PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8111971-9 1993 Treatment of oocytes with phorbol 12-myristate 13-acetate, an activator of protein kinase C, for 30 min prior to the addition of 1-MA resulted in the inhibition of 1-MA-induced phosphorylation of eIF-4E, translational activation, and germinal vesicle breakdown. 1-methyladenine 129-133 eukaryotic translation initiation factor 4E Homo sapiens 196-202 8111971-9 1993 Treatment of oocytes with phorbol 12-myristate 13-acetate, an activator of protein kinase C, for 30 min prior to the addition of 1-MA resulted in the inhibition of 1-MA-induced phosphorylation of eIF-4E, translational activation, and germinal vesicle breakdown. 1-methyladenine 164-168 eukaryotic translation initiation factor 4E Homo sapiens 196-202 8111971-11 1993 Another possibility is that eIF-4E is phosphorylated by an unknown kinase that is activated by the cascade of reactions stimulated by 1-MA. 1-methyladenine 134-138 eukaryotic translation initiation factor 4E Homo sapiens 28-34 27889448-5 2016 This phospho-regulatory circuit is engaged by cancer therapeutics, such as rigosertib and paclitaxel/Taxol, that activate JNK through mitotic and oxidative stress as well as by physiological regulators of the JNK cascade and may function as a signaling checkpoint to suppress the Ras pathway during conditions of cellular stress. Paclitaxel 101-106 mitogen-activated protein kinase 8 Homo sapiens 209-212 22433870-0 2012 Tyrosine-phosphorylated caveolin-1 (Tyr-14) increases sensitivity to paclitaxel by inhibiting BCL2 and BCLxL proteins via c-Jun N-terminal kinase (JNK). Paclitaxel 69-79 mitogen-activated protein kinase 8 Homo sapiens 122-145 27563006-8 2016 After paclitaxel treatment, GLT-1 was significantly down-regulated, and the phosphorylation of ERK1/2 and JNK were obviously up-regulated. Paclitaxel 6-16 mitogen-activated protein kinase 8 Homo sapiens 106-109 25496994-6 2015 Treatment with taxol, a microtubule stabilizing agent, attenuates rotenone-induced phosphorylation and presumably activation of JNK. Paclitaxel 15-20 mitogen-activated protein kinase 8 Homo sapiens 128-131 25351906-6 2015 5-FU and paclitaxel treatment increased the number of SP cells and JNK phosphorylation, and decreased cell survival. Paclitaxel 9-19 mitogen-activated protein kinase 8 Homo sapiens 67-70 24787013-6 2014 EBV sensitized TP53-mutated BL cells to all spindle poisons tested, including vincristine and taxol, an effect that was systematically downmodulated by pretreatment of cells with inhibitors of p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases. Paclitaxel 94-99 mitogen-activated protein kinase 8 Homo sapiens 226-229 23681233-0 2013 Hypoxia counteracts taxol-induced apoptosis in MDA-MB-231 breast cancer cells: role of autophagy and JNK activation. Paclitaxel 20-25 mitogen-activated protein kinase 8 Homo sapiens 101-104 23681233-9 2013 Taxol also induced c-Jun N-terminal kinase (JNK) activation and phosphorylation of its substrates B-cell CLL/lymphoma 2 (Bcl2) and BCL2-like 1 (BclXL) under normoxia and hypoxia very early after taxol exposure. Paclitaxel 0-5 mitogen-activated protein kinase 8 Homo sapiens 19-42 23681233-9 2013 Taxol also induced c-Jun N-terminal kinase (JNK) activation and phosphorylation of its substrates B-cell CLL/lymphoma 2 (Bcl2) and BCL2-like 1 (BclXL) under normoxia and hypoxia very early after taxol exposure. Paclitaxel 0-5 mitogen-activated protein kinase 8 Homo sapiens 44-47 23681233-12 2013 The results showed that JNK activation promotes resistance against taxol-induced apoptosis under normoxia and hypoxia without being involved in induction of autophagy. Paclitaxel 67-72 mitogen-activated protein kinase 8 Homo sapiens 24-27 23681233-13 2013 In conclusion, the resistance against taxol-induced cell death observed under hypoxia can be explained by a more effective autophagic flow activated via the classical mTOR pathway and by a mechanism involving JNK, which could be dependent on Bcl2 and BclXL phosphorylation but independent of JNK-induced autophagy activation. Paclitaxel 38-43 mitogen-activated protein kinase 8 Homo sapiens 209-212 23681233-13 2013 In conclusion, the resistance against taxol-induced cell death observed under hypoxia can be explained by a more effective autophagic flow activated via the classical mTOR pathway and by a mechanism involving JNK, which could be dependent on Bcl2 and BclXL phosphorylation but independent of JNK-induced autophagy activation. Paclitaxel 38-43 mitogen-activated protein kinase 8 Homo sapiens 292-295 22323130-0 2012 Resistance to paclitaxel in hepatoma cells is related to static JNK activation and prohibition into entry of mitosis. Paclitaxel 14-24 mitogen-activated protein kinase 8 Homo sapiens 64-67 22323130-10 2012 In death-reluctant cells, inbuild-phospho-JNK levels were high but no longer activated in response to paclitaxel. Paclitaxel 102-112 mitogen-activated protein kinase 8 Homo sapiens 42-45 21074392-5 2012 Moreover, taxol caused an increase in c-Jun NH(2)-terminal kinase (JNK) and p38 activities, two of the well known mediators of the stress activation pathways. Paclitaxel 10-15 mitogen-activated protein kinase 8 Homo sapiens 38-65 21074392-5 2012 Moreover, taxol caused an increase in c-Jun NH(2)-terminal kinase (JNK) and p38 activities, two of the well known mediators of the stress activation pathways. Paclitaxel 10-15 mitogen-activated protein kinase 8 Homo sapiens 67-70 21074392-7 2012 Furthermore, our data indicated that Bcl-2alpha was down-regulated in taxol-treated cells and its expression was modulated by ROS and JNK activity. Paclitaxel 70-75 mitogen-activated protein kinase 8 Homo sapiens 134-137 21074392-8 2012 The activities of caspase-9 and -3 were also increased upon treatment with taxol; however, pre-treatment of cells with NAC or JNK inhibitor (SP600125) impeded taxol-mediated caspase activation and apoptosis in K562 cells, suggesting that JNK acts upstream of the caspases. Paclitaxel 75-80 mitogen-activated protein kinase 8 Homo sapiens 126-129 21074392-8 2012 The activities of caspase-9 and -3 were also increased upon treatment with taxol; however, pre-treatment of cells with NAC or JNK inhibitor (SP600125) impeded taxol-mediated caspase activation and apoptosis in K562 cells, suggesting that JNK acts upstream of the caspases. Paclitaxel 75-80 mitogen-activated protein kinase 8 Homo sapiens 238-241 21074392-8 2012 The activities of caspase-9 and -3 were also increased upon treatment with taxol; however, pre-treatment of cells with NAC or JNK inhibitor (SP600125) impeded taxol-mediated caspase activation and apoptosis in K562 cells, suggesting that JNK acts upstream of the caspases. Paclitaxel 159-164 mitogen-activated protein kinase 8 Homo sapiens 126-129 21074392-8 2012 The activities of caspase-9 and -3 were also increased upon treatment with taxol; however, pre-treatment of cells with NAC or JNK inhibitor (SP600125) impeded taxol-mediated caspase activation and apoptosis in K562 cells, suggesting that JNK acts upstream of the caspases. Paclitaxel 159-164 mitogen-activated protein kinase 8 Homo sapiens 238-241 21074392-9 2012 Taken together, these results indicate that taxol induces apoptosis in chronic myelogenous leukemia cells by inducing intracellular oxidative stress and JNK activation pathway. Paclitaxel 44-49 mitogen-activated protein kinase 8 Homo sapiens 153-156 26985944-0 2016 Paclitaxel induces apoptosis in leukemia cells through a JNK activation-dependent pathway. Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 57-60 26985944-3 2016 In this paper, we focused on the role of c-Jun N-terminal kinase (JNK) pathways in PTX-induced apoptosis and proliferation inhibition. Paclitaxel 83-86 mitogen-activated protein kinase 8 Homo sapiens 41-64 26985944-3 2016 In this paper, we focused on the role of c-Jun N-terminal kinase (JNK) pathways in PTX-induced apoptosis and proliferation inhibition. Paclitaxel 83-86 mitogen-activated protein kinase 8 Homo sapiens 66-69 26985944-4 2016 The effects of PTX were examined in human leukemia cell lines and patients" chronic lymphocytic leukemia (CLL) cells in relation to mitochondrial events, apoptosis, and perturbation of JNK activation using flow cytometry, siRNA, mitochondrial membrane potential determination, and western blotting. Paclitaxel 15-18 mitogen-activated protein kinase 8 Homo sapiens 185-188 26985944-5 2016 Exposure of cells to PTX at concentrations >= 10 nM for 18 or 24 h resulted in a significant release of cytochrome c from mitochondria to the cytosol, cleavages of procaspase 3 and poly (ADP-ribose) polymerase (PARP), and JNK activation, leading to apoptosis. Paclitaxel 21-24 mitogen-activated protein kinase 8 Homo sapiens 225-228 26985944-7 2016 Moreover, both pharmacological JNK inhibitors SP600125 and JNK siRNA dramatically blocked PTX-induced apoptosis, cytochrome c release, caspase 3, and PARP cleavage. Paclitaxel 90-93 mitogen-activated protein kinase 8 Homo sapiens 31-34 26985944-7 2016 Moreover, both pharmacological JNK inhibitors SP600125 and JNK siRNA dramatically blocked PTX-induced apoptosis, cytochrome c release, caspase 3, and PARP cleavage. Paclitaxel 90-93 mitogen-activated protein kinase 8 Homo sapiens 59-62 26985944-8 2016 These findings demonstrate that JNK activation plays a critical role in the induction of apoptosis mediated by PTX in human leukemia cell lines and CLL patient-derived primary cancer cells, and this event is upstream of cytochrome c release, caspase 3, and PARP cleavage. Paclitaxel 111-114 mitogen-activated protein kinase 8 Homo sapiens 32-35 26246283-4 2016 Paclitaxel-induced JNK (c-Jun N-terminal kinase) activation is critical for Bcl-2 modulation. Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 19-22 26246283-4 2016 Paclitaxel-induced JNK (c-Jun N-terminal kinase) activation is critical for Bcl-2 modulation. Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 24-47 26534836-0 2016 Time-staggered inhibition of JNK effectively sensitizes chemoresistant ovarian cancer cells to cisplatin and paclitaxel. Paclitaxel 109-119 mitogen-activated protein kinase 8 Homo sapiens 29-32 26534836-3 2016 In the present study, while investigating the mechanism underlying the chemoresistance of ovarian cancer, we found that JNK may have a key role in the resistance of ovarian cancer cells to cisplatin and paclitaxel. Paclitaxel 203-213 mitogen-activated protein kinase 8 Homo sapiens 120-123 26534836-4 2016 Importantly, whereas simultaneous application of a JNK inhibitor and either of the chemotherapeutic agents had contrasting effects for cisplatin (enhanced cytotoxicity) and paclitaxel (decreased cytotoxicity), JNK inhibitor treatment prior to chemotherapeutic agent application invariably enhanced the cytotoxicity of both drugs, suggesting that the basal JNK activity is commonly involved in the chemoresistance of ovarian cancer cells to cisplatin and paclitaxel in contrast to drug-induced JNK activity which may have different roles for these two drugs. Paclitaxel 173-183 mitogen-activated protein kinase 8 Homo sapiens 51-54 26534836-4 2016 Importantly, whereas simultaneous application of a JNK inhibitor and either of the chemotherapeutic agents had contrasting effects for cisplatin (enhanced cytotoxicity) and paclitaxel (decreased cytotoxicity), JNK inhibitor treatment prior to chemotherapeutic agent application invariably enhanced the cytotoxicity of both drugs, suggesting that the basal JNK activity is commonly involved in the chemoresistance of ovarian cancer cells to cisplatin and paclitaxel in contrast to drug-induced JNK activity which may have different roles for these two drugs. Paclitaxel 454-464 mitogen-activated protein kinase 8 Homo sapiens 51-54 22433870-14 2012 Thus, we highlight novel roles for CAV1 variants in cell death; wtCAV1 promotes cell death, whereas CAV1beta promotes cell survival by preventing inactivation of BCL2 and BCLxL via JNK in paclitaxel-mediated apoptosis. Paclitaxel 188-198 mitogen-activated protein kinase 8 Homo sapiens 181-184 22800348-7 2012 JNK signal was inhibited in FaDu or FaDu/T cells and the inhibited JNK was reactivated by taxol or anisomycin (an activator for MAPK signal transduction pathways). Paclitaxel 90-95 mitogen-activated protein kinase 8 Homo sapiens 0-3 22800348-7 2012 JNK signal was inhibited in FaDu or FaDu/T cells and the inhibited JNK was reactivated by taxol or anisomycin (an activator for MAPK signal transduction pathways). Paclitaxel 90-95 mitogen-activated protein kinase 8 Homo sapiens 67-70 22433870-0 2012 Tyrosine-phosphorylated caveolin-1 (Tyr-14) increases sensitivity to paclitaxel by inhibiting BCL2 and BCLxL proteins via c-Jun N-terminal kinase (JNK). Paclitaxel 69-79 mitogen-activated protein kinase 8 Homo sapiens 147-150 19944065-9 2010 The c-Jun terminal NH2 kinase (JNK) inhibitor SP600125 reduced thrombin/paclitaxel-induced TF expression. Paclitaxel 72-82 mitogen-activated protein kinase 8 Homo sapiens 31-34 20145041-6 2010 In addition, hyperactive JNK attenuated the apoptosis of breast cancer cells treated by the chemotherapy drug paclitaxel, which is in contrast to the requirement for inducible JNK activity in response to cytotoxic chemotherapy. Paclitaxel 110-120 mitogen-activated protein kinase 8 Homo sapiens 25-28 19944065-10 2010 Furthermore, EGCG significantly inhibited the phosphorylation of JNK to 49% of thrombin/paclitaxel-stimulated HAECs at 60min. Paclitaxel 88-98 mitogen-activated protein kinase 8 Homo sapiens 65-68 19048624-5 2009 The combination of paclitaxel with CRM197 had an inhibitory effect on cell proliferation and enhanced apoptosis via the inhibition of ERK and Akt activation and the stimulation of p38 and JNK activation. Paclitaxel 19-29 mitogen-activated protein kinase 8 Homo sapiens 188-191 19048624-3 2009 Paclitaxel induced transient ERK activation and sustained activation of JNK and p38 MAPK through the ectodomain shedding of HB-EGF in SKOV3 cells. Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 72-75 19048624-4 2009 In addition, the overexpression of HB-EGF in paclitaxel-treated SKOV3 cells resulted in modulation of paclitaxel-evoked MAPK signaling, including marked activation of ERK and Akt, and minimized activation of JNK and p38 MAPK, indicating that HB-EGF is involved in drug sensitivity through the balance of anti-apoptotic and pro-apoptotic signals induced by paclitaxel. Paclitaxel 45-55 mitogen-activated protein kinase 8 Homo sapiens 208-211 19717209-0 2009 Potentiation of paclitaxel-induced apoptosis by galectin-13 overexpression via activation of Ask-1-p38-MAP kinase and JNK/SAPK pathways and suppression of Akt and ERK1/2 activation in U-937 human macrophage cells. Paclitaxel 16-26 mitogen-activated protein kinase 8 Homo sapiens 118-121 19717209-6 2009 In addition, pharmacological inhibition of JNK and p38-MAPK pathways protected the cells from paclitaxel-induced cell death. Paclitaxel 94-104 mitogen-activated protein kinase 8 Homo sapiens 43-46 19674193-8 2009 GRP78 knockdown or EGCG potentiates taxol- and vinblastine-induced activation of pro-apoptosis arms of the ER stress response, such as JNK phosphorylation, caspase-7 and PARP cleavage. Paclitaxel 36-41 mitogen-activated protein kinase 8 Homo sapiens 135-138 19674193-9 2009 Inhibition of JNK and caspase-7 abrogates EGCG sensitization of breast cancer cells to taxol and vinblastine. Paclitaxel 87-92 mitogen-activated protein kinase 8 Homo sapiens 14-17 19385049-5 2009 In the present study,the well-characterized human neuroblastoma cell line SH-SY5Y served as a model system to separate physiological and pro-apoptotic JNK actions in the response to the cytoskeleton-interfering substances colchicine, cytochalasin D and taxol. Paclitaxel 253-258 mitogen-activated protein kinase 8 Homo sapiens 151-154 17987264-3 2008 Treatment of glioblastoma cells with TXL triggered production of reactive oxygen species (ROS), induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), and activated the redox-sensitive c-Jun NH(2)-terminal kinase 1 (JNK1) pathway. Paclitaxel 37-40 mitogen-activated protein kinase 8 Homo sapiens 202-231 18690538-6 2008 Paclitaxel-induced phosphorylation of c-JUN N-terminal kinase (JNK), but not p38, extracellular signal-regulated kinase and Akt, was markedly suppressed in U373MG cells that stably expressed Ran. Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 38-61 18690538-6 2008 Paclitaxel-induced phosphorylation of c-JUN N-terminal kinase (JNK), but not p38, extracellular signal-regulated kinase and Akt, was markedly suppressed in U373MG cells that stably expressed Ran. Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 63-66 18690538-7 2008 These results suggest that Ran suppresses paclitaxel-induced cell death through the downregulation of JNK-mediated signal pathways. Paclitaxel 42-52 mitogen-activated protein kinase 8 Homo sapiens 102-105 18341588-0 2008 Distinct signaling pathways of microtubule inhibitors--vinblastine and Taxol induce JNK-dependent cell death but through AP-1-dependent and AP-1-independent mechanisms, respectively. Paclitaxel 71-76 mitogen-activated protein kinase 8 Homo sapiens 84-87 18341588-6 2008 However, inhibition of JNK or an absence of JNK protected against both vinblastine- and Taxol-induced cell death. Paclitaxel 88-93 mitogen-activated protein kinase 8 Homo sapiens 23-26 18341588-6 2008 However, inhibition of JNK or an absence of JNK protected against both vinblastine- and Taxol-induced cell death. Paclitaxel 88-93 mitogen-activated protein kinase 8 Homo sapiens 44-47 18341588-7 2008 These results suggest that although JNK activation plays an important role in cell death induced by both agents, vinblastine and Taxol differ markedly with respect to signaling downstream of JNK, with AP-1-dependent and -independent mechanisms, respectively. Paclitaxel 129-134 mitogen-activated protein kinase 8 Homo sapiens 191-194 17987264-3 2008 Treatment of glioblastoma cells with TXL triggered production of reactive oxygen species (ROS), induced phosphorylation of p38 mitogen-activated protein kinase (MAPK), and activated the redox-sensitive c-Jun NH(2)-terminal kinase 1 (JNK1) pathway. Paclitaxel 37-40 mitogen-activated protein kinase 8 Homo sapiens 233-237 18068334-0 2008 Taxol-induced mitochondrial stress in melanoma cells is mediated by activation of c-Jun N-terminal kinase (JNK) and p38 pathways via uncoupling protein 2. Paclitaxel 0-5 mitogen-activated protein kinase 8 Homo sapiens 107-110 18068334-9 2008 Our data provide evidence that taxol-induced mitochondrial stress occurs through the activation of both JNK and p38 pathways, and suggest a novel role for UCP2 in the modulation of taxol-induced apoptosis of melanoma cells. Paclitaxel 31-36 mitogen-activated protein kinase 8 Homo sapiens 104-107 18068334-5 2008 Taxol resulted in the activation of apoptosis signal regulated kinase (ASK)1, c-jun NH(2)-terminal kinase (JNK), p38(MAPK) and extracellular-regulated kinase (ERK) together with the downregulation of uncoupling protein 2 (UCP2). Paclitaxel 0-5 mitogen-activated protein kinase 8 Homo sapiens 78-105 18068334-5 2008 Taxol resulted in the activation of apoptosis signal regulated kinase (ASK)1, c-jun NH(2)-terminal kinase (JNK), p38(MAPK) and extracellular-regulated kinase (ERK) together with the downregulation of uncoupling protein 2 (UCP2). Paclitaxel 0-5 mitogen-activated protein kinase 8 Homo sapiens 107-110 18068334-8 2008 Pretreatment of melanoma cells with the JNK inhibitor (SP600125) or the p38 inhibitor (SB203580) blocked taxol-induced UCP2 downregulation, ROS generation and apoptosis, whereas the ERK inhibitor (PD98059) had no such effect. Paclitaxel 105-110 mitogen-activated protein kinase 8 Homo sapiens 40-43 17568772-8 2007 Moreover, such SGK1 depletion prevented the dexamethasone-induced increase in SGK1 expression, as well as the inhibitory effects of dexamethasone on paclitaxel-induced SEK1-JNK signaling and apoptosis in MDA-MB-231 breast cancer cells. Paclitaxel 149-159 mitogen-activated protein kinase 8 Homo sapiens 173-176 16972069-10 2007 PTX induced JNK activity or AKT mediated BAD phosphorylation was unaffected by cell cycle inhibitors. Paclitaxel 0-3 mitogen-activated protein kinase 8 Homo sapiens 12-15 16287090-0 2006 Inactivation of Id-1 in prostate cancer cells: A potential therapeutic target in inducing chemosensitization to taxol through activation of JNK pathway. Paclitaxel 112-117 mitogen-activated protein kinase 8 Homo sapiens 140-143 16969513-8 2006 Furthermore, we observed that paclitaxel, ceramide, or combo-induced EGFR phosphorylation was inhibited by EGFR inhibitor, PD153035, while paclitaxel, ceramide, or combo-induced JNK and ERK phosphorylation was blocked by EGFR inhibitor, PD153035 and ERK inhibitor, U126. Paclitaxel 30-40 mitogen-activated protein kinase 8 Homo sapiens 178-181 16547493-3 2006 In an attempt to explore what genes are transcriptionally regulated by the activated JNK signaling pathway upon paclitaxel treatment, we used cDNA microarrays to analyse the changes of gene expression in human ovarian cancer cells that were treated with paclitaxel and/or the JNK inhibitor SP600125. Paclitaxel 112-122 mitogen-activated protein kinase 8 Homo sapiens 85-88 16547493-3 2006 In an attempt to explore what genes are transcriptionally regulated by the activated JNK signaling pathway upon paclitaxel treatment, we used cDNA microarrays to analyse the changes of gene expression in human ovarian cancer cells that were treated with paclitaxel and/or the JNK inhibitor SP600125. Paclitaxel 112-122 mitogen-activated protein kinase 8 Homo sapiens 276-279 16547493-3 2006 In an attempt to explore what genes are transcriptionally regulated by the activated JNK signaling pathway upon paclitaxel treatment, we used cDNA microarrays to analyse the changes of gene expression in human ovarian cancer cells that were treated with paclitaxel and/or the JNK inhibitor SP600125. Paclitaxel 254-264 mitogen-activated protein kinase 8 Homo sapiens 85-88 16547493-3 2006 In an attempt to explore what genes are transcriptionally regulated by the activated JNK signaling pathway upon paclitaxel treatment, we used cDNA microarrays to analyse the changes of gene expression in human ovarian cancer cells that were treated with paclitaxel and/or the JNK inhibitor SP600125. Paclitaxel 254-264 mitogen-activated protein kinase 8 Homo sapiens 276-279 16547493-4 2006 Among 20 genes that were specifically regulated by the paclitaxel-activated JNK pathway, interleukin (IL)-6 was shown to elicit function through the JAK-STAT signaling pathway in an autocrine and/or paracrine fashion. Paclitaxel 55-65 mitogen-activated protein kinase 8 Homo sapiens 76-79 16547493-6 2006 Dissection on regulatory pathways for IL-6 indicated that (i) when ovarian cancer cells were treated with paclitaxel at low but clinically achievable concentrations (exemplified by 1 microM in this study), the JNK signaling pathway was the major stimulator of IL-6 gene regulation and (ii) at suprapharmacologically high concentrations (exemplified by 50 microM), paclitaxel exerted lipopolysaccharide-like effects, most likely through the Toll-like receptor 4 signaling pathway. Paclitaxel 106-116 mitogen-activated protein kinase 8 Homo sapiens 210-213 16547493-6 2006 Dissection on regulatory pathways for IL-6 indicated that (i) when ovarian cancer cells were treated with paclitaxel at low but clinically achievable concentrations (exemplified by 1 microM in this study), the JNK signaling pathway was the major stimulator of IL-6 gene regulation and (ii) at suprapharmacologically high concentrations (exemplified by 50 microM), paclitaxel exerted lipopolysaccharide-like effects, most likely through the Toll-like receptor 4 signaling pathway. Paclitaxel 364-374 mitogen-activated protein kinase 8 Homo sapiens 210-213 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). Paclitaxel 64-74 mitogen-activated protein kinase 8 Homo sapiens 227-243 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). Paclitaxel 64-74 mitogen-activated protein kinase 8 Homo sapiens 245-248 16794185-8 2006 Paclitaxel potently activated c-Jun terminal NH2 kinase (JNK) as compared with thrombin alone, whereas the thrombin-mediated phosphorylation of p38 and extracellular signal-regulated kinase remained unaffected. Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 57-60 16794185-12 2006 Paclitaxel increases endothelial TF expression via its stabilizing effect on microtubules and selective activation of JNK. Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 118-121 16287090-7 2006 Furthermore, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for taxol-induced apoptosis, was also activated in the si-Id-1 transfected cells. Paclitaxel 87-92 mitogen-activated protein kinase 8 Homo sapiens 13-36 16287090-7 2006 Furthermore, c-Jun N-terminal kinase (JNK), one of the common pathways responsible for taxol-induced apoptosis, was also activated in the si-Id-1 transfected cells. Paclitaxel 87-92 mitogen-activated protein kinase 8 Homo sapiens 38-41 16287090-8 2006 Inhibition of JNK activity by a specific inhibitor, SP600125, blocked the si-Id-1-induced sensitivity to taxol. Paclitaxel 105-110 mitogen-activated protein kinase 8 Homo sapiens 14-17 15467450-0 2004 JNK is associated with Bcl-2 and PP1 in mitochondria: paclitaxel induces its activation and its association with the phosphorylated form of Bcl-2. Paclitaxel 54-64 mitogen-activated protein kinase 8 Homo sapiens 0-3 16397234-3 2006 To further investigate its mechanism of action, we treated MCF-7 cells with paclitaxel and showed a dose-dependent increase in nuclear localization of FOXO3a, which coincided with decreased Akt signaling but increased c-Jun NH2-terminal kinase 1/2 (JNK1/2), p38, and extracellular signal-regulated kinase 1/2 (ERK1/2) activity. Paclitaxel 76-86 mitogen-activated protein kinase 8 Homo sapiens 249-255 16397234-4 2006 Flow cytometry revealed that paclitaxel-induced apoptosis of MCF-7 cells and of other paclitaxel-sensitive breast cancer cell lines was maintained in the presence of inhibitors of p38 (SB203580) or mitogen-activated protein/ERK kinase 1 signaling (PD98059) but abrogated when cells were treated with the JNK1/2 inhibitor SP600125. Paclitaxel 29-39 mitogen-activated protein kinase 8 Homo sapiens 304-310 16397234-6 2006 Moreover, conditional activation of JNK mimicked paclitaxel activity and led to dephosphorylation of Akt and FOXO3a. Paclitaxel 49-59 mitogen-activated protein kinase 8 Homo sapiens 36-39 16397234-8 2006 Taken together, the data show that cell death of breast cancer cells in response to paclitaxel is dependent upon JNK activation, resulting in Akt inhibition and increased FOXO3a activity. Paclitaxel 84-94 mitogen-activated protein kinase 8 Homo sapiens 113-116 15467449-5 2004 Unexpectedly, enforced expression of p21(Cip1/WAF1) diminished paclitaxel-mediated inactivation of ERK, and reduced paclitaxel-induced activation of JNK as well as Bcl-2 phosphorylation. Paclitaxel 116-126 mitogen-activated protein kinase 8 Homo sapiens 149-152 17119350-2 2006 We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by paclitaxel. Paclitaxel 378-388 mitogen-activated protein kinase 8 Homo sapiens 132-157 17119350-2 2006 We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by paclitaxel. Paclitaxel 378-388 mitogen-activated protein kinase 8 Homo sapiens 159-162 17119350-2 2006 We have previously demonstrated that phosphorylation of Fas-associated death domain-containing protein (FADD) at 194 serine through c-jun NH2-terminal kinase (JNK) activation sensitizes breast cancer cells to chemotherapy through accelerating cell cycle arrest at G2/M, and that Bcl-2 phosphorylation downstream of JNK/FADD plays an important role in cell growth suppression by paclitaxel. Paclitaxel 378-388 mitogen-activated protein kinase 8 Homo sapiens 315-318 15788689-7 2005 The JNK inhibitor SP600125 substantially decreased the activation of caspases and apoptosis induced by MSeA combination with SN38 or etoposide and completely blocked these events induced by MSeA/paclitaxel. Paclitaxel 195-205 mitogen-activated protein kinase 8 Homo sapiens 4-7 15467450-1 2004 It has been shown that the activation of JNK after paclitaxel-induced microtubule damage is parallel to Bcl-2 phosphorylation, cell cycle arrest in mitosis and apoptosis. Paclitaxel 51-61 mitogen-activated protein kinase 8 Homo sapiens 41-44 15467450-2 2004 Using subcellular fractionation and immunocytochemistry, we found here that a pool of activated JNK is located in mitochondria of HeLa cells treated with paclitaxel. Paclitaxel 154-164 mitogen-activated protein kinase 8 Homo sapiens 96-99 15467450-3 2004 Furthermore, whereas the JNK protein is present in a tripartite complex with the anti-apoptotic Bcl-2 protein and the PP1 phosphatase in mitochondria isolated from control cells, the activated form of JNK was associated with the phosphorylated form of Bcl-2, but devoid of PP1, in mitochondria isolated from paclitaxel-treated cells. Paclitaxel 308-318 mitogen-activated protein kinase 8 Homo sapiens 25-28 15467450-3 2004 Furthermore, whereas the JNK protein is present in a tripartite complex with the anti-apoptotic Bcl-2 protein and the PP1 phosphatase in mitochondria isolated from control cells, the activated form of JNK was associated with the phosphorylated form of Bcl-2, but devoid of PP1, in mitochondria isolated from paclitaxel-treated cells. Paclitaxel 308-318 mitogen-activated protein kinase 8 Homo sapiens 201-204 15467450-7 2004 Taken together, these data show that JNK activation provides a molecular linkage from microtubule damages to the mitochondrial apoptotic machinery and also point to a pivotal role for the JNK/Bcl-2/PP1 complex in the control of apoptosis following paclitaxel treatment. Paclitaxel 248-258 mitogen-activated protein kinase 8 Homo sapiens 37-40 15467450-7 2004 Taken together, these data show that JNK activation provides a molecular linkage from microtubule damages to the mitochondrial apoptotic machinery and also point to a pivotal role for the JNK/Bcl-2/PP1 complex in the control of apoptosis following paclitaxel treatment. Paclitaxel 248-258 mitogen-activated protein kinase 8 Homo sapiens 188-191 15001534-4 2004 Inhibition of paclitaxel-induced c-jun NH2-terminal kinase (JNK) activation by treatment with a specific inhibitor, SP600125, or overexpression of a dominant-negative mutant form of upstream kinases, MEK kinase 1 (MEKK1) and mitogen-activated protein kinase kinase (MKK) 7, significantly reduced the increase in phosphorylated FADD. Paclitaxel 14-24 mitogen-activated protein kinase 8 Homo sapiens 33-58 15001534-4 2004 Inhibition of paclitaxel-induced c-jun NH2-terminal kinase (JNK) activation by treatment with a specific inhibitor, SP600125, or overexpression of a dominant-negative mutant form of upstream kinases, MEK kinase 1 (MEKK1) and mitogen-activated protein kinase kinase (MKK) 7, significantly reduced the increase in phosphorylated FADD. Paclitaxel 14-24 mitogen-activated protein kinase 8 Homo sapiens 60-63 15001534-5 2004 It is noteworthy that pretreatment with paclitaxel significantly up-regulated MEKK1 expression, resulting in enhancement of etoposide- or cisplatin-induced MEKK1/MKK7-dependent JNK activation and apoptosis in LNCaP and DU145 cells. Paclitaxel 40-50 mitogen-activated protein kinase 8 Homo sapiens 177-180 14500571-6 2004 We confirmed a previous report showing that paclitaxel induces cell damage via the ASK1-c-Jun N-terminal protein kinase (JNK) cascade. Paclitaxel 44-54 mitogen-activated protein kinase 8 Homo sapiens 83-119 14724588-4 2004 Here, we show that the majority of both paclitaxel- and UV-induced apoptosis can be inhibited by the pharmacological JNK inhibitor, SP600125, in MCF-7 cells. Paclitaxel 40-50 mitogen-activated protein kinase 8 Homo sapiens 117-120 14500571-6 2004 We confirmed a previous report showing that paclitaxel induces cell damage via the ASK1-c-Jun N-terminal protein kinase (JNK) cascade. Paclitaxel 44-54 mitogen-activated protein kinase 8 Homo sapiens 121-124 14500571-9 2004 These results indicate that E2 inhibits paclitaxel-induced cell damage by inhibiting JNK activity via phosphorylation of Akt-ASK1. Paclitaxel 40-50 mitogen-activated protein kinase 8 Homo sapiens 85-88 14500571-7 2004 E2 inhibited the paclitaxel-induced JNK activation, and the E2-induced inhibition of the paclitaxel-induced JNK activation was attenuated in cells treated with either ICI182,780 or LY294002 or transfected with ASK1S83A, in which a consensus Akt phosphorylation site at serine-83 was converted to alanine. Paclitaxel 17-27 mitogen-activated protein kinase 8 Homo sapiens 36-39 14500571-7 2004 E2 inhibited the paclitaxel-induced JNK activation, and the E2-induced inhibition of the paclitaxel-induced JNK activation was attenuated in cells treated with either ICI182,780 or LY294002 or transfected with ASK1S83A, in which a consensus Akt phosphorylation site at serine-83 was converted to alanine. Paclitaxel 89-99 mitogen-activated protein kinase 8 Homo sapiens 108-111 12555062-5 2003 Paclitaxel-induced p70S6K(T421/S424) phosphorylation requires both de novo RNA and protein synthesis via multiple signaling pathways including ERK1/2 MAP kinase, JNK, PKC, Ca(++), PI3K, and mammalian target of rapamycin (mTOR). Paclitaxel 0-10 mitogen-activated protein kinase 8 Homo sapiens 162-165 14514687-1 2003 We show here that JNK1 activity is rapidly up-regulated and prolonged by specific mechanisms during apoptosis induced by paclitaxel- or ginsenoside-Rh2 in SK-HEP-1 cells. Paclitaxel 121-131 mitogen-activated protein kinase 8 Homo sapiens 18-22 12510025-3 2003 trans-Resveratrol also reverses the sustained phosphorylation of JNK/SAPK, which specifically occurs after paclitaxel exposure.Overall, our observations demonstrate that (a) the toxic action of paclitaxel on neuronal-like cells is not only related to the effect of the drug on tubulin, but also to its capacity to activate several intracellular pathways leading to inactivation of Bcl-2, thus causing cells to die by apoptosis, (b) trans-resveratrol significantly reduces paclitaxel-induced apoptosis by modulating the cellular signaling pathways which commit the cell to apoptosis. Paclitaxel 107-117 mitogen-activated protein kinase 8 Homo sapiens 65-73 12510025-3 2003 trans-Resveratrol also reverses the sustained phosphorylation of JNK/SAPK, which specifically occurs after paclitaxel exposure.Overall, our observations demonstrate that (a) the toxic action of paclitaxel on neuronal-like cells is not only related to the effect of the drug on tubulin, but also to its capacity to activate several intracellular pathways leading to inactivation of Bcl-2, thus causing cells to die by apoptosis, (b) trans-resveratrol significantly reduces paclitaxel-induced apoptosis by modulating the cellular signaling pathways which commit the cell to apoptosis. Paclitaxel 194-204 mitogen-activated protein kinase 8 Homo sapiens 65-73 12510025-3 2003 trans-Resveratrol also reverses the sustained phosphorylation of JNK/SAPK, which specifically occurs after paclitaxel exposure.Overall, our observations demonstrate that (a) the toxic action of paclitaxel on neuronal-like cells is not only related to the effect of the drug on tubulin, but also to its capacity to activate several intracellular pathways leading to inactivation of Bcl-2, thus causing cells to die by apoptosis, (b) trans-resveratrol significantly reduces paclitaxel-induced apoptosis by modulating the cellular signaling pathways which commit the cell to apoptosis. Paclitaxel 194-204 mitogen-activated protein kinase 8 Homo sapiens 65-73 12555073-4 2003 Taxol and other chemotherapy drugs induce c-Jun N-terminal kinase (JNK), a kinase that conveys cellular stress and death signals. Paclitaxel 0-5 mitogen-activated protein kinase 8 Homo sapiens 42-65 12555073-4 2003 Taxol and other chemotherapy drugs induce c-Jun N-terminal kinase (JNK), a kinase that conveys cellular stress and death signals. Paclitaxel 0-5 mitogen-activated protein kinase 8 Homo sapiens 67-70 12555073-8 2003 In contrast, overexpression of JNK significantly enhances Taxol-induced apoptosis and inhibits IGF-I survival effects. Paclitaxel 58-63 mitogen-activated protein kinase 8 Homo sapiens 31-34 12555073-10 2003 The inhibitory effect of JNK appears to be mediated by serine phosphorylation of IRS-1 (insulin receptor substrate) since both Taxol and IGF-I treatment enhanced Ser(312) IRS-1 phosphorylation, while LY294002 blocked IGF-I-mediated phosphorylation. Paclitaxel 127-132 mitogen-activated protein kinase 8 Homo sapiens 25-28 14529677-6 2003 pan-JNK expression was higher in specimens treated with both platinum agents (P = 0.038) and paclitaxel (P = 0.033). Paclitaxel 93-103 mitogen-activated protein kinase 8 Homo sapiens 4-7 12691824-4 2003 In addition, paclitaxel greatly increased c-Jun N-terminal protein kinase (JNK) activity whereas showing a small enhancing effect on extracellular-regulated kinases (ERK) activity. Paclitaxel 13-23 mitogen-activated protein kinase 8 Homo sapiens 42-73 12691824-4 2003 In addition, paclitaxel greatly increased c-Jun N-terminal protein kinase (JNK) activity whereas showing a small enhancing effect on extracellular-regulated kinases (ERK) activity. Paclitaxel 13-23 mitogen-activated protein kinase 8 Homo sapiens 75-78 12691824-7 2003 Thus, the findings suggest that paclitaxel-induced apoptosis is mediated by JNK and occurs in parallel with suppression of the Raf-1 kinase activity in parental MCF-7 cells. Paclitaxel 32-42 mitogen-activated protein kinase 8 Homo sapiens 76-79 12555062-8 2003 Inhibition of PKC and JNK prevents paclitaxel-induced p70S6K inactivation. Paclitaxel 35-45 mitogen-activated protein kinase 8 Homo sapiens 22-25 12121974-7 2002 Activation of JNK and its downstream caspase-3 by paclitaxel or vinblastine is significantly down-regulated in gamma-synuclein-expressing cells, indicating that the paclitaxel- or vinblastine-activated apoptosis pathway is blocked by gamma-synuclein. Paclitaxel 50-60 mitogen-activated protein kinase 8 Homo sapiens 14-17 12121974-7 2002 Activation of JNK and its downstream caspase-3 by paclitaxel or vinblastine is significantly down-regulated in gamma-synuclein-expressing cells, indicating that the paclitaxel- or vinblastine-activated apoptosis pathway is blocked by gamma-synuclein. Paclitaxel 165-175 mitogen-activated protein kinase 8 Homo sapiens 14-17 11598801-8 2001 The anti-neoplastic agent, paclitaxel, activates ASK1 and JNK, and promotes the in vitro assembly of stable microtubules. Paclitaxel 27-37 mitogen-activated protein kinase 8 Homo sapiens 58-61 11461094-0 2001 Involvement of JNK-mediated pathway in EGF-mediated protection against paclitaxel-induced apoptosis in SiHa human cervical cancer cells. Paclitaxel 71-81 mitogen-activated protein kinase 8 Homo sapiens 15-18 11461094-5 2001 Co-exposure of SiHa cells to SB202190 at concentrations that inhibit JNK abolished the protective effect of EGF on SiHa cells against paclitaxel-induced apoptosis. Paclitaxel 134-144 mitogen-activated protein kinase 8 Homo sapiens 69-72 11461094-6 2001 Our findings indicate that the JNK signaling pathway plays an important role in EGF-mediated protection from paclitaxel-induced apoptosis in SiHa cells. Paclitaxel 109-119 mitogen-activated protein kinase 8 Homo sapiens 31-34 11425893-4 2001 Data from non-neuronal cells indicate that taxol-induced apoptosis requires activation of N-terminal c-Jun protein kinase (JNK) that phosphorylates and inactivates Bcl-2. Paclitaxel 43-48 mitogen-activated protein kinase 8 Homo sapiens 101-121 11425893-4 2001 Data from non-neuronal cells indicate that taxol-induced apoptosis requires activation of N-terminal c-Jun protein kinase (JNK) that phosphorylates and inactivates Bcl-2. Paclitaxel 43-48 mitogen-activated protein kinase 8 Homo sapiens 123-126 11425893-9 2001 However, taxol activated a subpool of JNK in the nucleus and stimulated c-Jun phosphorylation. Paclitaxel 9-14 mitogen-activated protein kinase 8 Homo sapiens 38-41 11425893-10 2001 JNK inhibition or expression of a dominant-negative c-Jun abrogated taxol-induced apoptosis in cortical neurons, suggesting a role for JNK and JNK-mediated transcription in taxol-stimulated apoptosis. Paclitaxel 68-73 mitogen-activated protein kinase 8 Homo sapiens 0-3 11425893-10 2001 JNK inhibition or expression of a dominant-negative c-Jun abrogated taxol-induced apoptosis in cortical neurons, suggesting a role for JNK and JNK-mediated transcription in taxol-stimulated apoptosis. Paclitaxel 173-178 mitogen-activated protein kinase 8 Homo sapiens 0-3 11425893-10 2001 JNK inhibition or expression of a dominant-negative c-Jun abrogated taxol-induced apoptosis in cortical neurons, suggesting a role for JNK and JNK-mediated transcription in taxol-stimulated apoptosis. Paclitaxel 173-178 mitogen-activated protein kinase 8 Homo sapiens 135-138 11425893-10 2001 JNK inhibition or expression of a dominant-negative c-Jun abrogated taxol-induced apoptosis in cortical neurons, suggesting a role for JNK and JNK-mediated transcription in taxol-stimulated apoptosis. Paclitaxel 173-178 mitogen-activated protein kinase 8 Homo sapiens 135-138 11278851-4 2001 All three mitogen-activated protein kinase (MAPK) family members, c-Jun N-terminal kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (ERK) were activated upon paclitaxel treatment. Paclitaxel 175-185 mitogen-activated protein kinase 8 Homo sapiens 66-89 11278851-4 2001 All three mitogen-activated protein kinase (MAPK) family members, c-Jun N-terminal kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (ERK) were activated upon paclitaxel treatment. Paclitaxel 175-185 mitogen-activated protein kinase 8 Homo sapiens 91-94