PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25914345-0 2015 JNK and NFkappaB dependence of apoptosis induced by vinblastine in human acute promyelocytic leukaemia cells. Vinblastine 52-63 mitogen-activated protein kinase 8 Homo sapiens 0-3 25914345-8 2015 Vinblastine treatment suppressed NFkappaB expression and depressed NFkappaB-DNA binding activity while maintaining JNK activation that subsequently resulted in apoptotic response through caspase-dependent pathway. Vinblastine 0-11 mitogen-activated protein kinase 8 Homo sapiens 115-118 25914345-9 2015 Our study provides a possible anti-cancer mechanism of vinblastine action on NB4 cells by deregulation of the intracellular signalling cascade affecting to JNK activation and NFkappaB expression. Vinblastine 55-66 mitogen-activated protein kinase 8 Homo sapiens 156-159 25914345-10 2015 Moreover, JNK activation and NFkappaB depression can be very significant factors in apoptosis induction by vinblastine. Vinblastine 107-118 mitogen-activated protein kinase 8 Homo sapiens 10-13 19427996-3 2009 In KB-3 cells, we have shown previously that vinblastine activates c-Jun NH(2)-terminal protein kinase (JNK) and causes Bax mitochondrial translocation and activation. Vinblastine 45-56 mitogen-activated protein kinase 8 Homo sapiens 67-102 20510207-0 2010 Up-regulation of connexin 32 gene by 5-aza-2"-deoxycytidine enhances vinblastine-induced cytotoxicity in human renal carcinoma cells via the activation of JNK signalling. Vinblastine 69-80 mitogen-activated protein kinase 8 Homo sapiens 155-158 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. Vinblastine 47-58 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. Vinblastine 97-108 mitogen-activated protein kinase 8 Homo sapiens 14-17 19427996-3 2009 In KB-3 cells, we have shown previously that vinblastine activates c-Jun NH(2)-terminal protein kinase (JNK) and causes Bax mitochondrial translocation and activation. Vinblastine 45-56 mitogen-activated protein kinase 8 Homo sapiens 104-107 19427996-5 2009 The JNK inhibitor SP600125 inhibited vinblastine-induced JNK activation and in concert inhibited Bax mitochondrial translocation, Bax oligomerization, and Bax activation. Vinblastine 37-48 mitogen-activated protein kinase 8 Homo sapiens 4-7 19427996-5 2009 The JNK inhibitor SP600125 inhibited vinblastine-induced JNK activation and in concert inhibited Bax mitochondrial translocation, Bax oligomerization, and Bax activation. Vinblastine 37-48 mitogen-activated protein kinase 8 Homo sapiens 57-60 19427996-6 2009 Furthermore, the JNK inhibitor blocked vinblastine-induced apoptosis. Vinblastine 39-50 mitogen-activated protein kinase 8 Homo sapiens 17-20 12907245-0 2003 The JNK, ERK and p53 pathways play distinct roles in apoptosis mediated by the antitumor agents vinblastine, doxorubicin, and etoposide. Vinblastine 96-107 mitogen-activated protein kinase 8 Homo sapiens 4-7 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. Vinblastine 55-66 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. Vinblastine 71-82 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. Vinblastine 71-82 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. Vinblastine 113-124 mitogen-activated protein kinase 8 Homo sapiens 191-194 17126817-2 2007 Treatment of a wide variety of cells with the microtubule inhibitor vinblastine leads to a robust increase in c-Jun expression, JNK-mediated c-Jun phosphorylation, and activation of AP-1-dependent transcription. Vinblastine 68-79 mitogen-activated protein kinase 8 Homo sapiens 128-131 16555127-1 2006 Vinca alkaloids (VAs) such as Vincristine, Vinblastine and Vinorelbine are antineoplastic drugs that inhibit tubulin polymerisation into microtubules, induce mitotic G2/M arrest, activate c-Jun N-terminal kinase (JNK) and induce apoptosis. Vinblastine 43-54 mitogen-activated protein kinase 8 Homo sapiens 188-211 16555127-1 2006 Vinca alkaloids (VAs) such as Vincristine, Vinblastine and Vinorelbine are antineoplastic drugs that inhibit tubulin polymerisation into microtubules, induce mitotic G2/M arrest, activate c-Jun N-terminal kinase (JNK) and induce apoptosis. Vinblastine 43-54 mitogen-activated protein kinase 8 Homo sapiens 213-216 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. Vinblastine 64-75 mitogen-activated protein kinase 8 Homo sapiens 14-17 12221076-4 2002 With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine. Vinblastine 267-278 mitogen-activated protein kinase 8 Homo sapiens 103-109 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. Vinblastine 180-191 mitogen-activated protein kinase 8 Homo sapiens 14-17 11245462-3 2001 We show that these compounds elicit different effects on MAPKs with vinblastine, but not paclitaxel, increasing both c-Jun-NH2-terminal kinase (JNK) and p38 activity. Vinblastine 68-79 mitogen-activated protein kinase 8 Homo sapiens 117-142 11245462-6 2001 This apoptotic induction was attributed to JNK activation because: (a) non-JNK-activating concentrations of vinblastine failed to increase apoptosis in the presence of PD098059; (b) apoptosis induced by paclitaxel, which did not activate JNK, was not potentiated by PD098059; and (c) transduction of an inhibitor of JNK activity partially suppressed both JNK activity and apoptosis induced by vinblastine plus PD098059. Vinblastine 108-119 mitogen-activated protein kinase 8 Homo sapiens 43-46 11245462-6 2001 This apoptotic induction was attributed to JNK activation because: (a) non-JNK-activating concentrations of vinblastine failed to increase apoptosis in the presence of PD098059; (b) apoptosis induced by paclitaxel, which did not activate JNK, was not potentiated by PD098059; and (c) transduction of an inhibitor of JNK activity partially suppressed both JNK activity and apoptosis induced by vinblastine plus PD098059. Vinblastine 108-119 mitogen-activated protein kinase 8 Homo sapiens 75-78 11245462-6 2001 This apoptotic induction was attributed to JNK activation because: (a) non-JNK-activating concentrations of vinblastine failed to increase apoptosis in the presence of PD098059; (b) apoptosis induced by paclitaxel, which did not activate JNK, was not potentiated by PD098059; and (c) transduction of an inhibitor of JNK activity partially suppressed both JNK activity and apoptosis induced by vinblastine plus PD098059. Vinblastine 108-119 mitogen-activated protein kinase 8 Homo sapiens 75-78 11245462-6 2001 This apoptotic induction was attributed to JNK activation because: (a) non-JNK-activating concentrations of vinblastine failed to increase apoptosis in the presence of PD098059; (b) apoptosis induced by paclitaxel, which did not activate JNK, was not potentiated by PD098059; and (c) transduction of an inhibitor of JNK activity partially suppressed both JNK activity and apoptosis induced by vinblastine plus PD098059. Vinblastine 108-119 mitogen-activated protein kinase 8 Homo sapiens 75-78 11245462-6 2001 This apoptotic induction was attributed to JNK activation because: (a) non-JNK-activating concentrations of vinblastine failed to increase apoptosis in the presence of PD098059; (b) apoptosis induced by paclitaxel, which did not activate JNK, was not potentiated by PD098059; and (c) transduction of an inhibitor of JNK activity partially suppressed both JNK activity and apoptosis induced by vinblastine plus PD098059. Vinblastine 108-119 mitogen-activated protein kinase 8 Homo sapiens 75-78 11245462-6 2001 This apoptotic induction was attributed to JNK activation because: (a) non-JNK-activating concentrations of vinblastine failed to increase apoptosis in the presence of PD098059; (b) apoptosis induced by paclitaxel, which did not activate JNK, was not potentiated by PD098059; and (c) transduction of an inhibitor of JNK activity partially suppressed both JNK activity and apoptosis induced by vinblastine plus PD098059. Vinblastine 393-404 mitogen-activated protein kinase 8 Homo sapiens 43-46 11245462-7 2001 Additionally, we found that the activation of JNK by vinblastine occurred upstream of effector caspase activation because treatment with a pan-specific caspase inhibitor (valine-alanine-aspartate-fluoromethylketone) resulted in complete abrogation of apoptosis with no effect on MAPK signaling. Vinblastine 53-64 mitogen-activated protein kinase 8 Homo sapiens 46-49 11245462-8 2001 Taken together, these data suggest that inhibition of the MEK-->ERK signal transduction cascade alleviates cell cycle dependence for vinblastine-induced apoptosis by a mechanism that requires JNK activation. Vinblastine 136-147 mitogen-activated protein kinase 8 Homo sapiens 195-198 11245462-3 2001 We show that these compounds elicit different effects on MAPKs with vinblastine, but not paclitaxel, increasing both c-Jun-NH2-terminal kinase (JNK) and p38 activity. Vinblastine 68-79 mitogen-activated protein kinase 8 Homo sapiens 144-147 10623471-3 2000 All four agents tested (vinblastine, vincristine, Taxol, and colchicine) caused significant (6- to 13-fold) activation of JNK, concomitant inactivation of ERK, and a reduction in basal p38 MAPK activity. Vinblastine 24-35 mitogen-activated protein kinase 8 Homo sapiens 122-125 11103805-5 2000 We show that Bcl-2 phosphorylation and JNK activation, as well as extracellular response kinase and p38 inactivation, occur not only in response to vinblastine but also as discrete transient events at G2-M phase in untreated synchronized KB-3 cells. Vinblastine 148-159 mitogen-activated protein kinase 8 Homo sapiens 39-42 10913135-6 2000 In addition, AS-JNK1/2 inhibited vinblastine-induced phosphorylation of Bcl-2 by 85% and that of Bcl-X(L) by 65%. Vinblastine 33-44 mitogen-activated protein kinase 8 Homo sapiens 16-22 10913135-7 2000 Stable expression of the JNK scaffold protein JIP-1 blocked vinblastine-induced phosphorylation of c-Jun and ATF-2, but did not affect Bcl-2/Bcl-X(L) phosphorylation, confirming a bifurcation in JNK signaling involving both nuclear and non-nuclear substrates. Vinblastine 60-71 mitogen-activated protein kinase 8 Homo sapiens 25-28 10913135-7 2000 Stable expression of the JNK scaffold protein JIP-1 blocked vinblastine-induced phosphorylation of c-Jun and ATF-2, but did not affect Bcl-2/Bcl-X(L) phosphorylation, confirming a bifurcation in JNK signaling involving both nuclear and non-nuclear substrates. Vinblastine 60-71 mitogen-activated protein kinase 8 Homo sapiens 195-198 10913135-0 2000 Vinblastine-induced phosphorylation of Bcl-2 and Bcl-XL is mediated by JNK and occurs in parallel with inactivation of the Raf-1/MEK/ERK cascade. Vinblastine 0-11 mitogen-activated protein kinase 8 Homo sapiens 71-74 10913135-2 2000 Because microtubule inhibitors activate JNK, we sought to determine whether JNK was responsible for Bcl-2/Bcl-X(L) phosphorylation in KB-3 cells treated with vinblastine. Vinblastine 158-169 mitogen-activated protein kinase 8 Homo sapiens 76-79 10913135-3 2000 Two major endogenous forms of JNK, p46(JNK1) and p54(JNK2), were present in KB-3 cells, and both isoforms were activated by vinblastine as determined by Mono Q chromatography. Vinblastine 124-135 mitogen-activated protein kinase 8 Homo sapiens 30-33 10913135-3 2000 Two major endogenous forms of JNK, p46(JNK1) and p54(JNK2), were present in KB-3 cells, and both isoforms were activated by vinblastine as determined by Mono Q chromatography. Vinblastine 124-135 mitogen-activated protein kinase 8 Homo sapiens 39-43 10913135-5 2000 A combination of AS-JNK1 with AS-JNK2 inhibited by 80% vinblastine-induced phosphorylation of two known JNK substrates, c-Jun and ATF-2. Vinblastine 55-66 mitogen-activated protein kinase 8 Homo sapiens 20-24 10913135-5 2000 A combination of AS-JNK1 with AS-JNK2 inhibited by 80% vinblastine-induced phosphorylation of two known JNK substrates, c-Jun and ATF-2. Vinblastine 55-66 mitogen-activated protein kinase 8 Homo sapiens 20-23 9478937-3 1998 We have observed that paclitaxel (Taxol), docetaxel (Taxotere), vinblastine, vincristine, nocodazole, and colchicine activate the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signaling pathway in a variety of human cells. Vinblastine 64-75 mitogen-activated protein kinase 8 Homo sapiens 187-195 8940082-4 1996 Treatment with vinblastine or etoposide (VP-16) also activated JNK, with maximum increases of 6.5- and 4.3-fold, respectively. Vinblastine 15-26 mitogen-activated protein kinase 8 Homo sapiens 63-66 8940082-9 1996 Under conditions optimal for JNK activation, Adriamycin, vinblastine, and VP-16 all induced MDR1 mRNA expression in KB-3 cells. Vinblastine 57-68 mitogen-activated protein kinase 8 Homo sapiens 29-32