PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21924351-3 2012 Here we show that treatment of cells with nocodazole or paclitaxel does cause phosphorylation of BIM(EL), which is independent of ERK1/2. Paclitaxel 56-66 mitogen-activated protein kinase 3 Homo sapiens 130-136 23478574-3 2013 Paclitaxel exposure activated the Erk1/2/MAPK pathway and promoted the accumulation of the early response transcription factor Egr-1 in MCF-7 cells. Paclitaxel 0-10 mitogen-activated protein kinase 3 Homo sapiens 34-40 23478574-6 2013 These findings suggest that Erk1/2-induced Egr-1 accumulation activates MDR1 transcription and thereby induces the drug resistance observed in paclitaxel-resistant MCF-7 cells. Paclitaxel 143-153 mitogen-activated protein kinase 3 Homo sapiens 28-34 23879997-13 2013 CONCLUSIONS: Human melanoma A375 cells produce resistance to paclitaxel (0.001 to 0.1 micromol/L) by activating MAPK signaling and PI3K/AKT signaling pathways. Paclitaxel 61-71 mitogen-activated protein kinase 3 Homo sapiens 112-116 21391217-5 2012 Furthermore, the activity of ERK1/2 was enhanced by the combination of K8 and paclitaxel, and an ERK1/2 inhibitor dramatically inhibited NAG-1 expression in human lung cancer cells. Paclitaxel 78-88 mitogen-activated protein kinase 3 Homo sapiens 29-35 21391217-8 2012 In addition, treatment of nude mice with K8 combined with paclitaxel induced phospho-ERK1/2 and NAG-1 expression in vivo. Paclitaxel 58-68 mitogen-activated protein kinase 3 Homo sapiens 85-91 21391217-10 2012 Our results reveal that activation of NAG-1 by K8 enhanced the therapeutic efficacy of paclitaxel in human lung cancer cells via the ERK1/2 signaling pathway. Paclitaxel 87-97 mitogen-activated protein kinase 3 Homo sapiens 133-139 18688857-8 2008 The suppressive action of paclitaxel on meningioma cell growth was enhanced in the presence of fluvastatin or the mitogen-actvated protein kinase (ERK1/2) inhibitor PD98059. Paclitaxel 26-36 mitogen-activated protein kinase 3 Homo sapiens 147-153 22005063-0 2011 Paclitaxel induced B7-H1 expression in cancer cells via the MAPK pathway. Paclitaxel 0-10 mitogen-activated protein kinase 3 Homo sapiens 60-64 22005063-3 2011 Moreover, PTX treatment induced Erk1/2 phosphorylation in both cell lines. Paclitaxel 10-13 mitogen-activated protein kinase 3 Homo sapiens 32-38 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 3 Homo sapiens 163-169 18688857-10 2008 In conclusion, our in vitro results suggest that paclitaxel alone or in combination with other inhibitors of cell growth (statins, MAPK inhibitors) could provide a potential tool for the treatment of TLR4 expressing meningiomas. Paclitaxel 49-59 mitogen-activated protein kinase 3 Homo sapiens 131-135 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 3 Homo sapiens 310-316 18487950-7 2008 Subsequent application of specific inhibitors revealed that the paclitaxel-induced cell death is highly impaired by active Erk1/2 and Akt, whereas the cisplatin-induced cell death is independent of both kinases. Paclitaxel 64-74 mitogen-activated protein kinase 3 Homo sapiens 123-129 17936423-8 2007 Cytochalasin D and paclitaxel, but not phalloidin and colchicine, blocked ERK1/2 phosphorylation. Paclitaxel 19-29 mitogen-activated protein kinase 3 Homo sapiens 74-80 16395709-3 2006 In fact, p38 MAPK activity is stimulated by HGF and further increased by the combined treatment with HGF and either CDDP or PTX. Paclitaxel 124-127 mitogen-activated protein kinase 3 Homo sapiens 13-17 16395709-7 2006 Altogether data show that p38 MAPK is necessary for HGF sensitization of ovarian cancer cells to low-doses of CDDP and PTX and might be sufficient to overcome activation of survival pathways. Paclitaxel 119-122 mitogen-activated protein kinase 3 Homo sapiens 30-34 18594523-7 2008 Evaluation of signalling pathways showed that MnSOD siRNA enhanced doxorubicin- and paclitaxel-induced phosphorylation of extracellular signal-regulated kinase 1/2. Paclitaxel 84-94 mitogen-activated protein kinase 3 Homo sapiens 122-163 17400763-5 2007 In contrast, the extracellular signal-regulated kinase 1/2 activities have only a partial effect, being able to modulate Bad phosphorylation but not paclitaxel-induced apoptosis in hypoxia. Paclitaxel 149-159 mitogen-activated protein kinase 3 Homo sapiens 17-56 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 3 Homo sapiens 224-227 15688426-13 2005 We show that Chk1 elimination attenuates the paclitaxel-induced activation of the anti-apoptotic p42/p44 (ERK1/2) MAP kinase pathway, additionally contributing to the sensitization. Paclitaxel 45-55 mitogen-activated protein kinase 3 Homo sapiens 106-112 15778245-6 2005 MT stabilization by taxol (5 microM, 1 h) attenuated nocodazole-induced ERK1/2 and p38 MAPK activation and phosphorylation of p38 MAPK substrate 27-kDa heat shock protein and regulatory myosin light chains, the proteins involved in actin polymerization and actomyosin contraction. Paclitaxel 20-25 mitogen-activated protein kinase 3 Homo sapiens 72-78 15834684-8 2005 On the other hand, the MAP kinase ERK1/2 is modestly inhibited by paclitaxel. Paclitaxel 66-76 mitogen-activated protein kinase 3 Homo sapiens 34-40 15657900-7 2005 As single agents, FAS blocker C75 and Taxol induced a significant stimulation of the proliferation and cell survival mitogen-activated protein kinase extracellular signal-regulated kinase (ERK1/ERK2 MAPK) activity, whereas, in combination, they interfered with ERK1/ERK2 activation. Paclitaxel 38-43 mitogen-activated protein kinase 3 Homo sapiens 189-193 15657900-7 2005 As single agents, FAS blocker C75 and Taxol induced a significant stimulation of the proliferation and cell survival mitogen-activated protein kinase extracellular signal-regulated kinase (ERK1/ERK2 MAPK) activity, whereas, in combination, they interfered with ERK1/ERK2 activation. Paclitaxel 38-43 mitogen-activated protein kinase 3 Homo sapiens 261-265 15592521-10 2005 Strikingly, CYR61 overexpression impaired the accumulation of wild-type p53 following Taxol exposure, while inhibition of alphavbeta3 or ERK1/ERK2 MAPK signalings completely restored Taxol-induced upregulation of p53. Paclitaxel 183-188 mitogen-activated protein kinase 3 Homo sapiens 137-141 15590693-0 2005 Glucocorticoid receptor-induced MAPK phosphatase-1 (MPK-1) expression inhibits paclitaxel-associated MAPK activation and contributes to breast cancer cell survival. Paclitaxel 79-89 mitogen-activated protein kinase 3 Homo sapiens 32-36 15590693-6 2005 Paclitaxel treatment resulted in MAPK activation and apoptosis of MDA-MB-231 breast cancer cells, and both processes were inhibited by Dex pretreatment. Paclitaxel 0-10 mitogen-activated protein kinase 3 Homo sapiens 33-37 11461121-5 2001 Here we demonstrate that Taxol activates ERK 1/2 and p38 MAP-kinases in human ovarian carcinoma cells with distinct kinetics. Paclitaxel 25-30 mitogen-activated protein kinase 3 Homo sapiens 41-48 14742744-7 2004 The importance of activated MAP kinases for DOR internalization is further demonstrated by glutamate and paclitaxel because these substances induce phosphorylation of ERK1/2 and concomitantly prevent DOR sequestration by etorphine. Paclitaxel 105-115 mitogen-activated protein kinase 3 Homo sapiens 167-173 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 3 Homo sapiens 143-149 11710832-5 2001 Inhibition of the ERK1/2 MAP kinase pathway using UO126 or PD098059 re-sensitised the Taxol resistant cells at least 20-fold. Paclitaxel 86-91 mitogen-activated protein kinase 3 Homo sapiens 18-24 11710832-6 2001 Importantly, when Mdr-1 cDNA was stably expressed in the wild-type cell line to generate a highly Taxol-resistant sub-line, 1847/MDR5, ERK1/2 MAP kinases again became activated. Paclitaxel 98-103 mitogen-activated protein kinase 3 Homo sapiens 135-141 15466208-7 2004 Rituximab-mediated effects were corroborated by using specific inhibitors of the ERK1/2 pathway, which also reduced Bcl-(xL) levels and sensitized the NHL B cells to paclitaxel-induced apoptosis. Paclitaxel 166-176 mitogen-activated protein kinase 3 Homo sapiens 81-87 14688474-3 2003 Studies by a number of laboratories have also linked suppression of mitogen activated protein kinase (MAPK) signaling to enhanced Taxol toxicity. Paclitaxel 130-135 mitogen-activated protein kinase 3 Homo sapiens 102-106 11461121-0 2001 The role of ERK 1/2 and p38 MAP-kinase pathways in taxol-induced apoptosis in human ovarian carcinoma cells. Paclitaxel 51-56 mitogen-activated protein kinase 3 Homo sapiens 12-19 11461121-6 2001 Activation of ERK1/2 has been observed at low concentrations of Taxol (1-100 nM) within 0.5-6 h, whereas longer exposure(24 h) to nanomolar concentrations of Taxol resulted in an abrogation of the ERK1/2 phosphorylation/activation. Paclitaxel 64-69 mitogen-activated protein kinase 3 Homo sapiens 14-20 11461121-6 2001 Activation of ERK1/2 has been observed at low concentrations of Taxol (1-100 nM) within 0.5-6 h, whereas longer exposure(24 h) to nanomolar concentrations of Taxol resulted in an abrogation of the ERK1/2 phosphorylation/activation. Paclitaxel 158-163 mitogen-activated protein kinase 3 Homo sapiens 14-20 11461121-6 2001 Activation of ERK1/2 has been observed at low concentrations of Taxol (1-100 nM) within 0.5-6 h, whereas longer exposure(24 h) to nanomolar concentrations of Taxol resulted in an abrogation of the ERK1/2 phosphorylation/activation. Paclitaxel 158-163 mitogen-activated protein kinase 3 Homo sapiens 197-203 11461121-12 2001 We conclude that the alternative use of ERK1/2 and p38 MAP-kinase pathways may be necessary for the transition from proliferation state to Taxol-induced apoptosisin human ovarian carcinoma cells. Paclitaxel 139-144 mitogen-activated protein kinase 3 Homo sapiens 40-46 10773023-8 2000 The ERK1/2 activity in these cells decreased rapidly after paclitaxel treatment or serum withdrawal, but was maintained at a 2-fold higher level in the presence of ET-1 for at least 4 h. These results suggest that the ERK1/2 pathway is activated by ET-1, and blocking this pathway abolishes the antiapoptotic effect of ET-1. Paclitaxel 59-69 mitogen-activated protein kinase 3 Homo sapiens 4-10 10773023-8 2000 The ERK1/2 activity in these cells decreased rapidly after paclitaxel treatment or serum withdrawal, but was maintained at a 2-fold higher level in the presence of ET-1 for at least 4 h. These results suggest that the ERK1/2 pathway is activated by ET-1, and blocking this pathway abolishes the antiapoptotic effect of ET-1. Paclitaxel 59-69 mitogen-activated protein kinase 3 Homo sapiens 218-224 34365218-5 2021 Further, majority of the non-platinum drugs except irinotecan increased ERK1/2 activation in platinum-taxol resistant cells as observed by live-cell BRET assessment which were associated with p90RSK1/2 and BAD activation along with upregulation of multidrug transporter gene ABCC1 and cell survival genes like cyclin D1 and Bcl2. Paclitaxel 102-107 mitogen-activated protein kinase 3 Homo sapiens 72-78 10376521-2 1999 Taxol-induced apoptosis was associated with phosphorylation of both c-Raf-1 and Bcl-2 and activation of ERK and JNK MAP kinases. Paclitaxel 0-5 mitogen-activated protein kinase 3 Homo sapiens 104-107 10376521-5 1999 The serine protease inhibitor did not alter JNK activity, but it enhanced Taxol-induced activation of ERK1/2. Paclitaxel 74-79 mitogen-activated protein kinase 3 Homo sapiens 102-108 10376521-6 1999 Treatment of cells with the inhibitor of MEK activation, PD98059, prevented Taxol-induced ERK activation both in the presence and absence of TPCK, but did not influence survival of either Taxol- or Taxol plus TPCK-treated cells. Paclitaxel 76-81 mitogen-activated protein kinase 3 Homo sapiens 90-93 10376521-8 1999 Thus, while the Taxol-induced phosphorylations of c-Raf-1 and Bcl-2 proteins appear to be coupled, these events can be disassociated from ERK1/2 activation. Paclitaxel 16-21 mitogen-activated protein kinase 3 Homo sapiens 138-144 34365218-4 2021 Utilizing improved PIP3-AKT and ERK1/2 activation Bioluminescence Resonance Energy Transfer (BRET) sensors, we report chemotherapy-induced ERK1/2 activation predominantly in cisplatin-paclitaxel resistant EOC cells and increased activation of both ERK1/2 and AKT in malignant ascites derived cancer cells from platinum-resistant patients but not from treatment-naive or platinum-sensitive relapse patients. Paclitaxel 184-194 mitogen-activated protein kinase 3 Homo sapiens 139-145 34685613-8 2021 Furthermore, the MAPK inhibitors indicated that 7-Epitaxol induces apoptosis and autophagy marker proteins (cleaved-PARP and LC3-I/II) by reducing the phosphorylation of ERK1/2. Paclitaxel 48-58 mitogen-activated protein kinase 3 Homo sapiens 170-176 34685613-9 2021 In conclusion, these findings indicate the involvement of 7-Epitaxol in inducing apoptosis and autophagy through ERK1/2 signaling pathway, which identify 7-Epitaxol as a potent cytotoxic agent in HNSCC. Paclitaxel 58-68 mitogen-activated protein kinase 3 Homo sapiens 113-119 34685613-9 2021 In conclusion, these findings indicate the involvement of 7-Epitaxol in inducing apoptosis and autophagy through ERK1/2 signaling pathway, which identify 7-Epitaxol as a potent cytotoxic agent in HNSCC. Paclitaxel 154-164 mitogen-activated protein kinase 3 Homo sapiens 113-119 31786845-12 2019 CONCLUSIONS: Inhibitor PD98059 combined with paclitaxel can affect the expression of ERK1/2 in ERK1/2 signaling pathway, effectively inhibit the proliferation and invasive abilities of CRC cells, increase the apoptotic ability of CRC cells, and is expected to become a potential drug for clinical treatment of CRC. Paclitaxel 45-55 mitogen-activated protein kinase 3 Homo sapiens 85-91 31786845-12 2019 CONCLUSIONS: Inhibitor PD98059 combined with paclitaxel can affect the expression of ERK1/2 in ERK1/2 signaling pathway, effectively inhibit the proliferation and invasive abilities of CRC cells, increase the apoptotic ability of CRC cells, and is expected to become a potential drug for clinical treatment of CRC. Paclitaxel 45-55 mitogen-activated protein kinase 3 Homo sapiens 95-101 31334335-5 2019 FoxM1 contributed to the PHB1/C-RAF interaction and phosphorylation of ERK1/2 kinases, thus promoting paclitaxel resistance. Paclitaxel 102-112 mitogen-activated protein kinase 3 Homo sapiens 71-77 31293426-6 2019 Furthermore, we found that combined treatment of TMP and PTX suppressed angiogenesis by inhibiting both ERK1/2 and Akt pathways and promoted apoptosis of tumor cells compared to TMP or PTX treatment alone. Paclitaxel 57-60 mitogen-activated protein kinase 3 Homo sapiens 104-110 31334335-11 2019 It was regulated by FoxM1 to maintain phosphorylation of ERK1/2 in drug-resistant cells, and FoxM1 simultaneously enhanced the function of ABCA2, which collectively contributed to paclitaxel resistance. Paclitaxel 180-190 mitogen-activated protein kinase 3 Homo sapiens 57-63 30429459-2 2018 Here we uncovered that either sulforaphane-cysteine (SFN-Cys) or sulforaphane-N-acetyl-cysteine (SFN-NAC) induced apoptosis via phosphorylated ERK1/2-mediated upregulation of 26 S proteasome and Hsp70, and downregulation of betaIII-tubulin, XIAP, Tau, Stathmin1 and alpha-tubulin causing microtubule disruption in human PTX-resistant non-small cell lung cancer (NSCLC) cells. Paclitaxel 320-323 mitogen-activated protein kinase 3 Homo sapiens 143-149 30094097-7 2018 In addition, treatment with oxaliplatin, paclitaxel, vincristine, or bortezomib enhanced ERK1/2 and c-Jun N-terminal kinase (JNK) phosphorylation in the spinal cord lumbar segments 4-6, and when combined with trametinib, can prevent chemotherapy-induced neuropathy via the suppression of ERK1/2 activation, but does not affect JNK activation. Paclitaxel 41-51 mitogen-activated protein kinase 3 Homo sapiens 89-95 30221728-0 2018 Combination of pristimerin and paclitaxel additively induces autophagy in human breast cancer cells via ERK1/2 regulation. Paclitaxel 31-41 mitogen-activated protein kinase 3 Homo sapiens 104-110 30094097-7 2018 In addition, treatment with oxaliplatin, paclitaxel, vincristine, or bortezomib enhanced ERK1/2 and c-Jun N-terminal kinase (JNK) phosphorylation in the spinal cord lumbar segments 4-6, and when combined with trametinib, can prevent chemotherapy-induced neuropathy via the suppression of ERK1/2 activation, but does not affect JNK activation. Paclitaxel 41-51 mitogen-activated protein kinase 3 Homo sapiens 288-294 30064123-12 2018 Furthermore, CA increased the PTX-induced activation of Bax, Bid, and downstream cleaved PARP, and phosphorylation of extracellular signal regulated kinase1/2 and c-Jun NH2-terminal protein kinase1/2. Paclitaxel 30-33 mitogen-activated protein kinase 3 Homo sapiens 118-158 28415580-11 2017 Together, these results indicated that CXCR4 overexpression drives acquired paclitaxel resistance, partly by activating the PDGFA and PDGFB/PDGFRalpha autocrine signaling loops that activate AKT and ERK1/2. Paclitaxel 76-86 mitogen-activated protein kinase 3 Homo sapiens 199-205 29371916-0 2017 The IL-17B-IL-17 receptor B pathway promotes resistance to paclitaxel in breast tumors through activation of the ERK1/2 pathway. Paclitaxel 59-69 mitogen-activated protein kinase 3 Homo sapiens 113-119 27422607-6 2016 Pharmacological suppression of p38 MAPK activity prevents the up-regulation of p-glycoprotein expression and the consequent resistance against paclitaxel in HeyA8-DUSP1 cells. Paclitaxel 143-153 mitogen-activated protein kinase 3 Homo sapiens 35-39 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 3 Homo sapiens 95-101 27619088-7 2016 PTX would perturb the anodic/cathodic responses of the cell-covered biosensor by binding phosphate groups to deformed proteins due to extracellular signal-regulated kinase (ERK(1/2)) pathway. Paclitaxel 0-3 mitogen-activated protein kinase 3 Homo sapiens 134-180 27422607-9 2016 Collectively, these data indicated that DUSP1 may induce the resistance against paclitaxel through the p38 MAPK-mediated overexpression of p-glycoprotein in human ovarian cancer cells. Paclitaxel 80-90 mitogen-activated protein kinase 3 Homo sapiens 107-111