PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25157570-6 2014 Mechanistically, [6]-gingerol down-regulated Phorbol Myristate Acetate (PMA) induced phosphorylation of ERK1/2 and JNK MAP kinases and activation of AP-1 transcription factor, but had only little effects on phosphorylation of p38 MAP kinase and activation of NF-kappa B. Tetradecanoylphorbol Acetate 45-70 mitogen-activated protein kinase 8 Homo sapiens 115-118 25533502-6 2015 In vitro, butein inhibited the phosphorylation of c-Jun, binding to GST beads, mediated by JNK isolated from PMA-treated cells. Tetradecanoylphorbol Acetate 109-112 mitogen-activated protein kinase 8 Homo sapiens 91-94 25157570-6 2014 Mechanistically, [6]-gingerol down-regulated Phorbol Myristate Acetate (PMA) induced phosphorylation of ERK1/2 and JNK MAP kinases and activation of AP-1 transcription factor, but had only little effects on phosphorylation of p38 MAP kinase and activation of NF-kappa B. Tetradecanoylphorbol Acetate 72-75 mitogen-activated protein kinase 8 Homo sapiens 115-118 25540590-6 2014 With respect to signaling, TPA led to an early, strong, and relatively transient extracellular signal-regulated kinase (ERK)1/2 phosphorylation, and a less marked and even more transient phosphorylation of c-jun-N-terminal kinases (JNK1/2) and p38. Tetradecanoylphorbol Acetate 27-30 mitogen-activated protein kinase 8 Homo sapiens 232-238 25157570-7 2014 Additionally, it complemented the inhibitors of either ERK1/2 or JNK MAP kinase in bringing down the PMA-induced cell proliferation in SW-480 cells. Tetradecanoylphorbol Acetate 101-104 mitogen-activated protein kinase 8 Homo sapiens 65-68 24796531-6 2014 c-Jun increased expression of SPPR3 mainly via a PKC/JNK pathway in response to TPA in KYSE450 cells. Tetradecanoylphorbol Acetate 80-83 mitogen-activated protein kinase 8 Homo sapiens 53-56 23900581-8 2013 In addition, the knockdown of JNK-1 expression by siRNA-JNK-1 or siRNA-JNK-2 significantly impaired the upregulation of AP-1 luciferase reporter gene, but failed to decrease the levels of AP-1 reporter gene expression induced by TPA treatment. Tetradecanoylphorbol Acetate 229-232 mitogen-activated protein kinase 8 Homo sapiens 30-35 23884236-8 2013 In addition, treatment with ESM resulted in a reduction of PMA-stimulated phosphorylation of p38, extracellular regulated kinases (ERK) 1/2, and c-Jun N-terminal kinase (JNK). Tetradecanoylphorbol Acetate 59-62 mitogen-activated protein kinase 8 Homo sapiens 145-168 23884236-8 2013 In addition, treatment with ESM resulted in a reduction of PMA-stimulated phosphorylation of p38, extracellular regulated kinases (ERK) 1/2, and c-Jun N-terminal kinase (JNK). Tetradecanoylphorbol Acetate 59-62 mitogen-activated protein kinase 8 Homo sapiens 170-173 24433534-6 2014 Gen suppressed TPA-induced AP-1 activity through inhibitory phosphorylation of extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways, and TPA-stimulated inhibition of NF-kappaB nuclear translocation through IkappaB inhibitory signaling pathways. Tetradecanoylphorbol Acetate 15-18 mitogen-activated protein kinase 8 Homo sapiens 125-148 24433534-6 2014 Gen suppressed TPA-induced AP-1 activity through inhibitory phosphorylation of extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways, and TPA-stimulated inhibition of NF-kappaB nuclear translocation through IkappaB inhibitory signaling pathways. Tetradecanoylphorbol Acetate 15-18 mitogen-activated protein kinase 8 Homo sapiens 150-153 23715767-7 2013 Suppression of Egr-1 expression by siRNA abrogated the ability of TPA to induce Egr-1 and JNK-1 activities, moderately increasing the p21 activity and abrogating the anti-apoptotic effect of Egr-1 observed in the prostate cancer cell lines. Tetradecanoylphorbol Acetate 66-69 mitogen-activated protein kinase 8 Homo sapiens 90-95 23774263-8 2013 In addition, RA reduced PMA-stimulated phosphorylation of p38, extracellular regulated kinases (ERK) 1/2, and c-Jun N-terminal kinase (JNK). Tetradecanoylphorbol Acetate 24-27 mitogen-activated protein kinase 8 Homo sapiens 110-133 23774263-8 2013 In addition, RA reduced PMA-stimulated phosphorylation of p38, extracellular regulated kinases (ERK) 1/2, and c-Jun N-terminal kinase (JNK). Tetradecanoylphorbol Acetate 24-27 mitogen-activated protein kinase 8 Homo sapiens 135-138 23715767-6 2013 The expression of Egr-1, p21 and JNK was strongly increased after treatment of the cells with TPA, tumor necrosis factor-alpha (TNF-alpha) or arsenite. Tetradecanoylphorbol Acetate 94-97 mitogen-activated protein kinase 8 Homo sapiens 33-36 23490067-5 2013 Furthermore, activation of extracellular-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) by TPA+AA was identified in HL-60 cells, and the ERK inhibitor, PD98059, but not the JNK inhibitor, SP600125, inhibited TPA+AA-induced NBT-positive cells. Tetradecanoylphorbol Acetate 218-221 mitogen-activated protein kinase 8 Homo sapiens 68-91 23490067-5 2013 Furthermore, activation of extracellular-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) by TPA+AA was identified in HL-60 cells, and the ERK inhibitor, PD98059, but not the JNK inhibitor, SP600125, inhibited TPA+AA-induced NBT-positive cells. Tetradecanoylphorbol Acetate 101-104 mitogen-activated protein kinase 8 Homo sapiens 68-91 23726966-7 2013 In addition, persicarin and I3G reduced PMA-stimulated phosphorylation of p38MAPK, extracellular regulated kinases (ERK) 1/2, and c-Jun N-terminal kinase (JNK). Tetradecanoylphorbol Acetate 40-43 mitogen-activated protein kinase 8 Homo sapiens 130-153 23726966-7 2013 In addition, persicarin and I3G reduced PMA-stimulated phosphorylation of p38MAPK, extracellular regulated kinases (ERK) 1/2, and c-Jun N-terminal kinase (JNK). Tetradecanoylphorbol Acetate 40-43 mitogen-activated protein kinase 8 Homo sapiens 155-158 23490067-5 2013 Furthermore, activation of extracellular-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) by TPA+AA was identified in HL-60 cells, and the ERK inhibitor, PD98059, but not the JNK inhibitor, SP600125, inhibited TPA+AA-induced NBT-positive cells. Tetradecanoylphorbol Acetate 101-104 mitogen-activated protein kinase 8 Homo sapiens 93-96 23490067-5 2013 Furthermore, activation of extracellular-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) by TPA+AA was identified in HL-60 cells, and the ERK inhibitor, PD98059, but not the JNK inhibitor, SP600125, inhibited TPA+AA-induced NBT-positive cells. Tetradecanoylphorbol Acetate 218-221 mitogen-activated protein kinase 8 Homo sapiens 93-96 22503685-5 2012 In addition, PMA-induced phosphorylation of ERK1/2 and JNK were suppressed by JNP3 treatment, whereas the phosphorylation of p38 MAPK was not affected by JNP3. Tetradecanoylphorbol Acetate 13-16 mitogen-activated protein kinase 8 Homo sapiens 55-58 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 8 Homo sapiens 77-80 22314224-6 2012 By transient transfection analysis with the MMP-1 promoter (-2846 to -29 nt) and AP-1 promoter, MMP-1 and AP-1 promoter activities were induced by phorbol myristate acetate (PMA) but were significantly inhibited by PD98059 (ERK1/2 inhibitor) or SP600125 (JNK inhibitor). Tetradecanoylphorbol Acetate 147-172 mitogen-activated protein kinase 8 Homo sapiens 255-258 22314224-6 2012 By transient transfection analysis with the MMP-1 promoter (-2846 to -29 nt) and AP-1 promoter, MMP-1 and AP-1 promoter activities were induced by phorbol myristate acetate (PMA) but were significantly inhibited by PD98059 (ERK1/2 inhibitor) or SP600125 (JNK inhibitor). Tetradecanoylphorbol Acetate 174-177 mitogen-activated protein kinase 8 Homo sapiens 255-258 22200849-6 2012 In addition, Jurkat T cells, transfected with various expression plasmids and/or stimulated with TPA, UV or ionomycin strongly induced the c-Jun N-terminal kinase (JNK) and p38, whereas the extracellular signal-regulated kinase (ERK)-1/2 kinase pathway was weekly activated. Tetradecanoylphorbol Acetate 97-100 mitogen-activated protein kinase 8 Homo sapiens 139-162 22200849-6 2012 In addition, Jurkat T cells, transfected with various expression plasmids and/or stimulated with TPA, UV or ionomycin strongly induced the c-Jun N-terminal kinase (JNK) and p38, whereas the extracellular signal-regulated kinase (ERK)-1/2 kinase pathway was weekly activated. Tetradecanoylphorbol Acetate 97-100 mitogen-activated protein kinase 8 Homo sapiens 164-167 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 8 Homo sapiens 194-197 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 8 Homo sapiens 179-182 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 8 Homo sapiens 291-294 21804018-8 2011 IRAK1/4 inhibitors, their small interfering RNAs, and JNK inhibitor also attenuated PMA-induced IL-1beta production. Tetradecanoylphorbol Acetate 84-87 mitogen-activated protein kinase 8 Homo sapiens 54-57 21089054-0 2011 Acteoside inhibits PMA-induced matrix metalloproteinase-9 expression via CaMK/ERK- and JNK/NF-kappaB-dependent signaling. Tetradecanoylphorbol Acetate 19-22 mitogen-activated protein kinase 8 Homo sapiens 87-90 21089054-6 2011 In addition, acteoside repressed the PMA-induced phosphorylation of ERK1/2 (ERK, extracellular regulated kinase) and JNK1/2. Tetradecanoylphorbol Acetate 37-40 mitogen-activated protein kinase 8 Homo sapiens 117-123 21089054-9 2011 CONCLUSION: Acteoside inhibited PMA-induced invasion and migration of human fibrosarcoma cells via Ca(2+) -dependent CaMK/ERK and JNK/NF-kappaB-signaling pathways. Tetradecanoylphorbol Acetate 32-35 mitogen-activated protein kinase 8 Homo sapiens 130-133 20458747-3 2010 Activation of extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK) by TPA was identified, and TPA-induced migration and MMP-9 activity was significantly blocked by ERK inhibitor PD98059 and U0126, but not JNK inhibitor SP600125. Tetradecanoylphorbol Acetate 119-122 mitogen-activated protein kinase 8 Homo sapiens 230-233 20458747-3 2010 Activation of extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK) by TPA was identified, and TPA-induced migration and MMP-9 activity was significantly blocked by ERK inhibitor PD98059 and U0126, but not JNK inhibitor SP600125. Tetradecanoylphorbol Acetate 95-98 mitogen-activated protein kinase 8 Homo sapiens 62-85 20152819-8 2010 Furthermore, DHA strongly repressed the PMA-induced phosphorylation of Raf/ERK and JNK, which are dependent on the PKCalpha pathway. Tetradecanoylphorbol Acetate 40-43 mitogen-activated protein kinase 8 Homo sapiens 83-86 20458747-3 2010 Activation of extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK) by TPA was identified, and TPA-induced migration and MMP-9 activity was significantly blocked by ERK inhibitor PD98059 and U0126, but not JNK inhibitor SP600125. Tetradecanoylphorbol Acetate 95-98 mitogen-activated protein kinase 8 Homo sapiens 87-90 20458747-3 2010 Activation of extracellular signal-regulated kinase (ERK) and c-Jun-N-terminal kinase (JNK) by TPA was identified, and TPA-induced migration and MMP-9 activity was significantly blocked by ERK inhibitor PD98059 and U0126, but not JNK inhibitor SP600125. Tetradecanoylphorbol Acetate 95-98 mitogen-activated protein kinase 8 Homo sapiens 230-233 20533305-4 2010 TRIC expression was induced by treatment with the PKC activator TPA and proinflammatory cytokines IL-1beta, TNFalpha, and IL-1alpha, whereas the changes were inhibited by a JNK inhibitor. Tetradecanoylphorbol Acetate 64-67 mitogen-activated protein kinase 8 Homo sapiens 173-176 20541543-6 2010 Moreover, palmitate treatment induced activation of protein kinase Ctheta (PKCtheta) while blocking PKCtheta significantly inhibited JNK and IKKbeta activation induced by palmitate or phorbol 12-myristate 13-acetate (PKC activator, PMA), and attenuated the palmitate-induced defects in insulin action. Tetradecanoylphorbol Acetate 184-215 mitogen-activated protein kinase 8 Homo sapiens 133-136 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 8 Homo sapiens 122-151 20590612-10 2010 CONCLUSIONS AND IMPLICATIONS: Metformin inhibited PMA-induced invasion and migration of human fibrosarcoma cells via Ca(2+)-dependent PKCalpha/ERK and JNK/AP-1-signalling pathways. Tetradecanoylphorbol Acetate 50-53 mitogen-activated protein kinase 8 Homo sapiens 151-154 19969058-12 2010 CONCLUSION: Bee venom inhibits PMA-induced MMP-9 expression and activity by inhibition of NF-kappaB via p38 MAPK and JNK signaling pathways in MCF-7 cells. Tetradecanoylphorbol Acetate 31-34 mitogen-activated protein kinase 8 Homo sapiens 117-120 20082219-5 2010 In addition, melittin suppressed the PMA-induced phosphorylations of ERK and JNK mitogen-activated protein kinases, upstream factors involved in Ap-1 and NF-kappaB. Tetradecanoylphorbol Acetate 37-40 mitogen-activated protein kinase 8 Homo sapiens 77-80 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 22-25 mitogen-activated protein kinase 8 Homo sapiens 221-244 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 22-25 mitogen-activated protein kinase 8 Homo sapiens 246-249 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 8 Homo sapiens 221-244 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 8 Homo sapiens 246-249 20492175-0 2010 Acacetin inhibits TPA-induced MMP-2 and u-PA expressions of human lung cancer cells through inactivating JNK signaling pathway and reducing binding activities of NF-kappaB and AP-1. Tetradecanoylphorbol Acetate 18-21 mitogen-activated protein kinase 8 Homo sapiens 105-108 20492175-7 2010 Further, the treatment of specific inhibitor for JNK (SP600125) to A549 cells could inhibit TPA-induced MMP-2 and u-PA expressions along with an inhibition on cell invasion and migration. Tetradecanoylphorbol Acetate 92-95 mitogen-activated protein kinase 8 Homo sapiens 49-52 20025870-7 2010 In contrast, treatment of HASM by PMA induces phosphorylation and activation of Ra, MEK1/2, ERK1/2, JNK, Elk-1, and c-Jun. Tetradecanoylphorbol Acetate 34-37 mitogen-activated protein kinase 8 Homo sapiens 100-103 20492175-4 2010 Data also showed acacetin could inhibit phosphorylation of c-Jun N-terminal kinase 1 and 2 (JNK1/2) involved in the down-regulating protein expressions and transcriptions of matrix metalloproteinase-2 (MMP-2) and urokinase-type plasminogen activator (u-PA) induced by TPA. Tetradecanoylphorbol Acetate 268-271 mitogen-activated protein kinase 8 Homo sapiens 59-90 20492175-8 2010 Taken together, these results suggest the antimetastatic effects of acacetin on the TPA-induced A549 cells might be by reducing MMP-2 and u-PA expressions through inhibiting phosphorylation of JNK and reducing NF-kappaB and AP-1 binding activities. Tetradecanoylphorbol Acetate 84-87 mitogen-activated protein kinase 8 Homo sapiens 193-196 20492175-4 2010 Data also showed acacetin could inhibit phosphorylation of c-Jun N-terminal kinase 1 and 2 (JNK1/2) involved in the down-regulating protein expressions and transcriptions of matrix metalloproteinase-2 (MMP-2) and urokinase-type plasminogen activator (u-PA) induced by TPA. Tetradecanoylphorbol Acetate 268-271 mitogen-activated protein kinase 8 Homo sapiens 92-98 19706284-0 2009 PMA induces expression from the herpes simplex virus thymidine kinase promoter via the activation of JNK and ERK in the presence of adenoviral E1A proteins. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 101-104 18070596-4 2008 Further mechanistic studies revealed that irisolidone inhibits the binding of NF-kappaB and AP-1 to the MMP-9 promoter and suppresses the PMA-induced phosphorylation of ERK and JNK, which are upstream signaling molecules in MMP-9 expression. Tetradecanoylphorbol Acetate 138-141 mitogen-activated protein kinase 8 Homo sapiens 177-180 18982452-6 2008 In addition, increased expression of JNK in the absence of NFkappaB resulted in a significant induction of cell death in oral tumors when either left untreated or treated with TNF-alpha and TPA. Tetradecanoylphorbol Acetate 190-193 mitogen-activated protein kinase 8 Homo sapiens 37-40 18982452-7 2008 Moreover, when JNK was inhibited by dominant negative JNK (APF), a significant decrease in cell death could be observed in TNF-alpha and TPA treated NFkappaB knock down oral tumors. Tetradecanoylphorbol Acetate 137-140 mitogen-activated protein kinase 8 Homo sapiens 15-18 18982452-7 2008 Moreover, when JNK was inhibited by dominant negative JNK (APF), a significant decrease in cell death could be observed in TNF-alpha and TPA treated NFkappaB knock down oral tumors. Tetradecanoylphorbol Acetate 137-140 mitogen-activated protein kinase 8 Homo sapiens 54-57 19010898-3 2008 Previous studies showed that c-Jun NH(2) terminal kinase (JNK) is required for 12-O-tetradecanoylphorbol-13-acetate (TPA)- and thapsigargin (TG)-induced apoptosis in the androgen-responsive prostate cancer cell line LNCaP. Tetradecanoylphorbol Acetate 79-115 mitogen-activated protein kinase 8 Homo sapiens 29-56 19010898-3 2008 Previous studies showed that c-Jun NH(2) terminal kinase (JNK) is required for 12-O-tetradecanoylphorbol-13-acetate (TPA)- and thapsigargin (TG)-induced apoptosis in the androgen-responsive prostate cancer cell line LNCaP. Tetradecanoylphorbol Acetate 79-115 mitogen-activated protein kinase 8 Homo sapiens 58-61 19010898-3 2008 Previous studies showed that c-Jun NH(2) terminal kinase (JNK) is required for 12-O-tetradecanoylphorbol-13-acetate (TPA)- and thapsigargin (TG)-induced apoptosis in the androgen-responsive prostate cancer cell line LNCaP. Tetradecanoylphorbol Acetate 117-120 mitogen-activated protein kinase 8 Homo sapiens 29-56 19010898-3 2008 Previous studies showed that c-Jun NH(2) terminal kinase (JNK) is required for 12-O-tetradecanoylphorbol-13-acetate (TPA)- and thapsigargin (TG)-induced apoptosis in the androgen-responsive prostate cancer cell line LNCaP. Tetradecanoylphorbol Acetate 117-120 mitogen-activated protein kinase 8 Homo sapiens 58-61 19010898-4 2008 Androgens protect LNCaP cells from TPA-induced or TG-induced apoptosis via down-regulation of JNK activation. Tetradecanoylphorbol Acetate 35-38 mitogen-activated protein kinase 8 Homo sapiens 94-97 17647275-7 2008 Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. Tetradecanoylphorbol Acetate 14-17 mitogen-activated protein kinase 8 Homo sapiens 65-68 17647275-10 2008 From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. Tetradecanoylphorbol Acetate 40-43 mitogen-activated protein kinase 8 Homo sapiens 146-149 19907102-4 2009 PMA-induced up-regulation of beta1 and beta2 integrin activation in THP-1 cells was downregulated by VPP, which significantly suppressed only the PMA-induced phosphorylation of JNK (p<0.05) in THP-1 cells. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 177-180 19907102-4 2009 PMA-induced up-regulation of beta1 and beta2 integrin activation in THP-1 cells was downregulated by VPP, which significantly suppressed only the PMA-induced phosphorylation of JNK (p<0.05) in THP-1 cells. Tetradecanoylphorbol Acetate 146-149 mitogen-activated protein kinase 8 Homo sapiens 177-180 19907102-5 2009 In addition, preincubation of THP-1 with SP600125, a specific inhibitor of JNK, resulted in significant reduction of the PMA-induced adhesion of THP-1. Tetradecanoylphorbol Acetate 121-124 mitogen-activated protein kinase 8 Homo sapiens 75-78 19639210-6 2009 The inhibitors against NF-kappaB and mitogen-activated protein kinases (MAP kinase) including ERK and JNK pathways suppressed TPA-induced luciferase activity of MMP-1, -3 and -7 promoters. Tetradecanoylphorbol Acetate 126-129 mitogen-activated protein kinase 8 Homo sapiens 102-105 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 8 Homo sapiens 81-84 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 8 Homo sapiens 55-58 17982670-10 2007 Distinctly, the expression of B7-DC mRNA and -H3 mRNA in response to TPA is also PI-3K- and JNK-dependent, respectively. Tetradecanoylphorbol Acetate 69-72 mitogen-activated protein kinase 8 Homo sapiens 92-95 17880928-8 2007 Furthermore, Rh2 significantly repressed the PMA-mediated activation of p38 MAPK, ERK and JNK, which are upstream modulators of NF-kappaB and AP-1. Tetradecanoylphorbol Acetate 45-48 mitogen-activated protein kinase 8 Homo sapiens 90-93 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 8 Homo sapiens 191-194 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 8 Homo sapiens 191-194 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 8 Homo sapiens 172-175 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 8 Homo sapiens 172-175 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 8 Homo sapiens 215-218 16740769-6 2006 RESULTS: Treatment of LNCaP cells with a combination of TPA and paclitaxel synergistically inhibited the growth and induced apoptosis in cultured LNCaP cells, and this treatment also induced a marked increase in phosphorylated c-Jun-NH2-kinase (JNK). Tetradecanoylphorbol Acetate 56-59 mitogen-activated protein kinase 8 Homo sapiens 227-243 17404068-9 2007 In addition, KG-135 inhibited TPA-induced phosphorylation of c-Jun N-terminal kinases (JNK) that regulates COX-2 expression in MCF-10A cells. Tetradecanoylphorbol Acetate 30-33 mitogen-activated protein kinase 8 Homo sapiens 61-85 17404068-9 2007 In addition, KG-135 inhibited TPA-induced phosphorylation of c-Jun N-terminal kinases (JNK) that regulates COX-2 expression in MCF-10A cells. Tetradecanoylphorbol Acetate 30-33 mitogen-activated protein kinase 8 Homo sapiens 87-90 17404068-10 2007 The JNK inhibitor SP600125 attenuated COX-2 expression in TPA-treated MCF-10A cells. Tetradecanoylphorbol Acetate 58-61 mitogen-activated protein kinase 8 Homo sapiens 4-7 17404068-11 2007 Taken together, the above findings suggest that KG-135 inhibits TPA-induced COX-2 expression in MCF-10A cells by blocking the JNK/AP-1 signaling pathway. Tetradecanoylphorbol Acetate 64-67 mitogen-activated protein kinase 8 Homo sapiens 126-129 17030510-7 2006 PMA treatment resulted in transient activation of mitogen-activated protein kinases (ERK1/2, JNK1/2, and p38) followed by dephosphorylation/inactivation. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 93-99 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 8 Homo sapiens 119-122 16740769-6 2006 RESULTS: Treatment of LNCaP cells with a combination of TPA and paclitaxel synergistically inhibited the growth and induced apoptosis in cultured LNCaP cells, and this treatment also induced a marked increase in phosphorylated c-Jun-NH2-kinase (JNK). Tetradecanoylphorbol Acetate 56-59 mitogen-activated protein kinase 8 Homo sapiens 245-248 16434970-6 2006 In addition, several JNK upstream activators, including the phorbol ester TPA, anisomycin and MAPK kinase kinase-1 (MEKK1), phosphorylated Nur77 and induced its nuclear export. Tetradecanoylphorbol Acetate 74-77 mitogen-activated protein kinase 8 Homo sapiens 21-24 16267831-10 2006 The expression of either wild-type or mutant p53 had a similar effect on TPA-induced Jun N-terminal kinase (JNK) activation, indicating specificity for the ERK pathway. Tetradecanoylphorbol Acetate 73-76 mitogen-activated protein kinase 8 Homo sapiens 85-106 16480952-0 2006 Differentiation-associated genes regulated by TPA-induced c-Jun expression via a PKC/JNK pathway in KYSE450 cells. Tetradecanoylphorbol Acetate 46-49 mitogen-activated protein kinase 8 Homo sapiens 85-88 16480952-6 2006 Expression of involucrin and keratin 4 in response to TPA was attenuated by pretreatments with GF109203X and SP600125, but not PD98059, suggesting involvement of PKC and JNK in this response. Tetradecanoylphorbol Acetate 54-57 mitogen-activated protein kinase 8 Homo sapiens 170-173 16480952-7 2006 Taken together, these results suggested that differentiation-associated genes were regulated by TPA-induced c-Jun/AP-1 mainly via a PKC/JNK pathway in esophageal cancer cell line KYSE450. Tetradecanoylphorbol Acetate 96-99 mitogen-activated protein kinase 8 Homo sapiens 136-139 16267831-10 2006 The expression of either wild-type or mutant p53 had a similar effect on TPA-induced Jun N-terminal kinase (JNK) activation, indicating specificity for the ERK pathway. Tetradecanoylphorbol Acetate 73-76 mitogen-activated protein kinase 8 Homo sapiens 108-111 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 8 Homo sapiens 42-45 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 8 Homo sapiens 81-84 14709334-4 2004 In this study, we found that phorbol 12-myristate 13-acetate (PMA) induced JNK activation only in non-small cell lung cancer (NSCLC) cells, but not in small cell lung cancer (SCLC) cells, whereas ERK activation was detected in both cell types. Tetradecanoylphorbol Acetate 29-60 mitogen-activated protein kinase 8 Homo sapiens 75-78 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 8 Homo sapiens 138-171 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 8 Homo sapiens 138-171 15252145-7 2004 However, nobiletin was found to augment the phosphorylation of c-Jun NH2-terminal kinase (JNK), a downstream signal factor of the PI3K-Akt pathway, in TPA-treated HT-1080 cells. Tetradecanoylphorbol Acetate 151-154 mitogen-activated protein kinase 8 Homo sapiens 63-88 15252145-7 2004 However, nobiletin was found to augment the phosphorylation of c-Jun NH2-terminal kinase (JNK), a downstream signal factor of the PI3K-Akt pathway, in TPA-treated HT-1080 cells. Tetradecanoylphorbol Acetate 151-154 mitogen-activated protein kinase 8 Homo sapiens 90-93 15252145-9 2004 Furthermore, nobiletin enhancement of TIMP-1 production in TPA-stimulated HT-1080 cells was found to be diminished by adding a JNK inhibitor, SP600125. Tetradecanoylphorbol Acetate 59-62 mitogen-activated protein kinase 8 Homo sapiens 127-130 15138488-3 2004 In this study, we found that TPA activates the c-Jun NH2-terminal kinase (JNK)/c-Jun/AP-1 pathway. Tetradecanoylphorbol Acetate 29-32 mitogen-activated protein kinase 8 Homo sapiens 47-72 15138488-3 2004 In this study, we found that TPA activates the c-Jun NH2-terminal kinase (JNK)/c-Jun/AP-1 pathway. Tetradecanoylphorbol Acetate 29-32 mitogen-activated protein kinase 8 Homo sapiens 74-77 15138488-4 2004 To explore the possible role that the JNK/c-Jun/AP-1 signal pathway has on TPA-induced apoptosis in LNCaP cells, we stably transfected the scaffold protein, JNK interacting protein 1 (JIP-1), which binds to JNK inhibiting its ability to phosphorylate c-Jun. Tetradecanoylphorbol Acetate 75-78 mitogen-activated protein kinase 8 Homo sapiens 38-41 15138488-4 2004 To explore the possible role that the JNK/c-Jun/AP-1 signal pathway has on TPA-induced apoptosis in LNCaP cells, we stably transfected the scaffold protein, JNK interacting protein 1 (JIP-1), which binds to JNK inhibiting its ability to phosphorylate c-Jun. Tetradecanoylphorbol Acetate 75-78 mitogen-activated protein kinase 8 Homo sapiens 157-160 15138488-5 2004 TPA (10(-9)-10(-7) mol l(-1)) caused phosphorylation of JNK in both wild-type and JIP-1-transfected (LNCaP-JIP-1) cells. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 56-59 15138488-8 2004 Thus, TPA stimulated c-Jun through JNK, and JIP-1 effectively blocked JNK. Tetradecanoylphorbol Acetate 6-9 mitogen-activated protein kinase 8 Homo sapiens 35-38 15138488-14 2004 Taken together, TPA, probably by stimulation of PKC, phosphorylates JNK, which phosphorylates and increases expression of c-Jun leading to AP-1 activity. Tetradecanoylphorbol Acetate 16-19 mitogen-activated protein kinase 8 Homo sapiens 68-71 14709334-4 2004 In this study, we found that phorbol 12-myristate 13-acetate (PMA) induced JNK activation only in non-small cell lung cancer (NSCLC) cells, but not in small cell lung cancer (SCLC) cells, whereas ERK activation was detected in both cell types. Tetradecanoylphorbol Acetate 62-65 mitogen-activated protein kinase 8 Homo sapiens 75-78 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 8 Homo sapiens 81-104 14661062-0 2004 Resveratrol inhibits phorbol myristate acetate-induced matrix metalloproteinase-9 expression by inhibiting JNK and PKC delta signal transduction. Tetradecanoylphorbol Acetate 21-46 mitogen-activated protein kinase 8 Homo sapiens 107-110 14661062-7 2004 Resveratrol inhibited PMA-mediated activation of c-Jun N-terminal kinase (JNK) and protein kinase C (PKC)-delta activation. Tetradecanoylphorbol Acetate 22-25 mitogen-activated protein kinase 8 Homo sapiens 49-78 15161022-7 2004 EGCG also abrogated the PMA-induced activation of extracellular-regulated protein kinase (Erk) and c-jun N-terminal kinase (JNK), which are upstream modulators of AP-1. Tetradecanoylphorbol Acetate 24-27 mitogen-activated protein kinase 8 Homo sapiens 99-122 15161022-7 2004 EGCG also abrogated the PMA-induced activation of extracellular-regulated protein kinase (Erk) and c-jun N-terminal kinase (JNK), which are upstream modulators of AP-1. Tetradecanoylphorbol Acetate 24-27 mitogen-activated protein kinase 8 Homo sapiens 124-127 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 8 Homo sapiens 106-109 14978257-0 2004 Phorbol 12-myristate 13-acetate protects Jurkat cells from methylglyoxal-induced apoptosis by preventing c-Jun N-terminal kinase-mediated leakage of cytochrome c in an extracellular signal-regulated kinase-dependent manner. Tetradecanoylphorbol Acetate 0-31 mitogen-activated protein kinase 8 Homo sapiens 105-128 14612503-7 2003 Furthermore, use of the c-Jun N-terminal kinase (JNK) inhibitor SB202190 showed that the combination of DHT/TPA increased JNK activation in LNCaP cells but not in LNCaP-p65 cells, demonstrating that NFkappaB may be able to suppress JNK activity. Tetradecanoylphorbol Acetate 108-111 mitogen-activated protein kinase 8 Homo sapiens 49-52 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 8 Homo sapiens 141-144 14672351-13 2003 In addition, TPA induced the activation of JNK in RAW(264.7) cells but had little effect on RANKL-induced activation of JNK. Tetradecanoylphorbol Acetate 13-16 mitogen-activated protein kinase 8 Homo sapiens 43-46 14978257-5 2004 Taken together, these results suggest that PMA-induced ERK activation can protect Jurkat cells from methylglyoxal-induced apoptosis and that activated ERK exerts its antiapoptotic effects on mitochondria by inhibiting activated JNK-induced permeabilization of the outer mitochondrial membrane. Tetradecanoylphorbol Acetate 43-46 mitogen-activated protein kinase 8 Homo sapiens 228-231 14612503-7 2003 Furthermore, use of the c-Jun N-terminal kinase (JNK) inhibitor SB202190 showed that the combination of DHT/TPA increased JNK activation in LNCaP cells but not in LNCaP-p65 cells, demonstrating that NFkappaB may be able to suppress JNK activity. Tetradecanoylphorbol Acetate 108-111 mitogen-activated protein kinase 8 Homo sapiens 122-125 14612503-7 2003 Furthermore, use of the c-Jun N-terminal kinase (JNK) inhibitor SB202190 showed that the combination of DHT/TPA increased JNK activation in LNCaP cells but not in LNCaP-p65 cells, demonstrating that NFkappaB may be able to suppress JNK activity. Tetradecanoylphorbol Acetate 108-111 mitogen-activated protein kinase 8 Homo sapiens 122-125 14612503-8 2003 These results indicate that androgen/AR facilitates TPA-induced apoptosis by interruption of the NFkappaB signaling pathway, leading to activation of JNK in LNCaP cells. Tetradecanoylphorbol Acetate 52-55 mitogen-activated protein kinase 8 Homo sapiens 150-153 12186945-5 2002 Growth-arresting signals are triggered either by transient and sustained JNK activation (by TPA and anisomycin, respectively) or by preventing both ERK and JNK activation (UO126) and are maintained, rather than induced, by p38. Tetradecanoylphorbol Acetate 92-95 mitogen-activated protein kinase 8 Homo sapiens 73-76 12593797-6 2003 Jurkat cells activated their JNK in response to phorbol myristate acetate (PMA), and the response of the entire population of Jurkat cells was graded. Tetradecanoylphorbol Acetate 48-73 mitogen-activated protein kinase 8 Homo sapiens 29-32 12593797-6 2003 Jurkat cells activated their JNK in response to phorbol myristate acetate (PMA), and the response of the entire population of Jurkat cells was graded. Tetradecanoylphorbol Acetate 75-78 mitogen-activated protein kinase 8 Homo sapiens 29-32 12824193-7 2003 Stimulation of PKC by phorbol 12-myristate 13-acetate (PMA) leads to the activation of ERK1/2, p38 MAPK, and JNK in LNCaP cells. Tetradecanoylphorbol Acetate 22-53 mitogen-activated protein kinase 8 Homo sapiens 109-112 12824193-7 2003 Stimulation of PKC by phorbol 12-myristate 13-acetate (PMA) leads to the activation of ERK1/2, p38 MAPK, and JNK in LNCaP cells. Tetradecanoylphorbol Acetate 55-58 mitogen-activated protein kinase 8 Homo sapiens 109-112 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 8 Homo sapiens 136-139 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 8 Homo sapiens 91-94 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 8 Homo sapiens 309-312 12091247-2 2002 We have recently shown that phorbol 13-myristate 12-acetate (PMA)-stimulated SPRR1B transcription in Clara-like H441 cells is mainly mediated by activator protein-1 (AP-1) and c-Jun N-terminal kinase-1 (JNK1). Tetradecanoylphorbol Acetate 61-64 mitogen-activated protein kinase 8 Homo sapiens 176-201 12091247-2 2002 We have recently shown that phorbol 13-myristate 12-acetate (PMA)-stimulated SPRR1B transcription in Clara-like H441 cells is mainly mediated by activator protein-1 (AP-1) and c-Jun N-terminal kinase-1 (JNK1). Tetradecanoylphorbol Acetate 61-64 mitogen-activated protein kinase 8 Homo sapiens 203-207 11792626-9 2002 Interestingly, unlike in S6 cells, a catalytically inactive c-Jun NH(2)-terminal kinase (JNK) 1 mutant significantly reduced the PMA-inducible SPRR1B promoter activity in H441 cells. Tetradecanoylphorbol Acetate 129-132 mitogen-activated protein kinase 8 Homo sapiens 60-95 11850819-4 2002 Here we show that c-Jun N-terminal Kinase (JNK) is activated strongly and in a sustained fashion by 12-O-tetradecanoylphorbol 13-acetate (TPA) and thapsigargin (TG), two agents which were previously shown to lead to apoptosis in the androgen responsive prostate cancer cell line LNCaP. Tetradecanoylphorbol Acetate 100-136 mitogen-activated protein kinase 8 Homo sapiens 18-41 11850819-4 2002 Here we show that c-Jun N-terminal Kinase (JNK) is activated strongly and in a sustained fashion by 12-O-tetradecanoylphorbol 13-acetate (TPA) and thapsigargin (TG), two agents which were previously shown to lead to apoptosis in the androgen responsive prostate cancer cell line LNCaP. Tetradecanoylphorbol Acetate 100-136 mitogen-activated protein kinase 8 Homo sapiens 43-46 11850819-4 2002 Here we show that c-Jun N-terminal Kinase (JNK) is activated strongly and in a sustained fashion by 12-O-tetradecanoylphorbol 13-acetate (TPA) and thapsigargin (TG), two agents which were previously shown to lead to apoptosis in the androgen responsive prostate cancer cell line LNCaP. Tetradecanoylphorbol Acetate 138-141 mitogen-activated protein kinase 8 Homo sapiens 18-41 11850819-4 2002 Here we show that c-Jun N-terminal Kinase (JNK) is activated strongly and in a sustained fashion by 12-O-tetradecanoylphorbol 13-acetate (TPA) and thapsigargin (TG), two agents which were previously shown to lead to apoptosis in the androgen responsive prostate cancer cell line LNCaP. Tetradecanoylphorbol Acetate 138-141 mitogen-activated protein kinase 8 Homo sapiens 43-46 11850819-9 2002 Specific inhibition of JNK by expression of the JNK Inhibitory Protein (JIP) dramatically inhibited both TPA- and TG-induced apoptosis. Tetradecanoylphorbol Acetate 105-108 mitogen-activated protein kinase 8 Homo sapiens 23-26 11956220-10 2002 Co-transfection of the MAO B promoter with dominant negative forms of Ras, Raf-1, MEKK1, MEK1, MEK3, MEK7, ERK2, JNK1, and p38/RK inhibit the PMA-dependent activation of the MAO B promoter. Tetradecanoylphorbol Acetate 142-145 mitogen-activated protein kinase 8 Homo sapiens 113-117 11353829-10 2001 Phorbol 12-myristate 13-acetate, which strongly activates ERK1/2, also inhibited TNF-alpha activation of JNK. Tetradecanoylphorbol Acetate 0-31 mitogen-activated protein kinase 8 Homo sapiens 105-108 11356718-3 2001 Insulin-induced JNK activation was potentiated by either preincubating cells with 2 nM GF109203X (PKC inhibitor) or down-regulation of PKC by overnight treatment with 100 nM tetradecanoyl phorbol acetate. Tetradecanoylphorbol Acetate 174-203 mitogen-activated protein kinase 8 Homo sapiens 16-19 11356718-4 2001 In contrast, brief preincubation with 100 nM tetradecanoyl phorbol acetate inhibited the insulin- induced JNK activation. Tetradecanoylphorbol Acetate 45-74 mitogen-activated protein kinase 8 Homo sapiens 106-109 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 8 Homo sapiens 95-120 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 8 Homo sapiens 31-34 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 8 Homo sapiens 122-125 11086177-7 2000 In addition, unlike the effects on other inducers of apoptosis, the activation of JNK and of the caspase-3-like protease by GGO was significantly delayed by 12-O-tetradecanoylphorbol-13-acetate (TPA), suggesting that the site of inhibition by TPA might be located upstream of the protease and JNK in the GGO-induced apoptotic signaling pathway. Tetradecanoylphorbol Acetate 157-193 mitogen-activated protein kinase 8 Homo sapiens 82-85 11086177-7 2000 In addition, unlike the effects on other inducers of apoptosis, the activation of JNK and of the caspase-3-like protease by GGO was significantly delayed by 12-O-tetradecanoylphorbol-13-acetate (TPA), suggesting that the site of inhibition by TPA might be located upstream of the protease and JNK in the GGO-induced apoptotic signaling pathway. Tetradecanoylphorbol Acetate 157-193 mitogen-activated protein kinase 8 Homo sapiens 293-296 11086177-7 2000 In addition, unlike the effects on other inducers of apoptosis, the activation of JNK and of the caspase-3-like protease by GGO was significantly delayed by 12-O-tetradecanoylphorbol-13-acetate (TPA), suggesting that the site of inhibition by TPA might be located upstream of the protease and JNK in the GGO-induced apoptotic signaling pathway. Tetradecanoylphorbol Acetate 195-198 mitogen-activated protein kinase 8 Homo sapiens 82-85 11086177-7 2000 In addition, unlike the effects on other inducers of apoptosis, the activation of JNK and of the caspase-3-like protease by GGO was significantly delayed by 12-O-tetradecanoylphorbol-13-acetate (TPA), suggesting that the site of inhibition by TPA might be located upstream of the protease and JNK in the GGO-induced apoptotic signaling pathway. Tetradecanoylphorbol Acetate 243-246 mitogen-activated protein kinase 8 Homo sapiens 82-85 10807930-0 2000 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced c-Jun N-terminal kinase (JNK) phosphatase renders immortalized or transformed epithelial cells refractory to TPA-inducible JNK activity. Tetradecanoylphorbol Acetate 0-36 mitogen-activated protein kinase 8 Homo sapiens 51-74 10807930-0 2000 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced c-Jun N-terminal kinase (JNK) phosphatase renders immortalized or transformed epithelial cells refractory to TPA-inducible JNK activity. Tetradecanoylphorbol Acetate 0-36 mitogen-activated protein kinase 8 Homo sapiens 76-79 10807930-0 2000 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced c-Jun N-terminal kinase (JNK) phosphatase renders immortalized or transformed epithelial cells refractory to TPA-inducible JNK activity. Tetradecanoylphorbol Acetate 0-36 mitogen-activated protein kinase 8 Homo sapiens 174-177 10807930-0 2000 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced c-Jun N-terminal kinase (JNK) phosphatase renders immortalized or transformed epithelial cells refractory to TPA-inducible JNK activity. Tetradecanoylphorbol Acetate 38-41 mitogen-activated protein kinase 8 Homo sapiens 51-74 10807930-0 2000 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced c-Jun N-terminal kinase (JNK) phosphatase renders immortalized or transformed epithelial cells refractory to TPA-inducible JNK activity. Tetradecanoylphorbol Acetate 38-41 mitogen-activated protein kinase 8 Homo sapiens 76-79 10807930-0 2000 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced c-Jun N-terminal kinase (JNK) phosphatase renders immortalized or transformed epithelial cells refractory to TPA-inducible JNK activity. Tetradecanoylphorbol Acetate 38-41 mitogen-activated protein kinase 8 Homo sapiens 174-177 10807930-0 2000 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced c-Jun N-terminal kinase (JNK) phosphatase renders immortalized or transformed epithelial cells refractory to TPA-inducible JNK activity. Tetradecanoylphorbol Acetate 160-163 mitogen-activated protein kinase 8 Homo sapiens 76-79 10807930-2 2000 JNK can be activated by the tumor promoting agent, 12-O-tetradecanoylphorbol-13-acetate (TPA) in normal human oral keratinocytes but not in human keratinocytes that have been immortalized (HOK-16B and HaCaT) or transformed (HOK-16B-Bap-T) nor in a cervical carcinoma cell line (HeLa). Tetradecanoylphorbol Acetate 51-87 mitogen-activated protein kinase 8 Homo sapiens 0-3 10807930-2 2000 JNK can be activated by the tumor promoting agent, 12-O-tetradecanoylphorbol-13-acetate (TPA) in normal human oral keratinocytes but not in human keratinocytes that have been immortalized (HOK-16B and HaCaT) or transformed (HOK-16B-Bap-T) nor in a cervical carcinoma cell line (HeLa). Tetradecanoylphorbol Acetate 89-92 mitogen-activated protein kinase 8 Homo sapiens 0-3 10807930-3 2000 The refractory JNK activation response to TPA is not due a defect in the JNK pathway, because JNK can be activated by other stimuli, e.g. UV irradiation and an alkylating agent N-methyl-N"-nitrosoguanidine in these immortalized or transformed cells. Tetradecanoylphorbol Acetate 42-45 mitogen-activated protein kinase 8 Homo sapiens 15-18 10807930-4 2000 More importantly, the refractory JNK and JNKK activation response to TPA can be restored by treatment of the cells with a combination of TPA and a protein-tyrosine phosphatase inhibitor, sodium orthovanadate. Tetradecanoylphorbol Acetate 69-72 mitogen-activated protein kinase 8 Homo sapiens 33-36 10807930-4 2000 More importantly, the refractory JNK and JNKK activation response to TPA can be restored by treatment of the cells with a combination of TPA and a protein-tyrosine phosphatase inhibitor, sodium orthovanadate. Tetradecanoylphorbol Acetate 137-140 mitogen-activated protein kinase 8 Homo sapiens 33-36 10807930-5 2000 Furthermore, pretreatment of cells with TPA partially inhibited UV- or N-methyl-N"-nitrosoguanidine-induced JNK activity. Tetradecanoylphorbol Acetate 40-43 mitogen-activated protein kinase 8 Homo sapiens 108-111 10807930-6 2000 These results suggest that a TPA-inducible, orthovanadate-sensitive protein-tyrosine phosphatase may specifically down-regulate JNK signaling pathway in these immortalized/transformed epithelial cells. Tetradecanoylphorbol Acetate 29-32 mitogen-activated protein kinase 8 Homo sapiens 128-131 10518804-4 1999 PMA/ionomycin treatment also mediated activation of SAPK1 (JNKs) which was inhibited by CsA. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 52-57 10514454-10 1999 Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway. Tetradecanoylphorbol Acetate 25-28 mitogen-activated protein kinase 8 Homo sapiens 82-85 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 8 Homo sapiens 130-133 10514454-10 1999 Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway. Tetradecanoylphorbol Acetate 70-73 mitogen-activated protein kinase 8 Homo sapiens 82-85 10514454-10 1999 Thus, trans-RA modulates TPA activity through its interaction through TPA-induced JNK/AP-1 pathway but not TPA-induced ERK/p21(WAF1) pathway. Tetradecanoylphorbol Acetate 70-73 mitogen-activated protein kinase 8 Homo sapiens 82-85 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 8 Homo sapiens 92-95 10357879-4 1999 In contrast, treatment of cells with phorbol 12-myristate 13-acetate (PMA) strongly activated not only JNK but also ERK, while not affecting p38 kinase. Tetradecanoylphorbol Acetate 37-68 mitogen-activated protein kinase 8 Homo sapiens 103-106 10357879-4 1999 In contrast, treatment of cells with phorbol 12-myristate 13-acetate (PMA) strongly activated not only JNK but also ERK, while not affecting p38 kinase. Tetradecanoylphorbol Acetate 70-73 mitogen-activated protein kinase 8 Homo sapiens 103-106 10344756-4 1999 TPA induced both phosphorylation of stress-activated protein kinase kinase 1 (SEK1) and c-Jun NH2-terminal kinase (JNK) in the activated Ki-ras-disrupted clones but not in HCT116. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 88-113 10344756-4 1999 TPA induced both phosphorylation of stress-activated protein kinase kinase 1 (SEK1) and c-Jun NH2-terminal kinase (JNK) in the activated Ki-ras-disrupted clones but not in HCT116. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 115-118 10344756-6 1999 Furthermore, TPA-induced SEK1-JNK activation was observed in a DLD-1-derived activated Ki-ras-disrupted clone but not in DLD-1. Tetradecanoylphorbol Acetate 13-16 mitogen-activated protein kinase 8 Homo sapiens 30-33 10344756-0 1999 Activated Ki-Ras suppresses 12-O-tetradecanoylphorbol-13-acetate-induced activation of the c-Jun NH2-terminal kinase pathway in human colon cancer cells. Tetradecanoylphorbol Acetate 28-64 mitogen-activated protein kinase 8 Homo sapiens 91-116 10344756-7 1999 The TPA-induced SEK1-JNK activation in these disrupted clones was completely inhibited by the protein kinase C (PKC) inhibitor, GF109203X (1 microM), but not by another PKC inhibitor, H7 (50 microM), whereas TPA-induced MEK1/2-ERK activation was partially and completely inhibited by GF109203X (1 microM) and H7 (50 microM), respectively. Tetradecanoylphorbol Acetate 4-7 mitogen-activated protein kinase 8 Homo sapiens 21-24 9674701-3 1998 In this report, we show that curcumin inhibits JNK activation by various agonists including PMA plus ionomycin, anisomycin, UV-C, gamma radiation, TNF-alpha, and sodium orthovanadate. Tetradecanoylphorbol Acetate 92-95 mitogen-activated protein kinase 8 Homo sapiens 47-50 10359012-3 1999 The activity of JNK1 was also significantly induced, with JNK1 protein levels increasing moderately during exposure to TPA. Tetradecanoylphorbol Acetate 119-122 mitogen-activated protein kinase 8 Homo sapiens 16-20 10359012-3 1999 The activity of JNK1 was also significantly induced, with JNK1 protein levels increasing moderately during exposure to TPA. Tetradecanoylphorbol Acetate 119-122 mitogen-activated protein kinase 8 Homo sapiens 58-62 9925763-4 1999 We tested whether the activities of the mitogen-activated protein kinases (ERK1/2 and JNK1) varied in response to EGF, TPA, or combinations of these agonists and if the same treatments altered patterns of immediate early gene expression. Tetradecanoylphorbol Acetate 119-122 mitogen-activated protein kinase 8 Homo sapiens 86-90 9743209-5 1998 In activated T cells toremifene clearly inhibits phorbol 12-myristate 13-acetate (PMA)-induced JNK activity, suggesting that the JNK pathway may also be involved in the up-regulation of TNF-R2 expression by antioestrogens. Tetradecanoylphorbol Acetate 49-80 mitogen-activated protein kinase 8 Homo sapiens 95-98 9743209-5 1998 In activated T cells toremifene clearly inhibits phorbol 12-myristate 13-acetate (PMA)-induced JNK activity, suggesting that the JNK pathway may also be involved in the up-regulation of TNF-R2 expression by antioestrogens. Tetradecanoylphorbol Acetate 49-80 mitogen-activated protein kinase 8 Homo sapiens 129-132 9743209-5 1998 In activated T cells toremifene clearly inhibits phorbol 12-myristate 13-acetate (PMA)-induced JNK activity, suggesting that the JNK pathway may also be involved in the up-regulation of TNF-R2 expression by antioestrogens. Tetradecanoylphorbol Acetate 82-85 mitogen-activated protein kinase 8 Homo sapiens 95-98 9743209-5 1998 In activated T cells toremifene clearly inhibits phorbol 12-myristate 13-acetate (PMA)-induced JNK activity, suggesting that the JNK pathway may also be involved in the up-regulation of TNF-R2 expression by antioestrogens. Tetradecanoylphorbol Acetate 82-85 mitogen-activated protein kinase 8 Homo sapiens 129-132 9686602-11 1998 Importantly, during C2-ceramide and PMA costimulation, the JNK pathway is not simply blocked by ERK activation; rather, cross-talk between these MAP kinase pathways acts to simultaneously augment ERK activity and down-regulate JNK activity. Tetradecanoylphorbol Acetate 36-39 mitogen-activated protein kinase 8 Homo sapiens 59-62 9686602-11 1998 Importantly, during C2-ceramide and PMA costimulation, the JNK pathway is not simply blocked by ERK activation; rather, cross-talk between these MAP kinase pathways acts to simultaneously augment ERK activity and down-regulate JNK activity. Tetradecanoylphorbol Acetate 36-39 mitogen-activated protein kinase 8 Homo sapiens 227-230 9674706-4 1998 PMA treatment of the u-PAR-deficient OVCAR-3 ovarian cancer cells, which contain low JNK activities, resulted in a rapid (5 min) increase in JNK activity. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 85-88 9674706-4 1998 PMA treatment of the u-PAR-deficient OVCAR-3 ovarian cancer cells, which contain low JNK activities, resulted in a rapid (5 min) increase in JNK activity. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 141-144 9674701-4 1998 Although both JNK and ERK activation by phorbol 12-myristate 13-acetate (PMA) plus ionomycin were suppressed by curcumin, the JNK pathway was more sensitive. Tetradecanoylphorbol Acetate 40-71 mitogen-activated protein kinase 8 Homo sapiens 14-17 9674701-4 1998 Although both JNK and ERK activation by phorbol 12-myristate 13-acetate (PMA) plus ionomycin were suppressed by curcumin, the JNK pathway was more sensitive. Tetradecanoylphorbol Acetate 73-76 mitogen-activated protein kinase 8 Homo sapiens 14-17 9535820-10 1998 Therefore, we conclude that TPA inhibits the induction of apoptosis in anisomycin-treated HL-60 cells through an ERK-dependent pathway and that this effect can be reversed by the attenuation of ERK activity accompanied with the stimulation of JNK/SAPK activity. Tetradecanoylphorbol Acetate 28-31 mitogen-activated protein kinase 8 Homo sapiens 243-246 9606192-2 1998 These signals, which can be replaced by the pharmacological agents phorbol ester (PMA) and Ca2+ ionophore, synergistically activate the mitogen-activated protein kinase (MAPK) JNK. Tetradecanoylphorbol Acetate 82-85 mitogen-activated protein kinase 8 Homo sapiens 176-179 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 8 Homo sapiens 154-157 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 8 Homo sapiens 17-20 9553058-8 1998 In T cells, overexpression of SPRK/MLK3, an activator of JNK/SAPK, strongly induces DSE-dependent transcription and dominant negative kinases of SEK and SAPK impair TPA/ionomycin-induced DSE activity. Tetradecanoylphorbol Acetate 165-168 mitogen-activated protein kinase 8 Homo sapiens 57-65 9535820-5 1998 We report the use of 12-O-tetradecanoylphorbol-13-acetate (TPA) in the inhibition of apoptosis in HL-60 cells stimulated with the JNK/SAPK activator anisomycin. Tetradecanoylphorbol Acetate 21-57 mitogen-activated protein kinase 8 Homo sapiens 130-138 9535820-5 1998 We report the use of 12-O-tetradecanoylphorbol-13-acetate (TPA) in the inhibition of apoptosis in HL-60 cells stimulated with the JNK/SAPK activator anisomycin. Tetradecanoylphorbol Acetate 59-62 mitogen-activated protein kinase 8 Homo sapiens 130-138 9478937-5 1998 Functional activation of the JNKK/SEK1-JNK/SAPK-c-Jun cascade (where JNKK/SEK1 is JNK kinase/SAPK kinase) was demonstrated by activation of a 12-O-tetradecanoylphorbol-13-acetate response element (TRE) reporter construct in a c-Jun dependent fashion. Tetradecanoylphorbol Acetate 142-178 mitogen-activated protein kinase 8 Homo sapiens 29-32 9547349-8 1998 Phorbol myristate acetate inhibited both ET-18-OCH3-induced apoptosis and sustained JNK activation; thus, persistent JNK activation by ET-18-OCH3 is associated with the capacity of this ether phospholipid to induce apoptosis. Tetradecanoylphorbol Acetate 0-25 mitogen-activated protein kinase 8 Homo sapiens 84-87 9547349-8 1998 Phorbol myristate acetate inhibited both ET-18-OCH3-induced apoptosis and sustained JNK activation; thus, persistent JNK activation by ET-18-OCH3 is associated with the capacity of this ether phospholipid to induce apoptosis. Tetradecanoylphorbol Acetate 0-25 mitogen-activated protein kinase 8 Homo sapiens 117-120 9514879-6 1998 The effects of 12-O-tetradecanoylphorbol beta-acetate (TPA) mimicked those of radiation on JNK cascade and 1-(5-isoquinolinesulphonyl)-2,5-dimethylpiperazine 2HCl (H7) and pretreatment with TPA blocked JNK activation following irradiation. Tetradecanoylphorbol Acetate 55-58 mitogen-activated protein kinase 8 Homo sapiens 91-94 9514879-6 1998 The effects of 12-O-tetradecanoylphorbol beta-acetate (TPA) mimicked those of radiation on JNK cascade and 1-(5-isoquinolinesulphonyl)-2,5-dimethylpiperazine 2HCl (H7) and pretreatment with TPA blocked JNK activation following irradiation. Tetradecanoylphorbol Acetate 55-58 mitogen-activated protein kinase 8 Homo sapiens 202-205 9478937-5 1998 Functional activation of the JNKK/SEK1-JNK/SAPK-c-Jun cascade (where JNKK/SEK1 is JNK kinase/SAPK kinase) was demonstrated by activation of a 12-O-tetradecanoylphorbol-13-acetate response element (TRE) reporter construct in a c-Jun dependent fashion. Tetradecanoylphorbol Acetate 142-178 mitogen-activated protein kinase 8 Homo sapiens 39-42 8999940-0 1997 Activation of 12-O-tetradecanoylphorbol-13-acetate response element- and dyad symmetry element-dependent transcription by interleukin-5 is mediated by Jun N-terminal kinase/stress-activated protein kinase kinases. Tetradecanoylphorbol Acetate 14-50 mitogen-activated protein kinase 8 Homo sapiens 151-172 9467967-7 1998 Protein kinase C (PKC) depletion by prolonged treatment of VSMC with phorbol 12-myristate 13-acetate (PMA) resulted in partial decrease in the responsiveness of JNK1 to arachidonic acid suggesting a role for both PKC-dependent and -independent mechanisms in the activation of JNK1 by this important fatty acid. Tetradecanoylphorbol Acetate 69-100 mitogen-activated protein kinase 8 Homo sapiens 161-165 9467967-7 1998 Protein kinase C (PKC) depletion by prolonged treatment of VSMC with phorbol 12-myristate 13-acetate (PMA) resulted in partial decrease in the responsiveness of JNK1 to arachidonic acid suggesting a role for both PKC-dependent and -independent mechanisms in the activation of JNK1 by this important fatty acid. Tetradecanoylphorbol Acetate 69-100 mitogen-activated protein kinase 8 Homo sapiens 276-280 9467967-7 1998 Protein kinase C (PKC) depletion by prolonged treatment of VSMC with phorbol 12-myristate 13-acetate (PMA) resulted in partial decrease in the responsiveness of JNK1 to arachidonic acid suggesting a role for both PKC-dependent and -independent mechanisms in the activation of JNK1 by this important fatty acid. Tetradecanoylphorbol Acetate 102-105 mitogen-activated protein kinase 8 Homo sapiens 161-165 9467967-7 1998 Protein kinase C (PKC) depletion by prolonged treatment of VSMC with phorbol 12-myristate 13-acetate (PMA) resulted in partial decrease in the responsiveness of JNK1 to arachidonic acid suggesting a role for both PKC-dependent and -independent mechanisms in the activation of JNK1 by this important fatty acid. Tetradecanoylphorbol Acetate 102-105 mitogen-activated protein kinase 8 Homo sapiens 276-280 9346918-6 1997 In contrast, 12-O-tetradecanoylphorbol-13-acetate-induced JNK activation could be observed in both JY and MS1418 cells. Tetradecanoylphorbol Acetate 13-49 mitogen-activated protein kinase 8 Homo sapiens 58-61 9169474-6 1997 A 1-min TPA pretreatment of GN4 cells inhibited thapsigargin-dependent JNK activation by 80-90%. Tetradecanoylphorbol Acetate 8-11 mitogen-activated protein kinase 8 Homo sapiens 71-74 9045910-6 1997 Pre-incubation of CD4+ T lymphocytes in the presence of anti-CD4 mAb or gp160 inhibits the activation of JNK in response to phorbol 12-myristate 13-acetate and ionomycin. Tetradecanoylphorbol Acetate 124-155 mitogen-activated protein kinase 8 Homo sapiens 105-108 9024981-1 1996 The effects of phorbol 12-myristate 13-acetate (PMA) on the activities of phospholipase D (PLD3), mitogen-activated protein kinase (ERK), and c-Jun N-terminal kinase (JNK) were studied in Jurkat, a human T cell line, and EL4, a murine T-cell line. Tetradecanoylphorbol Acetate 48-51 mitogen-activated protein kinase 8 Homo sapiens 142-165 8943238-8 1996 Co-treatment with a tyrosine phosphatase inhibitor (sodium orthovanadate) and T-cell activation signals (phorbol 12-myristate 13-acetate plus ionomycin) prolonged JNK induction, followed by T-cell apoptosis. Tetradecanoylphorbol Acetate 105-136 mitogen-activated protein kinase 8 Homo sapiens 163-166 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 8 Homo sapiens 108-111 8887624-4 1996 Cotransfection of RasN17, a dominant negative mutant of Ha-Ras, attenuated the shear-activated JNK and luciferase reporters driven by 12-O-tetradecanoylphorbol-13-acetate-responsive elements. Tetradecanoylphorbol Acetate 134-170 mitogen-activated protein kinase 8 Homo sapiens 95-98 8557665-4 1996 We demonstrate that JNK1 was activated by either the T-cell activation signals, anti-CD28 monoclonal antibody plus phorbol 12-myristate 13-acetate (PMA), or the apoptosis-inducing treatment, GR; however, the induction patterns were different. Tetradecanoylphorbol Acetate 115-146 mitogen-activated protein kinase 8 Homo sapiens 20-24 8557665-4 1996 We demonstrate that JNK1 was activated by either the T-cell activation signals, anti-CD28 monoclonal antibody plus phorbol 12-myristate 13-acetate (PMA), or the apoptosis-inducing treatment, GR; however, the induction patterns were different. Tetradecanoylphorbol Acetate 148-151 mitogen-activated protein kinase 8 Homo sapiens 20-24 7929360-7 1994 The kinetics of Raf-1, ERK, and JNK induction by epidermal growth factor, phorbol 12-myristate 13-acetate, or TNF alpha indicate distinct mechanisms of activation in human fibroblasts. Tetradecanoylphorbol Acetate 74-105 mitogen-activated protein kinase 8 Homo sapiens 32-35 8205621-3 1994 Full activation of the MAP kinases that phosphorylate the Jun activation domain, JNK1 and JNK2, required costimulation of T cells with either TPA and Ca2+ ionophore or antibodies to TCR and CD28. Tetradecanoylphorbol Acetate 142-145 mitogen-activated protein kinase 8 Homo sapiens 81-85 21454541-4 2011 Interestingly, silencing p23 from LNCaP prostate cancer cells using RNAi markedly enhanced PKCdelta-dependent apoptosis and activation of PKCdelta downstream effectors ROCK and JNK by phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 184-215 mitogen-activated protein kinase 8 Homo sapiens 177-180 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 8 Homo sapiens 253-256 34578957-0 2021 Kaempferol Blocks the Skin Fibroblastic Interleukin 1beta Expression and Cytotoxicity Induced by 12-O-tetradecanoylphorbol-13-acetate by Suppressing c-Jun N-terminal Kinase. Tetradecanoylphorbol Acetate 97-133 mitogen-activated protein kinase 8 Homo sapiens 149-172 34578957-5 2021 Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-Jun N-terminal kinase (JNK) induced by TPA. Tetradecanoylphorbol Acetate 165-168 mitogen-activated protein kinase 8 Homo sapiens 124-147 34578957-5 2021 Kaempferol blocked the production of the intracellular reactive oxygen species (ROS) responsible for the phosphorylation of c-Jun N-terminal kinase (JNK) induced by TPA. Tetradecanoylphorbol Acetate 165-168 mitogen-activated protein kinase 8 Homo sapiens 149-152 33865428-8 2021 Furthermore, IL-35 markedly inhibited the phosphorylation levels of ERK1/2, p38, and JNK1/2, in PMA plus A23187 induced HMC-1 cells. Tetradecanoylphorbol Acetate 96-99 mitogen-activated protein kinase 8 Homo sapiens 85-91 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 8 Homo sapiens 96-119 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 8 Homo sapiens 121-124 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 8 Homo sapiens 181-184 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 8 Homo sapiens 108-114 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 8 Homo sapiens 53-86 29371085-0 2018 (E)-2-Methoxy-4-(3-(4-methoxyphenyl) prop-1-en-1-yl) phenol attenuates PMA-induced inflammatory responses in human monocytic cells through PKCdelta/JNK/AP-1 pathways. Tetradecanoylphorbol Acetate 71-74 mitogen-activated protein kinase 8 Homo sapiens 148-151 30133131-6 2018 TPA-induced membrane translocation of PKCalpha, phosphorylation of JNK, and the nuclear translocations of AP-1 and NF-kappaB were downregulated by mLU8C-PU in MCF-7 cells. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 67-70 30133131-8 2018 These results indicate that mLU8C-PU inhibits migratory and invasive responses in MCF-7 breast cancer cells by suppressing MMP-9 and IL-8 expression through mitigating TPA-induced PKCalpha, JNK activation, and the nuclear translocation of AP-1 and NF-kappaB. Tetradecanoylphorbol Acetate 168-171 mitogen-activated protein kinase 8 Homo sapiens 190-193 29371085-5 2018 PMA induced the translocation of PKCs from the cytosol to the membrane and phosphorylated JNK. Tetradecanoylphorbol Acetate 0-3 mitogen-activated protein kinase 8 Homo sapiens 90-93 27654969-5 2016 Specific inhibitors and mutagenesis studies showed that PKCdelta, JNK1/2, Erk1/2, NF-kappaB, and AP-1 were critical for TPA-induced uPAR expression. Tetradecanoylphorbol Acetate 120-123 mitogen-activated protein kinase 8 Homo sapiens 66-72 29371085-6 2018 MMPP inhibited PMA-induced membrane translocation of PKCdelta, phosphorylation of JNK, and nuclear translocation of AP-1, resulting in downregulation of cyclooxygenase-2 and chemokine ligand 5 production. Tetradecanoylphorbol Acetate 15-18 mitogen-activated protein kinase 8 Homo sapiens 82-85 29371085-7 2018 These findings indicate that MMPP inhibits inflammatory responses in THP-1 cells by mitigating PMA-induced activation of PKCdelta and JNK and nuclear translocation of AP-1. Tetradecanoylphorbol Acetate 95-98 mitogen-activated protein kinase 8 Homo sapiens 134-137 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 8 Homo sapiens 156-159 27654969-6 2016 Application of DHA suppressed TPA-induced translocation of PKCdelta, activation of the JNK1/2 and Erk1/2 signaling pathways, and subsequent AP-1 and NF-kappaB transactivation. Tetradecanoylphorbol Acetate 30-33 mitogen-activated protein kinase 8 Homo sapiens 87-93 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 8 Homo sapiens 36-42 25866363-5 2015 It suppressed TPA-induced AP-1 activity through inhibiting the phosphorylation of the extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways, and it suppressed TPA-induced inhibition of NF-kappaB nuclear translocation through IkappaB. Tetradecanoylphorbol Acetate 14-17 mitogen-activated protein kinase 8 Homo sapiens 132-155 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 8 Homo sapiens 101-104 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 8 Homo sapiens 101-104 25866363-5 2015 It suppressed TPA-induced AP-1 activity through inhibiting the phosphorylation of the extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways, and it suppressed TPA-induced inhibition of NF-kappaB nuclear translocation through IkappaB. Tetradecanoylphorbol Acetate 14-17 mitogen-activated protein kinase 8 Homo sapiens 157-160 25866363-5 2015 It suppressed TPA-induced AP-1 activity through inhibiting the phosphorylation of the extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways, and it suppressed TPA-induced inhibition of NF-kappaB nuclear translocation through IkappaB. Tetradecanoylphorbol Acetate 200-203 mitogen-activated protein kinase 8 Homo sapiens 132-155