PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31357761-9 2019 SP600125 and SB203580 had inhibited oxidative stress and apoptosis induced by palmitic acid (including CYP2E1, MDA, Bax, Bcl-2, caspase3, CHOP) (P< 0.05). pyrazolanthrone 0-8 BCL2 associated X, apoptosis regulator Homo sapiens 116-119 31362241-8 2019 VSMCs treated with siRNA-ANXA3 or SP600125 showed decreased expression of JNK, caspase-3, osteopontin (OPN), Bax, and matrix metalloproteinase-9 (MMP-9), as well as phosphate (p)-JNK, but increased the expression of alpha smooth muscle actin (alpha-SMA), beta-tubulin, and Bcl-2. pyrazolanthrone 34-42 BCL2 associated X, apoptosis regulator Homo sapiens 109-112 30368882-7 2019 Pretreatment with JNK-specific inhibitors SP600125 markedly upregulated the reduced B-cell lymphoma 2 (Bcl-2) content and downregulated the increased Bcl-2-associated X protein (Bax) level and thereby eventually reduced the proportions of early and late apoptotic cells induced by ACR, while p38 suppression by SB202190 only reversed the decrease in Bcl-2 expression. pyrazolanthrone 42-50 BCL2 associated X, apoptosis regulator Homo sapiens 150-176 30368882-7 2019 Pretreatment with JNK-specific inhibitors SP600125 markedly upregulated the reduced B-cell lymphoma 2 (Bcl-2) content and downregulated the increased Bcl-2-associated X protein (Bax) level and thereby eventually reduced the proportions of early and late apoptotic cells induced by ACR, while p38 suppression by SB202190 only reversed the decrease in Bcl-2 expression. pyrazolanthrone 42-50 BCL2 associated X, apoptosis regulator Homo sapiens 178-181 30290166-8 2018 Pre-incubation with inhibitors of JNK (SP600125) and p38 (SB202190) significantly decreases the BAX/BCL2 ratio. pyrazolanthrone 39-47 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 30574018-15 2018 Furthermore, we found that the JNK inhibitor SP600125 completely diminished the mobility shift of YAP and its phosphorylation at Tyr357, the binding of YAP and p73, the transcription of Bax and p53AIP1 as well as the apoptosis induced by ABF. pyrazolanthrone 45-53 BCL2 associated X, apoptosis regulator Homo sapiens 186-189 29330470-9 2018 Simultaneously, inhibition of JNK by SP600125 abolished beta-Ecd-induced Bax downregulation in Abeta-challenged SH-SY5Y cells, whereas LY294002 failed to do so. pyrazolanthrone 37-45 BCL2 associated X, apoptosis regulator Homo sapiens 73-76 28546532-11 2017 Supplementation of JNK-specific inhibitor (SP600125) decreased expression of Bax and cleaved caspase 3/9, and alleviated ADMA-induced apoptosis. pyrazolanthrone 43-51 BCL2 associated X, apoptosis regulator Homo sapiens 77-80 28756921-6 2017 In cells treated with 40 mumol/L juglone and SP600125, the protein expressions of Bax, CytC, Fas, FasL and Caspase-3 were significantly lower than those of cells treated with 40 mumol/L juglone (P < 0.05), and the protein expressions of Bax, CytC, Fas, FasL and Caspase-3 reduced more remarkably as the SP600125 dosage increased (P < 0.05). pyrazolanthrone 45-53 BCL2 associated X, apoptosis regulator Homo sapiens 82-85 28756921-6 2017 In cells treated with 40 mumol/L juglone and SP600125, the protein expressions of Bax, CytC, Fas, FasL and Caspase-3 were significantly lower than those of cells treated with 40 mumol/L juglone (P < 0.05), and the protein expressions of Bax, CytC, Fas, FasL and Caspase-3 reduced more remarkably as the SP600125 dosage increased (P < 0.05). pyrazolanthrone 45-53 BCL2 associated X, apoptosis regulator Homo sapiens 240-243 29045468-9 2017 The JNK inhibitor SP600125 strongly inhibited Bax expression. pyrazolanthrone 18-26 BCL2 associated X, apoptosis regulator Homo sapiens 46-49 25958204-6 2015 SP600125 (SAPK/JNK inhibitor) and SB203580 (p38 MAPK inhibitor) attenuated down-regulation of Bcl-xL/Bcl-2, mitochondrial translocation of Bax, and cytochrome c release from mitochondria. pyrazolanthrone 0-8 BCL2 associated X, apoptosis regulator Homo sapiens 139-142 26296767-3 2015 In this study, we showed that the HCV-induced activation and mitochondrial accumulation of Bax were significantly attenuated by treatment with a general antioxidant, N-acetyl cysteine (NAC), or a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, with the result suggesting that the reactive oxygen species (ROS)/JNK signalling pathway is upstream of Bax activation in HCV-induced apoptosis. pyrazolanthrone 246-254 BCL2 associated X, apoptosis regulator Homo sapiens 91-94 27233606-7 2016 In the presence of SP600125, expression of cleaved caspase-9/-3 and p53 as well as the ratio of Bax to Bcl-2 was significantly decreased compared to treatment with TNF-alpha alone. pyrazolanthrone 19-27 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 26849940-7 2016 While, SP600125 (one JNK inhibitor) and SB203580 (one p38 inhibitor) markedly up-regulated Bcl-2 level, down-regulated the levels of Bax, cleaved caspase-3/9, and obviously boosted Cytochrome c release induced by dioscin. pyrazolanthrone 7-15 BCL2 associated X, apoptosis regulator Homo sapiens 133-136 27848251-9 2016 This subsequently increased Bax activation, leading to marked aRVS-induced apoptosis, whereas the JNK inhibitor SP600125 in aRVS extract treated SKOV-3 cells strongly inhibited Bax. pyrazolanthrone 112-120 BCL2 associated X, apoptosis regulator Homo sapiens 177-180 23326144-13 2012 Furthermore, the JNK specific inhibitor, SP600125, suppressed p-JNK, Bax and caspase-3 at the protein level in SGC790l cells following thermotherapy, compared to mock-inhibitor treatment, which was in line with the decreased rate of apoptosis. pyrazolanthrone 41-49 BCL2 associated X, apoptosis regulator Homo sapiens 69-72 25178491-7 2015 Specific JNK inhibitor SP600125 prevented the PYDDT-induced down-regulation of Bcl-2, mitochondrial translocation of Bax, activation of caspase 3, and apoptosis of SW620 cells. pyrazolanthrone 23-31 BCL2 associated X, apoptosis regulator Homo sapiens 117-120 20653470-7 2010 SP600125 also attenuated Bax protein content and p53 nuclear accumulation induced by H(2)O(2). pyrazolanthrone 0-8 BCL2 associated X, apoptosis regulator Homo sapiens 25-28 21250978-11 2011 RH1-induced generation and mitochondrial translocation of cleaved Bax were blocked by the JNK inhibitor, SP600125. pyrazolanthrone 105-113 BCL2 associated X, apoptosis regulator Homo sapiens 66-69 20709060-0 2010 The JNK inhibitor SP600125 enhances dihydroartemisinin-induced apoptosis by accelerating Bax translocation into mitochondria in human lung adenocarcinoma cells. pyrazolanthrone 18-26 BCL2 associated X, apoptosis regulator Homo sapiens 89-92 20709060-1 2010 The C-Jun N-terminal Kinase (JNK) inhibitor SP600125 is widely used to inhibit the JNK-mediated Bax activation and cell apoptosis. pyrazolanthrone 44-52 BCL2 associated X, apoptosis regulator Homo sapiens 96-99 20709060-2 2010 However, this report demonstrates that SP600125 synergistically enhances the dihydroartemisinin (DHA)-induced human lung adenocarcinoma cell apoptosis by accelerating Bax translocation and subsequent intrinsic apoptotic pathway involving mitochondrial membrane depolarization, cytochrome c release, caspase-9 and caspase-3 activation. pyrazolanthrone 39-47 BCL2 associated X, apoptosis regulator Homo sapiens 167-170 20709060-3 2010 The dynamical analysis of GFP-Bax mobility inside single living cells using fluorescence recovery after photobleaching revealed that SP600125 aggravated the DHA-induced decrease of Bax mobility and Bax translocation. pyrazolanthrone 133-141 BCL2 associated X, apoptosis regulator Homo sapiens 30-33 20709060-3 2010 The dynamical analysis of GFP-Bax mobility inside single living cells using fluorescence recovery after photobleaching revealed that SP600125 aggravated the DHA-induced decrease of Bax mobility and Bax translocation. pyrazolanthrone 133-141 BCL2 associated X, apoptosis regulator Homo sapiens 181-184 20709060-3 2010 The dynamical analysis of GFP-Bax mobility inside single living cells using fluorescence recovery after photobleaching revealed that SP600125 aggravated the DHA-induced decrease of Bax mobility and Bax translocation. pyrazolanthrone 133-141 BCL2 associated X, apoptosis regulator Homo sapiens 181-184 19699753-7 2009 Both SP600125 and SB203580 attenuated the activation of Bax and cytochrome c release, and reversed down-regulation of Bcl-2, XIAP, survivin, cyclin A, cyclin B, and Cdk1 in IQDMA-treated cells. pyrazolanthrone 5-13 BCL2 associated X, apoptosis regulator Homo sapiens 56-59 20423716-5 2010 SP600125, but not the vehicle, reduced JNK activation, attenuated mitochondrial Bax translocation and prevented the mitochondrial release of apoptosis-inducing factor at 4-12h. pyrazolanthrone 0-8 BCL2 associated X, apoptosis regulator Homo sapiens 80-83 20423716-11 2010 Our data suggest that the JNK inhibitor SP600125 protects against APAP-induced liver injury in part by attenuation of mitochondrial Bax translocation but mainly by preventing mitochondrial oxidant stress and peroxynitrite formation and thereby preventing the mitochondrial permeability transition pore opening, a key event in APAP-induced cell necrosis. pyrazolanthrone 40-48 BCL2 associated X, apoptosis regulator Homo sapiens 132-135 20144638-6 2010 SB202190 (p38 MAPK inhibitor) and SP600125 (JNK inhibitor) suppressed CMS-9-induced dissipation of mitochondrial membrane potential, Bcl-2 down-regulation, Bax up-regulation and increased mitochondrial translocation of Bax. pyrazolanthrone 34-42 BCL2 associated X, apoptosis regulator Homo sapiens 156-159 20144638-6 2010 SB202190 (p38 MAPK inhibitor) and SP600125 (JNK inhibitor) suppressed CMS-9-induced dissipation of mitochondrial membrane potential, Bcl-2 down-regulation, Bax up-regulation and increased mitochondrial translocation of Bax. pyrazolanthrone 34-42 BCL2 associated X, apoptosis regulator Homo sapiens 219-222 20346929-9 2010 Butyrate triggered the caspase apoptotic pathway, indicated by an enhanced Bax-to-Bcl-2 expression ratio and caspase cascade reaction, which was blocked by SP600125. pyrazolanthrone 156-164 BCL2 associated X, apoptosis regulator Homo sapiens 75-78 19427996-5 2009 The JNK inhibitor SP600125 inhibited vinblastine-induced JNK activation and in concert inhibited Bax mitochondrial translocation, Bax oligomerization, and Bax activation. pyrazolanthrone 18-26 BCL2 associated X, apoptosis regulator Homo sapiens 97-100 19540902-5 2009 SB202190 (p38 MAPK inhibitor) and SP600125 (JNK inhibitor) attenuated mitochondrial depolarization, degradation of Bcl-2/Bcl-xL, and mitochondrial translocation of Bax. pyrazolanthrone 34-42 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 19427996-5 2009 The JNK inhibitor SP600125 inhibited vinblastine-induced JNK activation and in concert inhibited Bax mitochondrial translocation, Bax oligomerization, and Bax activation. pyrazolanthrone 18-26 BCL2 associated X, apoptosis regulator Homo sapiens 130-133 19427996-5 2009 The JNK inhibitor SP600125 inhibited vinblastine-induced JNK activation and in concert inhibited Bax mitochondrial translocation, Bax oligomerization, and Bax activation. pyrazolanthrone 18-26 BCL2 associated X, apoptosis regulator Homo sapiens 130-133 19427996-7 2009 The ability of vinblastine to induce Bax translocation and the inhibitory effect of SP600125 were confirmed in cells stably expressing GFP-Bax. pyrazolanthrone 84-92 BCL2 associated X, apoptosis regulator Homo sapiens 139-142 17494073-8 2007 Moreover, the pharmacological inhibition of JNK by SP600125 inhibits Bax activation and cytochrome c release. pyrazolanthrone 51-59 BCL2 associated X, apoptosis regulator Homo sapiens 69-72 17904874-5 2007 Prolonged SP600125 treatment downregulated p21, Bax and Mdm2 expression, but increased the level of the cellular p53-Mdm2 complex. pyrazolanthrone 10-18 BCL2 associated X, apoptosis regulator Homo sapiens 48-51 18718914-5 2008 JNK inhibitor (SP600125) or p38 MAPK inhibitor (SB203580) pretreatment attenuated 15d-PGJ(2)-mediated apoptosis and suppressed the p21(Waf1) and Bax expressions without affecting p53 protein accumulation. pyrazolanthrone 15-23 BCL2 associated X, apoptosis regulator Homo sapiens 145-148 15936998-12 2005 Moreover, SP600125, a specific inhibitor of JNK, suppressed Bax expression induced by syndecan-2 overexpression, indicating that JNK activation mediates syndecan-2-induced apoptosis. pyrazolanthrone 10-18 BCL2 associated X, apoptosis regulator Homo sapiens 60-63 17113036-10 2007 Cell incubation with either PRIMA-1 or SP600125 (c-Jun NH2-terminal kinase inhibitor) resulted in the abrogation of adriamycin-induced c-Jun NH2-terminal kinase (JNK) activation, whereas Bax activation was not inhibited. pyrazolanthrone 39-47 BCL2 associated X, apoptosis regulator Homo sapiens 187-190 15356200-6 2004 SP600125 blocked translocation of the cell death effector Bax from the cytosol to the mitochondria after tFCI. pyrazolanthrone 0-8 BCL2 associated X, apoptosis regulator Homo sapiens 58-61 15117824-6 2004 We further show that a JNK-specific inhibitor SP600125 completely blocks TNF induced JNK activation, Bid cleavage, and Bax mitochondrial translocation, but only partially inhibits cytochrome c release and EC death, suggesting that TNF induces both JNK-dependent and JNK-independent apoptotic pathways in EC. pyrazolanthrone 46-54 BCL2 associated X, apoptosis regulator Homo sapiens 119-122 12527812-14 2003 Furthermore, SP600125 pretreatment effectively prevented the TRO-mediated changes in Bad, Bax, Bid cleavage, and cytochrome c release. pyrazolanthrone 13-21 BCL2 associated X, apoptosis regulator Homo sapiens 90-93 15034932-9 2004 Also, apoptosis was observed to be induced by SP600125, concomitant with the increase in c-myc, p53, and bax protein level. pyrazolanthrone 46-54 BCL2 associated X, apoptosis regulator Homo sapiens 105-108 15034932-11 2004 When the cells were treated with NDGA or SP600125 in the presence of antisense c-myc oligonucleotides, apoptosis was not observed and an increase of c-myc, p53, and bax proteins was not manifested. pyrazolanthrone 41-49 BCL2 associated X, apoptosis regulator Homo sapiens 165-168