PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29259009-7 2018 By activating MST1 and the JNK/c-Jun pathway, RASSF4 sensitized MM cells to bortezomib. Bortezomib 76-86 mitogen-activated protein kinase 8 Homo sapiens 27-30 33787860-6 2021 Bortezomib enhanced binding immunoglobulin protein/78-kDa glucose-regulated protein (Bip/GRP78) expression induced by endoplasmic reticulum stress and activated apoptosis-promoting molecules JNK and p38 in the cell lines. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 191-194 33674562-0 2021 Ciclopirox and bortezomib synergistically inhibits glioblastoma multiforme growth via simultaneously enhancing JNK/p38 MAPK and NF-kappaB signaling. Bortezomib 15-25 mitogen-activated protein kinase 8 Homo sapiens 111-114 33674562-7 2021 In combination with BTZ, CPX promotes apoptosis in GBM cells through the induction of reactive oxygen species (ROS)-mediated c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling. Bortezomib 20-23 mitogen-activated protein kinase 8 Homo sapiens 125-148 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. Bortezomib 69-79 mitogen-activated protein kinase 8 Homo sapiens 100-123 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. Bortezomib 69-79 mitogen-activated protein kinase 8 Homo sapiens 125-128 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. Bortezomib 69-79 mitogen-activated protein kinase 8 Homo sapiens 327-330 34144391-3 2021 Bortezomib-induced proteasomal inhibition caused severe hepatocellular injury independent of ER stress via proapoptotic Apoptosis Signal-regulating Kinase 1 (ASK1)- c-Jun N-terminal kinase (JNK1)- p38 signaling concomitant with inadequate peroxisome proliferator-activated receptor gamma (PPARgamma)- Nuclear factor erythroid 2-related factor 2 (Nrf2) -driven antioxidant response. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 190-194 33674562-7 2021 In combination with BTZ, CPX promotes apoptosis in GBM cells through the induction of reactive oxygen species (ROS)-mediated c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) signaling. Bortezomib 20-23 mitogen-activated protein kinase 8 Homo sapiens 150-153 23257432-7 2012 It is concluded that the apoptosis of U937 cells synergistically induced by bortezomib combined with low concentration Ara-C is possibly associated with up-regulation of phosphorylated form of JNK, P38 and down-regulation of phosphorylation of ERK induced by increase of ROS, resulting in decrease of mitochondrial potential. Bortezomib 76-86 mitogen-activated protein kinase 8 Homo sapiens 193-196 27390350-11 2016 RESULTS: Combination treatment with bortezomib- and oHSV-induced necroptotic cell death and increased the production of mitochondrial ROS and JNK phosphorylation. Bortezomib 36-46 mitogen-activated protein kinase 8 Homo sapiens 142-145 24158003-7 2013 Moreover, we observed that treatment with bortezomib plus 2ME maintains the activation of c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase kinase kinase 4/7 (MKK4/7). Bortezomib 42-52 mitogen-activated protein kinase 8 Homo sapiens 90-113 24158003-7 2013 Moreover, we observed that treatment with bortezomib plus 2ME maintains the activation of c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase kinase kinase 4/7 (MKK4/7). Bortezomib 42-52 mitogen-activated protein kinase 8 Homo sapiens 115-118 24158003-8 2013 Collectively, combination treatment with bortezomib and 2ME induces cell death via JNK-MKK4/7 activation by overproduction of mitochondrial ROS. Bortezomib 41-51 mitogen-activated protein kinase 8 Homo sapiens 83-86 24086672-0 2013 JNK and macroautophagy activation by bortezomib has a pro-survival effect in primary effusion lymphoma cells. Bortezomib 37-47 mitogen-activated protein kinase 8 Homo sapiens 0-3 24086672-4 2013 We found that bortezomib induced up-regulation of the pro-survival and pro-death ER stress molecules BIP and CHOP and activated c-Jun NH2-terminal kinase (JNK), resulting in Bcl-2 phosphorylation and induction of autophagy. Bortezomib 14-24 mitogen-activated protein kinase 8 Homo sapiens 128-153 24086672-4 2013 We found that bortezomib induced up-regulation of the pro-survival and pro-death ER stress molecules BIP and CHOP and activated c-Jun NH2-terminal kinase (JNK), resulting in Bcl-2 phosphorylation and induction of autophagy. Bortezomib 14-24 mitogen-activated protein kinase 8 Homo sapiens 155-158 24086672-5 2013 JNK and autophagy activation played a pro-survival role in this setting, thus their inhibition increased the bortezomib cytotoxic effect and PARP cleavage in PEL cells. Bortezomib 109-119 mitogen-activated protein kinase 8 Homo sapiens 0-3 29423023-10 2018 Bortezomib treatment also caused activation of the kinase JNK, which played a pro-proliferative and anti-apoptotic role. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 58-61 29423023-11 2018 Hence, the combination of bortezomib with a JNK inhibitor synergized to induce cell death. Bortezomib 26-36 mitogen-activated protein kinase 8 Homo sapiens 44-47 29026157-0 2017 Bortezomib promotes KHSV and EBV lytic cycle by activating JNK and autophagy. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 59-62 29026157-5 2017 In this study, we found that proteasome inhibitor bortezomib, a cytotoxic drug that efficiently target gammaherpesvirus-associated B cell lymphomas, triggered KSHV or EBV viral lytic cycle by activating JNK, in the course of ER stress, and inducing autophagy. Bortezomib 50-60 mitogen-activated protein kinase 8 Homo sapiens 203-206 25602436-0 2015 Bortezomib inhibits gastric carcinoma HGC-27 cells through the phospho-Jun N-terminal kinase (p-JNK) pathway in vitro. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 96-99 25602436-4 2015 Western blot showed that the Bortezomib strongly increased the levels of p-JNK, caspase-3, PARP, and bax proteins while it increased the level of bcl-2. Bortezomib 29-39 mitogen-activated protein kinase 8 Homo sapiens 75-78 24486574-5 2014 The combinational treatment of oxaliplatin and bortezomib promoted the JNK-Bcl-xL-Bax pathway which modulated the synergistic effect through the mitochondria-dependent apoptotic pathway. Bortezomib 47-57 mitogen-activated protein kinase 8 Homo sapiens 71-74 24190701-12 2014 Further, bortezomib-induced pro-apoptotic c-Jun N-terminal kinase (JNK) activation was also associated with ceramide production. Bortezomib 9-19 mitogen-activated protein kinase 8 Homo sapiens 42-65 24190701-12 2014 Further, bortezomib-induced pro-apoptotic c-Jun N-terminal kinase (JNK) activation was also associated with ceramide production. Bortezomib 9-19 mitogen-activated protein kinase 8 Homo sapiens 67-70 24190701-13 2014 JNK activation by bortezomib was suppressed by F-B1, but was enhanced by SKI-II and PDMP in pancreatic cancer cells. Bortezomib 18-28 mitogen-activated protein kinase 8 Homo sapiens 0-3 23079083-4 2013 In addition, bortezomib enhanced the phosphorylation of inositol-requiring transmembrane kinase and endonuclease 1alpha (IRE1alpha), apoptosis signal-regulating kinase 1 (ASK1), c-jun-N-terminal kinase (JNK) and p38, and the activation of the transcription factors AP-1, ATF-2, Ets-1, and HSF1. Bortezomib 13-23 mitogen-activated protein kinase 8 Homo sapiens 178-201 23079083-4 2013 In addition, bortezomib enhanced the phosphorylation of inositol-requiring transmembrane kinase and endonuclease 1alpha (IRE1alpha), apoptosis signal-regulating kinase 1 (ASK1), c-jun-N-terminal kinase (JNK) and p38, and the activation of the transcription factors AP-1, ATF-2, Ets-1, and HSF1. Bortezomib 13-23 mitogen-activated protein kinase 8 Homo sapiens 203-206 22006557-2 2013 We show that BTZ induces the phosphorylation of several mitogen-activated protein (MAP) kinases, including MEK/ERK, c-Jun N-terminal kinase (JNK), and p38 MAPK. Bortezomib 13-16 mitogen-activated protein kinase 8 Homo sapiens 116-139 22006557-2 2013 We show that BTZ induces the phosphorylation of several mitogen-activated protein (MAP) kinases, including MEK/ERK, c-Jun N-terminal kinase (JNK), and p38 MAPK. Bortezomib 13-16 mitogen-activated protein kinase 8 Homo sapiens 141-144 22006557-3 2013 BTZ-induced cell differentiation is almost completely reversed by PD98059, an inhibitor of MEK, which also attenuates the increase in phospho-JNK p46. Bortezomib 0-3 mitogen-activated protein kinase 8 Homo sapiens 142-145 21732139-1 2012 BACKGROUND: Previous study indicated that PS-341 induces cell death via JNK pathway in vitro in glioma. Bortezomib 42-48 mitogen-activated protein kinase 8 Homo sapiens 72-75 21993018-0 2012 Bortezomib induces autophagy in head and neck squamous cell carcinoma cells via JNK activation. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 80-83 22532603-6 2012 The proteasome inhibitor bortezomib blocked NF-kappaB activity, decreased phospho-ERK1/2, increased phospho-c-jun-NH(2)-kinase (p-JNK) levels, reduced expression of resistance factors, restored MART-1 expression to sufficient levels, which in combination allowed M244R lines be sensitized to F5 CTL killing. Bortezomib 25-35 mitogen-activated protein kinase 8 Homo sapiens 130-133 22822672-10 2012 CONCLUSION: The results demonstrate that SDG combined with Bortezomib can significantly induce apoptosis of A549 cells, its mechanisms may be involved in activation of the JNK pathway. Bortezomib 59-69 mitogen-activated protein kinase 8 Homo sapiens 172-175 21993018-4 2012 Pharmacologic inhibition of JNK, but not p38 MAPK, dramatically inhibited bortezomib induction of autophagy regulatory proteins and autophagosome formation. Bortezomib 74-84 mitogen-activated protein kinase 8 Homo sapiens 28-31 21993018-5 2012 These results demonstrate a key requirement for JNK signaling in the activation of autophagy by bortezomib. Bortezomib 96-106 mitogen-activated protein kinase 8 Homo sapiens 48-51 21993018-3 2012 Bortezomib treatment led to phosphorylation/activation of jun N-terminal kinase (JNK) enzymes and JNK-dependent phosphorylation of Bcl-2 on serine 70. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 58-79 21993018-3 2012 Bortezomib treatment led to phosphorylation/activation of jun N-terminal kinase (JNK) enzymes and JNK-dependent phosphorylation of Bcl-2 on serine 70. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 81-84 21993018-3 2012 Bortezomib treatment led to phosphorylation/activation of jun N-terminal kinase (JNK) enzymes and JNK-dependent phosphorylation of Bcl-2 on serine 70. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 98-101 21729547-0 2011 [Effect of different concentrations of bortezomib on the expression of ERK, JNK and P38 in daunorubicin-resistant K562 cells]. Bortezomib 39-49 mitogen-activated protein kinase 8 Homo sapiens 76-79 22606012-6 2012 These results suggested that curcumin might enhance the cytotoxicity of PS-341 by interacting with NF-kappaB, at least in part, through JNK mechanism. Bortezomib 72-78 mitogen-activated protein kinase 8 Homo sapiens 136-139 21729547-1 2011 The aim of this study was to investigate the effect of proteasome inhibitor bortezomib on the expression of ERK, JNK, and P38 in daunorubicin (DNR)-resistant K562 cells and its mechanism. Bortezomib 76-86 mitogen-activated protein kinase 8 Homo sapiens 113-116 21729547-4 2011 The results indicated that the expression of ERK and P38 were significantly suppressed (p < 0.05) and the expression of JNK was significantly enhanced (p < 0.05) in the cells treated by DNR combined with bortezomib. Bortezomib 210-220 mitogen-activated protein kinase 8 Homo sapiens 123-126 21729547-5 2011 It is concluded that bortezomib can decrease the expressions of protein ERK and P38 and enhance the expression of JNK, the bortezomib reverses the cellular drug-resistance and promote cell apoptosis through MAPK pathway. Bortezomib 21-31 mitogen-activated protein kinase 8 Homo sapiens 114-117 21729547-5 2011 It is concluded that bortezomib can decrease the expressions of protein ERK and P38 and enhance the expression of JNK, the bortezomib reverses the cellular drug-resistance and promote cell apoptosis through MAPK pathway. Bortezomib 123-133 mitogen-activated protein kinase 8 Homo sapiens 114-117 22087283-0 2011 The proteasome inhibitor bortezomib enhances ATRA-induced differentiation of neuroblastoma cells via the JNK mitogen-activated protein kinase pathway. Bortezomib 25-35 mitogen-activated protein kinase 8 Homo sapiens 105-108 22087283-9 2011 The combination of bortezomib and ATRA triggered increased differentiation through the activation of proteins, including RARalpha, RARbeta, RARgamma, p-JNK and p21, compared with ATRA treatment alone. Bortezomib 19-29 mitogen-activated protein kinase 8 Homo sapiens 152-155 21755010-10 2011 Combined use of 6-OAP and bortezomib induced potentiated cytotoxicity with inactivation of ERK1/2 and activation of JNK1/2 and Casp-8/-3. Bortezomib 26-36 mitogen-activated protein kinase 8 Homo sapiens 116-122 21176351-1 2010 The study was aimed to investigate the effects of bortezomib (BTZ) on the expression of ERK, JNK and P38 in daunorubicin (DNR)-resistant K562 cells (K562/DNR) and to clarify the molecular mechanism of BTZ in reversing the drug-resistance in leukemic cells. Bortezomib 50-60 mitogen-activated protein kinase 8 Homo sapiens 93-96 21176351-1 2010 The study was aimed to investigate the effects of bortezomib (BTZ) on the expression of ERK, JNK and P38 in daunorubicin (DNR)-resistant K562 cells (K562/DNR) and to clarify the molecular mechanism of BTZ in reversing the drug-resistance in leukemic cells. Bortezomib 62-65 mitogen-activated protein kinase 8 Homo sapiens 93-96 19267218-0 2010 Bmf is upregulated by PS-341-mediated cell death of glioma cells through JNK phosphorylation. Bortezomib 22-28 mitogen-activated protein kinase 8 Homo sapiens 73-76 19270531-4 2009 Pharmacologic or genetic (e.g., shRNA knockdown) interruption of JNK signaling attenuated HA14-1/bortezomib lethality and ER stress induction. Bortezomib 97-107 mitogen-activated protein kinase 8 Homo sapiens 65-68 19608275-7 2010 The enhanced cytotoxicity of ATO+bortezomib was associated with augmented STAT3 inhibition and JNK activation, up-regulation of Bim, p21, p27, p53 as well as down-regulation of Bcl-2. Bortezomib 33-43 mitogen-activated protein kinase 8 Homo sapiens 95-98 19270531-0 2009 Bcl-2 antagonists interact synergistically with bortezomib in DLBCL cells in association with JNK activation and induction of ER stress. Bortezomib 48-58 mitogen-activated protein kinase 8 Homo sapiens 94-97 19270531-7 2009 Finally, HA14-1 significantly increased bortezomib-mediated JNK activation, ER stress induction, and lethality in bortezomib-resistant cells. Bortezomib 40-50 mitogen-activated protein kinase 8 Homo sapiens 60-63 19270531-8 2009 Collectively these findings indicate that small molecule Bcl-2 antagonists promote bortezomib-mediated mitochondrial injury and lethality in DLBCL cells in association with enhanced JNK activation and ER stress induction. Bortezomib 83-93 mitogen-activated protein kinase 8 Homo sapiens 182-185 18559525-9 2008 Therefore, CGC-11093 enhances the anticancer activity of bortezomib by augmenting JNK-mediated apoptosis and blocking angiogenesis. Bortezomib 57-67 mitogen-activated protein kinase 8 Homo sapiens 82-85 18559525-8 2008 Furthermore, inhibition of JNK with a pharmacologic inhibitor or by selective knockdown blunted the efficacy of CGC-11093 and bortezomib. Bortezomib 126-136 mitogen-activated protein kinase 8 Homo sapiens 27-30 16528474-0 2006 JNK and AP-1 mediate apoptosis induced by bortezomib in HepG2 cells via FasL/caspase-8 and mitochondria-dependent pathways. Bortezomib 42-52 mitogen-activated protein kinase 8 Homo sapiens 0-3 16985072-0 2006 Cytotoxic synergy between the multikinase inhibitor sorafenib and the proteasome inhibitor bortezomib in vitro: induction of apoptosis through Akt and c-Jun NH2-terminal kinase pathways. Bortezomib 91-101 mitogen-activated protein kinase 8 Homo sapiens 151-176 16528474-8 2006 In addition, bortezomib caused activation of JNK1, which in turn increased the level of phospho-c-Jun as well as stimulated the activation of caspase-3 and t-Bid, two fundamental apoptotic factors. Bortezomib 13-23 mitogen-activated protein kinase 8 Homo sapiens 45-49 16528474-10 2006 Both JNK-1 and AP-1 thus exerted a crucial role in bortezomib-induced apoptosis. Bortezomib 51-61 mitogen-activated protein kinase 8 Homo sapiens 5-10 15217830-6 2004 Furthermore, PK + bortezomib activates c-Jun NH2 terminal kinase (JNK), which translocates to mitochondria, thereby facilitating release of cyto-c and Smac from mitochondria to cytosol. Bortezomib 18-28 mitogen-activated protein kinase 8 Homo sapiens 39-64 16357177-6 2005 Importantly, combined therapy with bortezomib plus cisplatin induced JNK activation and apoptosis in orthotopic pancreatic tumors resulting in a reduction in tumor burden. Bortezomib 35-45 mitogen-activated protein kinase 8 Homo sapiens 69-72 15735676-6 2005 We have previously shown that PS-341 treatment triggers phosphorylation of c-Jun NH(2)-terminal kinase (JNK), which subsequently induces caspase-dependent apoptosis; conversely, JNK inhibition blocks PS-341-induced apoptosis. Bortezomib 30-36 mitogen-activated protein kinase 8 Homo sapiens 75-102 15735676-6 2005 We have previously shown that PS-341 treatment triggers phosphorylation of c-Jun NH(2)-terminal kinase (JNK), which subsequently induces caspase-dependent apoptosis; conversely, JNK inhibition blocks PS-341-induced apoptosis. Bortezomib 30-36 mitogen-activated protein kinase 8 Homo sapiens 104-107 15735676-6 2005 We have previously shown that PS-341 treatment triggers phosphorylation of c-Jun NH(2)-terminal kinase (JNK), which subsequently induces caspase-dependent apoptosis; conversely, JNK inhibition blocks PS-341-induced apoptosis. Bortezomib 30-36 mitogen-activated protein kinase 8 Homo sapiens 178-181 15735676-6 2005 We have previously shown that PS-341 treatment triggers phosphorylation of c-Jun NH(2)-terminal kinase (JNK), which subsequently induces caspase-dependent apoptosis; conversely, JNK inhibition blocks PS-341-induced apoptosis. Bortezomib 200-206 mitogen-activated protein kinase 8 Homo sapiens 75-102 15735676-6 2005 We have previously shown that PS-341 treatment triggers phosphorylation of c-Jun NH(2)-terminal kinase (JNK), which subsequently induces caspase-dependent apoptosis; conversely, JNK inhibition blocks PS-341-induced apoptosis. Bortezomib 200-206 mitogen-activated protein kinase 8 Homo sapiens 104-107 15735676-6 2005 We have previously shown that PS-341 treatment triggers phosphorylation of c-Jun NH(2)-terminal kinase (JNK), which subsequently induces caspase-dependent apoptosis; conversely, JNK inhibition blocks PS-341-induced apoptosis. Bortezomib 200-206 mitogen-activated protein kinase 8 Homo sapiens 178-181 16357177-4 2005 Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism. Bortezomib 19-29 mitogen-activated protein kinase 8 Homo sapiens 126-153 16357177-4 2005 Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism. Bortezomib 19-29 mitogen-activated protein kinase 8 Homo sapiens 155-158 15531918-9 2005 PS-341 activated JNK/c-Jun signaling in GBM cells, and the JNK inhibitor SP600125 blocked the JNK signaling to reverse partially the PS-341 growth inhibition. Bortezomib 0-6 mitogen-activated protein kinase 8 Homo sapiens 17-20 15217830-6 2004 Furthermore, PK + bortezomib activates c-Jun NH2 terminal kinase (JNK), which translocates to mitochondria, thereby facilitating release of cyto-c and Smac from mitochondria to cytosol. Bortezomib 18-28 mitogen-activated protein kinase 8 Homo sapiens 66-69 15217830-7 2004 Blocking JNK, by either dominant-negative mutant (DN-JNK) or cotreatment with a specific JNK inhibitor SP600125, abrogates both PK + bortezomib-induced release of cyto-c/Smac and induction of apoptosis. Bortezomib 133-143 mitogen-activated protein kinase 8 Homo sapiens 9-12 15217830-7 2004 Blocking JNK, by either dominant-negative mutant (DN-JNK) or cotreatment with a specific JNK inhibitor SP600125, abrogates both PK + bortezomib-induced release of cyto-c/Smac and induction of apoptosis. Bortezomib 133-143 mitogen-activated protein kinase 8 Homo sapiens 53-56 15217830-7 2004 Blocking JNK, by either dominant-negative mutant (DN-JNK) or cotreatment with a specific JNK inhibitor SP600125, abrogates both PK + bortezomib-induced release of cyto-c/Smac and induction of apoptosis. Bortezomib 133-143 mitogen-activated protein kinase 8 Homo sapiens 53-56 14965369-5 2004 Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role. Bortezomib 114-120 mitogen-activated protein kinase 8 Homo sapiens 24-27 15093752-5 2004 Conversely, pharmacologic MEK/ERK1/2 inhibition promoted Bortezomib-mediated JNK activation and apoptosis. Bortezomib 57-67 mitogen-activated protein kinase 8 Homo sapiens 77-80 15093752-8 2004 Together, these findings suggest that in human leukemia cells, Bortezomib-induced oxidative injury operates at a proximal point in the cell death cascade to antagonize cytoprotective ERK1/2 signaling, promote activation of the stress-related JNK pathway, and to trigger mitochondrial dysfunction, caspase activation, and apoptosis. Bortezomib 63-73 mitogen-activated protein kinase 8 Homo sapiens 242-245 15093752-9 2004 They also suggest the presence of a feedback loop wherein Bortezomib-mediated ERK1/2 inactivation contributes to JNK activation, thereby amplifying the cell death process. Bortezomib 58-68 mitogen-activated protein kinase 8 Homo sapiens 113-116 15093752-2 2004 Treatment of Jurkat or U937 cells with Bortezomib resulted in activation of c-Jun-N-terminal kinase (JNK) and p38 MAPK (mitogen-activated protein kinase), inactivation of extracellular signal-regulating kinase 1/2 (ERK1/2), cytochrome c release, caspase-9, -3, and -8 activation, and apoptosis. Bortezomib 39-49 mitogen-activated protein kinase 8 Homo sapiens 76-99 15093752-2 2004 Treatment of Jurkat or U937 cells with Bortezomib resulted in activation of c-Jun-N-terminal kinase (JNK) and p38 MAPK (mitogen-activated protein kinase), inactivation of extracellular signal-regulating kinase 1/2 (ERK1/2), cytochrome c release, caspase-9, -3, and -8 activation, and apoptosis. Bortezomib 39-49 mitogen-activated protein kinase 8 Homo sapiens 101-104 15093752-3 2004 Bortezomib-mediated cytochrome c release and caspase activation were blocked by the pharmacologic JNK inhibitor SP600125, but lethality was not diminished by the p38 MAPK inhibitor SB203580. Bortezomib 0-10 mitogen-activated protein kinase 8 Homo sapiens 98-101 14965369-0 2004 Proteasome inhibitor PS-341 induces growth arrest and apoptosis of non-small cell lung cancer cells via the JNK/c-Jun/AP-1 signaling. Bortezomib 21-27 mitogen-activated protein kinase 8 Homo sapiens 108-111 14965369-4 2004 Also, PS-341 caused phosphorylation of c-Jun NH(2)-terminal kinase (JNK) and c-Jun, and enhanced AP-1/DNA binding activities in these cells as measured by western blotting and enzyme-linked immunosorbent assay (ELISA), respectively. Bortezomib 6-12 mitogen-activated protein kinase 8 Homo sapiens 39-66 14965369-4 2004 Also, PS-341 caused phosphorylation of c-Jun NH(2)-terminal kinase (JNK) and c-Jun, and enhanced AP-1/DNA binding activities in these cells as measured by western blotting and enzyme-linked immunosorbent assay (ELISA), respectively. Bortezomib 6-12 mitogen-activated protein kinase 8 Homo sapiens 68-71 14965369-5 2004 Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role. Bortezomib 114-120 mitogen-activated protein kinase 8 Homo sapiens 75-78 14965369-5 2004 Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role. Bortezomib 114-120 mitogen-activated protein kinase 8 Homo sapiens 75-78 14965369-5 2004 Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role. Bortezomib 382-388 mitogen-activated protein kinase 8 Homo sapiens 24-27 14965369-5 2004 Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role. Bortezomib 382-388 mitogen-activated protein kinase 8 Homo sapiens 75-78 14965369-5 2004 Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role. Bortezomib 382-388 mitogen-activated protein kinase 8 Homo sapiens 75-78 12393500-5 2003 Inhibition of JNK activity abrogates PS-341-induced MM cell death. Bortezomib 37-43 mitogen-activated protein kinase 8 Homo sapiens 14-17 12393500-4 2003 We here demonstrate molecular mechanisms whereby PS-341 mediates anti-MM activity by inducing p53 and MDM2 protein expression; inducing the phosphorylation (Ser15) of p53 protein; activating c-Jun NH(2)-terminal kinase (JNK), caspase-8, and caspase-3; and cleaving the DNA protein kinase catalytic subunit, ATM, and MDM2. Bortezomib 49-55 mitogen-activated protein kinase 8 Homo sapiens 191-218 12393500-4 2003 We here demonstrate molecular mechanisms whereby PS-341 mediates anti-MM activity by inducing p53 and MDM2 protein expression; inducing the phosphorylation (Ser15) of p53 protein; activating c-Jun NH(2)-terminal kinase (JNK), caspase-8, and caspase-3; and cleaving the DNA protein kinase catalytic subunit, ATM, and MDM2. Bortezomib 49-55 mitogen-activated protein kinase 8 Homo sapiens 220-223