553058-4 1998 TPA/ionomycin treatment of T cells stimulates both mitogen-activated ERK, as well as the stress-activated mitogen-activated protein kinase family members JNK/SAPK and p38. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 14 Homo sapiens 167-170 9515796-0 1998 Inhibition of the p38 mitogen-activated protein kinase by SB 203580 blocks PMA-induced Mr 92,000 type IV collagenase secretion and in vitro invasion. Tetradecanoylphorbol Acetate 75-78 mitogen-activated protein kinase 14 Homo sapiens 18-21 33386632-7 2021 CS-DPSCs showed a lower phosphorylation rate of p38 and p44/42 in PMA-treated cells than healthy donor DPSCs compared with untreated control cells. Tetradecanoylphorbol Acetate 66-69 mitogen-activated protein kinase 14 Homo sapiens 48-51 32140039-0 2020 Eupatilin downregulates phorbol 12-myristate 13-acetate-induced MUC5AC expression via inhibition of p38/ERK/JNK MAPKs signal pathway in human airway epithelial cells. Tetradecanoylphorbol Acetate 24-55 mitogen-activated protein kinase 14 Homo sapiens 100-103 30518116-5 2018 We concluded that CGA isomers exert anti-inflammatory activity in a mixture of interferon gamma (IFNgamma) and phorbol myristate acetate (PMA)-challenged Caco-2 cells, by decreasing the phosphorylation of p38 cascade and up-regulating NFkappaB signaling. Tetradecanoylphorbol Acetate 111-136 mitogen-activated protein kinase 14 Homo sapiens 205-208 32736685-9 2020 In conclusion, the deletion of Prx I triggered the DMBA/TPA-induced skin tumor formation in vivo and in vitro by regulating the reactive oxygen species (ROS)-p38 mitogen-activated protein kinase (MAPK) pathway. Tetradecanoylphorbol Acetate 56-59 mitogen-activated protein kinase 14 Homo sapiens 158-194 30871060-9 2019 GA also inhibited the PMA-induced phosphorylation of IkappaB kinase alpha/beta (IKKalpha/beta), c-Jun N-terminal kinase (JNK) and p38 proteins (P38), suggesting that IKKalpha/beta, JNK and P38 activation is dependent on PKC activity. Tetradecanoylphorbol Acetate 22-25 mitogen-activated protein kinase 14 Homo sapiens 130-133 30871060-9 2019 GA also inhibited the PMA-induced phosphorylation of IkappaB kinase alpha/beta (IKKalpha/beta), c-Jun N-terminal kinase (JNK) and p38 proteins (P38), suggesting that IKKalpha/beta, JNK and P38 activation is dependent on PKC activity. Tetradecanoylphorbol Acetate 22-25 mitogen-activated protein kinase 14 Homo sapiens 144-147 30871060-9 2019 GA also inhibited the PMA-induced phosphorylation of IkappaB kinase alpha/beta (IKKalpha/beta), c-Jun N-terminal kinase (JNK) and p38 proteins (P38), suggesting that IKKalpha/beta, JNK and P38 activation is dependent on PKC activity. Tetradecanoylphorbol Acetate 22-25 mitogen-activated protein kinase 14 Homo sapiens 189-192 30590137-0 2019 Suppression of PMA-induced human fibrosarcoma HT-1080 invasion and metastasis by kahweol via inhibiting Akt/JNK1/2/p38 MAPK signal pathway and NF-kappaB dependent transcriptional activities. Tetradecanoylphorbol Acetate 15-18 mitogen-activated protein kinase 14 Homo sapiens 115-118 30590137-8 2019 KA repressed the PMA-induced phosphorylation of Akt, c-Jun N-terminal kinase (JNK) 1/2, and p38 MAPK, which are signaling molecules upstream of MMP-9 expression. Tetradecanoylphorbol Acetate 17-20 mitogen-activated protein kinase 14 Homo sapiens 92-95 30665329-11 2019 The combination of ERK and p38 inhibitors completely reversed the effects of PMA ( P <0.05). Tetradecanoylphorbol Acetate 77-80 mitogen-activated protein kinase 14 Homo sapiens 27-30 30518116-5 2018 We concluded that CGA isomers exert anti-inflammatory activity in a mixture of interferon gamma (IFNgamma) and phorbol myristate acetate (PMA)-challenged Caco-2 cells, by decreasing the phosphorylation of p38 cascade and up-regulating NFkappaB signaling. Tetradecanoylphorbol Acetate 138-141 mitogen-activated protein kinase 14 Homo sapiens 205-208 30545441-5 2018 Also, Tat-ATOX1 protein markedly inhibited LPS- and TPA-induced inflammatory responses by decreasing cyclooxygenase- 2 (COX-2) and inducible nitric oxide synthase (iNOS) and further inhibited phosphorylation of mitogen activated protein kinases (MAPKs; JNK, ERK and p38) and the nuclear factor-kappaB (NF-kappaB) signaling pathway. Tetradecanoylphorbol Acetate 52-55 mitogen-activated protein kinase 14 Homo sapiens 266-269 29601810-10 2018 On the contrary, phorbol 12-myristate 13-acetate (PMA)-induced phosphorylation of Src, AKT, P38, PKC and membrane localization of p47ph x and P40ph x remained unaffected. Tetradecanoylphorbol Acetate 17-48 mitogen-activated protein kinase 14 Homo sapiens 92-95 29601810-10 2018 On the contrary, phorbol 12-myristate 13-acetate (PMA)-induced phosphorylation of Src, AKT, P38, PKC and membrane localization of p47ph x and P40ph x remained unaffected. Tetradecanoylphorbol Acetate 50-53 mitogen-activated protein kinase 14 Homo sapiens 92-95