PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24716979-0 2014 Curcumin inhibits MHCC97H liver cancer cells by activating ROS/TLR-4/caspase signaling pathway. Reactive Oxygen Species 59-62 caspase 8 Homo sapiens 69-76 25586525-10 2015 Inhibition of p38 MAPK decreased ROS production, and inhibition of either p38 MAPK or ROS production attenuated apoptotic cell death and activation of caspase-8 and -9. Reactive Oxygen Species 86-89 caspase 8 Homo sapiens 151-167 25275027-4 2014 The FAS receptor and caspase-8 are required for amplification of ROS signaling triggered by individual compounds, but are dispensable when the synergistic effect is established. Reactive Oxygen Species 65-68 caspase 8 Homo sapiens 21-30 24927175-4 2014 Our results are the first to demonstrate that tazarotene induces mitochondria-dependent cleavage of caspase-9 and -3 and PARP in BCC cells by producing reactive oxygen species (ROS) and activating caspase-8 through both ROS and death receptor signaling. Reactive Oxygen Species 220-223 caspase 8 Homo sapiens 197-206 25112602-0 2014 Cartilage polysaccharide induces apoptosis in K562 cells through a reactive oxygen species-mediated caspase pathway. Reactive Oxygen Species 67-90 caspase 8 Homo sapiens 100-107 25447764-8 2015 In this work we demonstrate that after 8 h of incubation with deoxyadenosine and deoxycoformycin, caspase-8 is activated, mitochondrial mass increases and mitochondrial reactive oxygen species decrease. Reactive Oxygen Species 169-192 caspase 8 Homo sapiens 98-107 25018064-1 2014 Our recent studies have demonstrated the key roles of reactive oxygen species (ROS)-mediated caspase-8- and Bax-dependent apoptotic pathways in dihydroartemisinin (DHA)-induced apoptosis of A549 cells. Reactive Oxygen Species 54-77 caspase 8 Homo sapiens 93-102 25018064-1 2014 Our recent studies have demonstrated the key roles of reactive oxygen species (ROS)-mediated caspase-8- and Bax-dependent apoptotic pathways in dihydroartemisinin (DHA)-induced apoptosis of A549 cells. Reactive Oxygen Species 79-82 caspase 8 Homo sapiens 93-102 25018064-8 2014 Collectively, DHA presents more potent proapoptotic actions in A549GR cells preferentially over normal A549 cells via ROS-dependent apoptotic pathway, in which Bax and caspases are involved. Reactive Oxygen Species 118-121 caspase 8 Homo sapiens 168-176 24716979-3 2014 Also, we showed that increased intracellular ROS formation activated the TLR-4/MyD-88 signaling pathway, resulting in activation of caspase-8 and caspase-3, which eventually led to apoptosis in MHCC97H cells. Reactive Oxygen Species 45-48 caspase 8 Homo sapiens 132-141 23826964-6 2013 The apoptotic effect of brefeldin A seems to be mediated by formation of reactive oxygen species and depletion of GSH, which results in the activation of apoptotic caspases. Reactive Oxygen Species 73-96 caspase 8 Homo sapiens 164-172 22289270-10 2012 The other pathway includes increase in ROS, which resulted in activation of NF-kappaB, expression of FasL and triggered FasL-dependent pathway, which also involves caspase-8. Reactive Oxygen Species 39-42 caspase 8 Homo sapiens 164-173 23892367-10 2013 In contrast, RIPK3 participates in caspase-8 activation by acting downstream of the cytosolic death complex assembly, possibly via reactive oxygen species generation. Reactive Oxygen Species 131-154 caspase 8 Homo sapiens 35-44 23921841-0 2013 Licochalcone A enhances geldanamycin-induced apoptosis through reactive oxygen species-mediated caspase activation. Reactive Oxygen Species 63-86 caspase 8 Homo sapiens 96-103 23536891-2 2013 DHA treatment induced a concentration- and time-dependent reactive oxygen species (ROS)-mediated cell death with typical apoptotic characteristics such as breakdown of mitochondrial membrane potential (Deltapsim), caspases activation, DNA fragmentation and phosphatidylserine (PS) externalization. Reactive Oxygen Species 58-81 caspase 8 Homo sapiens 214-222 23536891-2 2013 DHA treatment induced a concentration- and time-dependent reactive oxygen species (ROS)-mediated cell death with typical apoptotic characteristics such as breakdown of mitochondrial membrane potential (Deltapsim), caspases activation, DNA fragmentation and phosphatidylserine (PS) externalization. Reactive Oxygen Species 83-86 caspase 8 Homo sapiens 214-222 23685456-11 2013 These results demonstrated that Dex-mediated activation of caspase-9 via ROS generation and ERK1/2 pathway activation resulted in the activation of caspase-8 and the increment of XAF1, thereby induced apoptosis of EBV-transformed B cells. Reactive Oxygen Species 73-76 caspase 8 Homo sapiens 148-157 22434375-7 2012 Collectively, our data firstly demonstrate that ARTE triggers a ROS-mediated positive feedback amplification activation loop between caspase-8 and -9 independent of mitochondria, which dominantly mediated the ARTE-induced apoptosis via a caspase-3-independent apoptotic pathway in ASTC-a-1 cells. Reactive Oxygen Species 64-67 caspase 8 Homo sapiens 133-149 22365665-4 2012 In the absence of IAPs, rapid and full generation of active IL-1beta by the NLRP3-caspase-1 inflammasome, or by caspase-8, required the kinase RIP3 and reactive oxygen species production. Reactive Oxygen Species 152-175 caspase 8 Homo sapiens 112-121 22160723-7 2011 These cells exhibited a high yield of ROS-induced DNA single- and double-strand breaks and activation of the ATR-Chk1-ATM-Chk2-p53 pathway that led to Fas and caspase-8, -3, and -7 activation, whereas macrophages and DCs derived from them were protected. Reactive Oxygen Species 38-41 caspase 8 Homo sapiens 159-180 21519916-10 2011 Overall, our findings suggest that cryptotanshinone can sensitize TNF-alpha-induced apoptosis in human myeloid leukemia KBM-5 cells, which appears through ROS-dependent activation of caspase-8 and p38. Reactive Oxygen Species 155-158 caspase 8 Homo sapiens 183-192 19646526-9 2009 Thus, this study illustrates that intracellular reactive oxygen species regulated by cytosolic 2-cysPrx is involved in the TNF-alpha-induced apoptotic cell death via controlling caspase activation. Reactive Oxygen Species 48-71 caspase 8 Homo sapiens 178-185 20954801-8 2011 Caspase inhibitors partially altered ROS levels, but did not reduce GSH-depleted cell number, in GA-treated HPF cells. Reactive Oxygen Species 37-40 caspase 8 Homo sapiens 0-7 20799830-0 2010 Single-cell analysis of dihydroartemisinin-induced apoptosis through reactive oxygen species-mediated caspase-8 activation and mitochondrial pathway in ASTC-a-1 cells using fluorescence imaging techniques. Reactive Oxygen Species 69-92 caspase 8 Homo sapiens 102-111 20799830-6 2010 Confocal imaging analysis in a single living cell and Western blot assay showed that DHA triggered ROS-dependent Bax translocation, mitochondrial membrane depolarization, alteration of mitochondrial morphology, cytochrome c release, caspase-9, caspase-8, and caspase-3 activation, indicating the coexistence of ROS-mediated mitochondrial and death receptor pathway. Reactive Oxygen Species 99-102 caspase 8 Homo sapiens 244-253 20799830-7 2010 Collectively, our findings demonstrate for the first time that DHA induces cell apoptosis by triggering ROS-mediated caspase-8/Bid activation and the mitochondrial pathway, which provides some novel insights into the application of DHA as a potential anticancer drug and a new therapeutic strategy by targeting ROS signaling in lung adenocarcinoma therapy in the future. Reactive Oxygen Species 104-107 caspase 8 Homo sapiens 117-126 21308745-4 2011 Cyclosporin A or the caspase-8 inhibitor Z-IETD-FMK blocked AE-induced loss of mitochondrial membrane potential and prevented increases in reactive oxygen species and Ca(++). Reactive Oxygen Species 139-162 caspase 8 Homo sapiens 21-30 21082355-0 2011 Modulation of ROS/MAPK signaling pathways by okadaic acid leads to cell death via, mitochondrial mediated caspase-dependent mechanism. Reactive Oxygen Species 14-17 caspase 8 Homo sapiens 106-113 21082355-9 2011 ROS scavenger-N-acetyl cysteine, mitochondrial stabilizer-cyclosporin-A, and broad spectrum caspase inhibitor Z-VAD-FMK inhibited the OA induced caspase-3 activation, DNA damage and cell death but caspase-8 inhibitor had no effect. Reactive Oxygen Species 0-3 caspase 8 Homo sapiens 197-206 17031493-8 2007 These data suggest that hydrogen peroxide is produced during TRAIL-receptor ligation, and that the increase of intracellular ROS regulates the activation of caspase-8 during apoptosis. Reactive Oxygen Species 125-128 caspase 8 Homo sapiens 157-166 19481559-0 2009 N,N-dimethyl phytosphingosine induces caspase-8-dependent cytochrome c release and apoptosis through ROS generation in human leukemia cells. Reactive Oxygen Species 101-104 caspase 8 Homo sapiens 38-47 18667818-9 2008 Moreover, the quenching of ROS generation by N-acetyl-L-cysteine administration, a scavenger of ROS, reversed the sanguinarine-induced apoptosis effects via inhibition of ROS production, MMP collapse, tBid expression and the subsequent activation of caspases. Reactive Oxygen Species 27-30 caspase 8 Homo sapiens 250-258 18667818-11 2008 CONCLUSION: Our data imply that sanguinarine-induced ROS are key mediators of MMP collapse, which leads to the release of cytochrome c followed by caspase activation, culminating in apoptosis. Reactive Oxygen Species 53-56 caspase 8 Homo sapiens 147-154 17904098-0 2007 Hypoxia/reoxygenation induces apoptosis through a ROS-mediated caspase-8/Bid/Bax pathway in human lymphocytes. Reactive Oxygen Species 50-53 caspase 8 Homo sapiens 63-72 17904098-7 2007 N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis. Reactive Oxygen Species 163-166 caspase 8 Homo sapiens 170-179 17904098-9 2007 Our results also suggest that ROS are critical regulators of caspase-8-mediated apoptosis in H/R-treated human lymphocytes. Reactive Oxygen Species 30-33 caspase 8 Homo sapiens 61-70 17907002-6 2007 Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway. Reactive Oxygen Species 36-39 caspase 8 Homo sapiens 278-287 17907002-6 2007 Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway. Reactive Oxygen Species 252-255 caspase 8 Homo sapiens 81-90 19481559-7 2009 In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis. Reactive Oxygen Species 117-120 caspase 8 Homo sapiens 232-241 19481559-7 2009 In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis. Reactive Oxygen Species 117-120 caspase 8 Homo sapiens 313-322 19481559-7 2009 In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis. Reactive Oxygen Species 117-120 caspase 8 Homo sapiens 232-241 19481559-7 2009 In addition, cells subjected to DMPS exhibited significantly increased reactive oxygen species (ROS) generation, and ROS scavengers, such as quercetin and Tiron, but not N-acetylcysteine (NAC), inhibited DMPS-induced activations of caspase-8, -3 and subsequent apoptotic cell death, indicating the role of ROS in caspase-8-mediated apoptosis. Reactive Oxygen Species 117-120 caspase 8 Homo sapiens 313-322 19481559-9 2009 Our results also suggest that ROS are critical regulators of caspase-8-mediated apoptosis in DMPS-treated leukemia cells. Reactive Oxygen Species 30-33 caspase 8 Homo sapiens 61-70 19406930-4 2009 The TRAIL cytotoxicity by Prx I knockdown was dependent on activation of caspase-8/3 cascades, which was ablated by addition of inhibitors for p38 MAPK, ROS or Nox, suggesting the association with Nox-driven redox signaling. Reactive Oxygen Species 153-156 caspase 8 Homo sapiens 73-82 19166881-4 2009 Our results showed that the expression of human CASP10 and CASP8 triggers certain apoptotic markers such as a massive production of reactive oxygen species (ROS), chromatin condensation and phosphatidylserine externalization, finally leading to cell death. Reactive Oxygen Species 132-155 caspase 8 Homo sapiens 59-64 19166881-4 2009 Our results showed that the expression of human CASP10 and CASP8 triggers certain apoptotic markers such as a massive production of reactive oxygen species (ROS), chromatin condensation and phosphatidylserine externalization, finally leading to cell death. Reactive Oxygen Species 157-160 caspase 8 Homo sapiens 59-64 17727829-9 2007 Taken together our present data showed that a rapid increase in intracellular ROS by MS5 triggers apoptosis via the Fas/caspase-8-mediated mitochondrial pathway suggesting that the presence of diketone makes the compound more potent to induce apoptosis. Reactive Oxygen Species 78-81 caspase 8 Homo sapiens 120-129 11134292-7 2001 Furthermore, E4orf4 induces accumulation of reactive oxygen species (ROS) in a caspase-8- and FADD/MORT1-dependent manner, and inhibition of ROS generation by 4,5-dihydroxy-1, 3-benzene-disulfonic acid (Tiron) inhibits E4orf4-induced apoptosis. Reactive Oxygen Species 44-67 caspase 8 Homo sapiens 79-88 16169029-4 2006 In the early stages, both rapid and transient ROS generation triggered apoptosis via Fas activation and subsequent caspase-8-dependent Bid cleavage, as well as by calpain-mediated mitochondrial Bax cleavage. Reactive Oxygen Species 46-49 caspase 8 Homo sapiens 115-124 16458195-8 2006 Studies using antioxidants and specific caspase inhibitors indicated that activation of caspase-8, but not caspase-9, mediates ROS-dependent caspase-3 activation and suggested that ROS from NADPH oxidase activate caspase-8. Reactive Oxygen Species 127-130 caspase 8 Homo sapiens 88-97 16458195-8 2006 Studies using antioxidants and specific caspase inhibitors indicated that activation of caspase-8, but not caspase-9, mediates ROS-dependent caspase-3 activation and suggested that ROS from NADPH oxidase activate caspase-8. Reactive Oxygen Species 127-130 caspase 8 Homo sapiens 213-222 16458195-8 2006 Studies using antioxidants and specific caspase inhibitors indicated that activation of caspase-8, but not caspase-9, mediates ROS-dependent caspase-3 activation and suggested that ROS from NADPH oxidase activate caspase-8. Reactive Oxygen Species 181-184 caspase 8 Homo sapiens 88-97 16458195-8 2006 Studies using antioxidants and specific caspase inhibitors indicated that activation of caspase-8, but not caspase-9, mediates ROS-dependent caspase-3 activation and suggested that ROS from NADPH oxidase activate caspase-8. Reactive Oxygen Species 181-184 caspase 8 Homo sapiens 213-222 16086031-7 2005 Reactive oxygen species (ROS) were also detected within 1 h after AF treatment, and the antioxidant N-acetyl-L-cysteine (NAC) effectively protected the cells from apoptosis by inhibiting the phosphorylation of p38 MAPK and the activation of caspases. Reactive Oxygen Species 0-23 caspase 8 Homo sapiens 241-249 15451068-9 2004 These results suggest the sequential mechanism of diclofenac-induced apoptosis of HL-60 cells: ROS generation suppresses Akt activity, thereby activating caspase-8, which stimulates Bid cleavage and induces cytochrome c release and the activation of caspase-9 and-3 in a CsA-insensitive mechanism. Reactive Oxygen Species 95-98 caspase 8 Homo sapiens 154-163 16103097-6 2005 Generation of ROS by CCCP was responsible for TRAIL-induced Bax and caspase activation because scavenging ROS completely abrogated apical caspase-8 activation and further downstream events leading to cell death. Reactive Oxygen Species 14-17 caspase 8 Homo sapiens 138-147 16103097-6 2005 Generation of ROS by CCCP was responsible for TRAIL-induced Bax and caspase activation because scavenging ROS completely abrogated apical caspase-8 activation and further downstream events leading to cell death. Reactive Oxygen Species 106-109 caspase 8 Homo sapiens 138-147 13129434-5 2004 This apoptotic pathway induced by abrin is caspase 3-dependent but caspase 8-independent and involves mitochondrial membrane potential damage and reactive oxygen species production. Reactive Oxygen Species 146-169 caspase 8 Homo sapiens 67-76 11134292-7 2001 Furthermore, E4orf4 induces accumulation of reactive oxygen species (ROS) in a caspase-8- and FADD/MORT1-dependent manner, and inhibition of ROS generation by 4,5-dihydroxy-1, 3-benzene-disulfonic acid (Tiron) inhibits E4orf4-induced apoptosis. Reactive Oxygen Species 69-72 caspase 8 Homo sapiens 79-88 34302634-12 2021 CONCLUSIONS: Our study is the first to demonstrate that lactucin-induced apoptosis is mediated by ROS production, which in turn activates the caspase-dependent apoptotic pathway by inhibiting BCL-2 and CFLARL expression in Caki-1 cells. Reactive Oxygen Species 98-101 caspase 8 Homo sapiens 142-149 9354463-6 1997 Cleavage of caspases was preceded by disturbance of mitochondrial membrane potential and by generation of reactive oxygen species. Reactive Oxygen Species 106-129 caspase 8 Homo sapiens 12-20 31392779-5 2019 Caspase activation is dependent on ROS as shown by the ability of CGs to generate ROS and the ROS-N-acetylcysteine (NAC) relationship, which inhibits apoptosis during cotreatment by preventing the formation of caspase-8 and -3. Reactive Oxygen Species 35-38 caspase 8 Homo sapiens 210-226 32616191-8 2020 Taken together, our results revealed that ZLTE induced caspase-dependent apoptosis via ROS generation, suggesting that ZLTE is a promising herbal medicine for the treatment of NSCLC. Reactive Oxygen Species 87-90 caspase 8 Homo sapiens 55-62 32093309-8 2020 In addition, upon enzyme upregulation, both the production of reactive oxygen species and activation of caspase-3 and caspase-8 were reduced. Reactive Oxygen Species 62-85 caspase 8 Homo sapiens 118-127 34479917-7 2021 Furthermore, paclitaxel induced ROS-mediated DNA damage that triggered the activation of the extrinsic pathway of apoptosis via the up-regulation of death receptor (DR5) and caspase-8 activation. Reactive Oxygen Species 32-35 caspase 8 Homo sapiens 174-183 31542488-10 2019 Furthermore, ROS production was found to be a consequence of caspase activation via caspases inhibition. Reactive Oxygen Species 13-16 caspase 8 Homo sapiens 61-68 31542488-10 2019 Furthermore, ROS production was found to be a consequence of caspase activation via caspases inhibition. Reactive Oxygen Species 13-16 caspase 8 Homo sapiens 84-92 31091501-11 2019 Furthermore, the expressions of caspase-3, caspase-8 caspase-9 and Bax were positively correlated with ROS level, but negatively correlated with T-AOC in testis. Reactive Oxygen Species 103-106 caspase 8 Homo sapiens 43-52 30365122-5 2019 The addition of 4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride, a scavenger of reactive oxygen species (ROS), inhibited the degradation of HSP90 client proteins and HSP90 cleavage that was induced by co-treatment as well as the cleavage of caspase-3, caspase-8, and caspase-9 and cell death. Reactive Oxygen Species 88-111 caspase 8 Homo sapiens 260-269 30309851-6 2019 Activation of caspase-8 and cleavage of B-cell receptor-associated protein 31 stimulate a pro-apoptotic crosstalk including release of calcium from the endoplasmic reticulum and an increase in the levels of reactive oxygen species resulting in amplification of mitochondrial apoptosis. Reactive Oxygen Species 207-230 caspase 8 Homo sapiens 14-23 30365122-5 2019 The addition of 4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride, a scavenger of reactive oxygen species (ROS), inhibited the degradation of HSP90 client proteins and HSP90 cleavage that was induced by co-treatment as well as the cleavage of caspase-3, caspase-8, and caspase-9 and cell death. Reactive Oxygen Species 113-116 caspase 8 Homo sapiens 260-269 30211553-7 2018 Therefore, these findings provide novel insight that ROS and p53 signalings mediate p38 phosphorylation and caspase activation in Kaempferol stimulated apoptosis in CRCs. Reactive Oxygen Species 53-56 caspase 8 Homo sapiens 108-115 30009775-1 2018 Recently, we have reported that Demethoxycurcumin induced Reactive oxygen species via inhibition of Mitochondrial Superoxide Dismutase is an initial event to trigger apoptosis through caspase-8 and 9 activation and to inhibit Akt/NF-kappaB survival signaling in human glioma U87 MG cells (Kumar et al., 2018). Reactive Oxygen Species 58-81 caspase 8 Homo sapiens 184-193 30211553-0 2018 Reactive Oxygen Species and p53 Mediated Activation of p38 and Caspases is Critically Involved in Kaempferol Induced Apoptosis in Colorectal Cancer Cells. Reactive Oxygen Species 0-23 caspase 8 Homo sapiens 63-71 30204479-7 2018 ROS production caused DNA damage and apoptosis was marked by cell cycle arrest, up-regulation of Bax and FasL protein as well as cleavage of caspase-9, caspase-8 and caspase-3 protein. Reactive Oxygen Species 0-3 caspase 8 Homo sapiens 152-161 30154785-7 2018 Human neutrophils pretreated with zVAD-fmk (pan-caspase inhibitor) and zIETD-fmk (caspase-8 inhibitor) increased reactive oxygen species (ROS) level in response to Leishmania infection, which is associated with necroptotic cell death. Reactive Oxygen Species 113-136 caspase 8 Homo sapiens 82-91 30154785-7 2018 Human neutrophils pretreated with zVAD-fmk (pan-caspase inhibitor) and zIETD-fmk (caspase-8 inhibitor) increased reactive oxygen species (ROS) level in response to Leishmania infection, which is associated with necroptotic cell death. Reactive Oxygen Species 138-141 caspase 8 Homo sapiens 82-91 29242562-0 2017 ROS-induced cleavage of NHLRC2 by caspase-8 leads to apoptotic cell death in the HCT116 human colon cancer cell line. Reactive Oxygen Species 0-3 caspase 8 Homo sapiens 34-43 29242562-3 2017 Here we show that the NHL-repeat-containing protein 2 (NHLRC2) thioredoxin-like domain protein is cleaved by caspase-8 in ROS-induced apoptosis in the HCT116 human colon cancer cell line. Reactive Oxygen Species 122-125 caspase 8 Homo sapiens 109-118 29242562-7 2017 Furthermore, siRNA-mediated knockdown of caspase-8 blocked the ROS-induced decrease in NHLRC2 protein levels. Reactive Oxygen Species 63-66 caspase 8 Homo sapiens 41-50 29242562-9 2017 These results suggest that excess ROS production causes a caspase-8-mediated decrease in NHLRC2 protein levels, leading to apoptotic cell death in colon cancer cells, and indicate an important role of NHLRC2 in the regulation of ROS-induced apoptosis. Reactive Oxygen Species 34-37 caspase 8 Homo sapiens 58-67 29242562-9 2017 These results suggest that excess ROS production causes a caspase-8-mediated decrease in NHLRC2 protein levels, leading to apoptotic cell death in colon cancer cells, and indicate an important role of NHLRC2 in the regulation of ROS-induced apoptosis. Reactive Oxygen Species 229-232 caspase 8 Homo sapiens 58-67 28888620-7 2017 In a cell-free reconstitution system, caspase-8-mediated Bid cleavage and recombinant tBid induced mitochondrial cytochrome c release and ROS generation, which were blocked by Bcl-xL and antioxidant enzymes. Reactive Oxygen Species 138-141 caspase 8 Homo sapiens 38-47 28888620-9 2017 These data provide evidence that the FADD/caspase-8/Bid/cytochrome c axis is a crucial linker between death receptors and mitochondria, where they play a role in ROS generation and apoptosis. Reactive Oxygen Species 162-165 caspase 8 Homo sapiens 42-51 28888620-0 2017 The caspase-8/Bid/cytochrome c axis links signals from death receptors to mitochondrial reactive oxygen species production. Reactive Oxygen Species 88-111 caspase 8 Homo sapiens 4-13 28888620-4 2017 ROS generation was accompanied by caspase-8 activation, Bid cleavage, and cytochrome c release; it was blocked in FADD- and caspase-8-deficient cells, as well as by caspase-8 knockdown and inhibitor. Reactive Oxygen Species 0-3 caspase 8 Homo sapiens 34-43 27393947-3 2016 In particular, it induced reactive oxygen species-mediated caspase-8/caspase-3-dependent apoptosis as revealed from the increased sub G1 cell population and changes in cell morphology. Reactive Oxygen Species 26-49 caspase 8 Homo sapiens 59-68 28888620-4 2017 ROS generation was accompanied by caspase-8 activation, Bid cleavage, and cytochrome c release; it was blocked in FADD- and caspase-8-deficient cells, as well as by caspase-8 knockdown and inhibitor. Reactive Oxygen Species 0-3 caspase 8 Homo sapiens 124-133 28888620-4 2017 ROS generation was accompanied by caspase-8 activation, Bid cleavage, and cytochrome c release; it was blocked in FADD- and caspase-8-deficient cells, as well as by caspase-8 knockdown and inhibitor. Reactive Oxygen Species 0-3 caspase 8 Homo sapiens 124-133 28542135-8 2017 In conclusion, the results demonstrated that furanodienone-triggered ROS plays a pivotal role in apoptosis as an upstream molecule-modulating activity of caspases in mitochondrial pathway via stimulating MAPKs signaling pathway. Reactive Oxygen Species 69-72 caspase 8 Homo sapiens 154-162 28154184-6 2017 More intriguingly, we find that it is sorafenib-induced ROS accumulation that enables TRAIL to activate caspase-8 in RCC. Reactive Oxygen Species 56-59 caspase 8 Homo sapiens 104-113 28238526-6 2017 Reactive oxygen species-induced mitochondrial DNA oxidative damage and BRCC36 deubiquitinating activity provide a missing link and mechanism by which innate immunity responds to environmental stress via caspase-8-involved NLRP3/NLRP6 inflammasomes. Reactive Oxygen Species 0-23 caspase 8 Homo sapiens 203-212 27993669-7 2017 In contrast, stimulation of cisplatin-induced cell death involved reactive oxygen species-mediated downregulation of FLIP-S, an inhibitor of caspase-8. Reactive Oxygen Species 66-89 caspase 8 Homo sapiens 141-150 27221553-0 2016 Hwang-Heuk-San induces apoptosis in HCT116 human colorectal cancer cells through the ROS-mediated activation of caspases and the inactivation of the PI3K/Akt signaling pathway. Reactive Oxygen Species 85-88 caspase 8 Homo sapiens 112-120 27571890-0 2016 Baicalein induces apoptosis via ROS-dependent activation of caspases in human bladder cancer 5637 cells. Reactive Oxygen Species 32-35 caspase 8 Homo sapiens 60-68 27571890-12 2016 In addition, the blocking of ROS generation decreases the apoptotic activity and antiproliferative effect of baicalein, indicating that baicalein induces apoptosis of 5637 cells through the ROS-dependent activation of caspases. Reactive Oxygen Species 29-32 caspase 8 Homo sapiens 218-226 27571890-12 2016 In addition, the blocking of ROS generation decreases the apoptotic activity and antiproliferative effect of baicalein, indicating that baicalein induces apoptosis of 5637 cells through the ROS-dependent activation of caspases. Reactive Oxygen Species 190-193 caspase 8 Homo sapiens 218-226 26971531-6 2016 In turn, baicalein increased the generation of reactive oxygen species (ROS); however, an ROS scavenger, N-acetylcysteine, notably attenuated baicalein-mediated loss of MMP and activation of caspases. Reactive Oxygen Species 90-93 caspase 8 Homo sapiens 191-199