PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33054537-9 2021 The time dependent induction of DNA breaks demonstrated in PC3 cells treated with MPO safe concentration stimulated ROS generation and apoptotic DNA damage through increased expression of tumor suppressor p53 and Bax genes and decreased expression of Bcl2 and MDM2 genes. ros 116-119 BCL2 associated X, apoptosis regulator Homo sapiens 213-216 32948186-8 2020 The results of Annexin V-FITC/PI, JC-1, Western blot and ROS analysis showed that the expression of cleaved caspase-3 and Bax were up-regulated Bcl-2 was down-regulated in Cepharanthine or Curcumin treated groups, while ROS and MMP value were decreased at different degrees and the apoptosis rate was reduced. ros 57-60 BCL2 associated X, apoptosis regulator Homo sapiens 122-125 33427275-5 2021 Furthermore, TTRh-CN can efficiently produce ROS in conjunction with lysosomes in situ upon light irradiation, which can damage lysosomes, up-regulate LC3 and Beclin1, increase BAX release, and induce cell apoptosis. ros 45-48 BCL2 associated X, apoptosis regulator Homo sapiens 177-180 32948186-8 2020 The results of Annexin V-FITC/PI, JC-1, Western blot and ROS analysis showed that the expression of cleaved caspase-3 and Bax were up-regulated Bcl-2 was down-regulated in Cepharanthine or Curcumin treated groups, while ROS and MMP value were decreased at different degrees and the apoptosis rate was reduced. ros 220-223 BCL2 associated X, apoptosis regulator Homo sapiens 122-125 31220110-9 2019 Mitochondrial damage and intracellular ROS production were observed upon treatment with AgNPs (10mug/mL) and PDT (0.5 mJ/cm2) showed significant reducing cell migration, expression of Bax and suppression of Bcl-2. ros 39-42 BCL2 associated X, apoptosis regulator Homo sapiens 184-187 29960166-0 2018 ROS mediated ER stress induces Bax-Bak dependent and independent apoptosis in response to Thioridazine. ros 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 31-34 30498348-9 2018 Cellular and molecular assays revealed that NGOs lead to ROS formation, cell cycle arrest, and apoptosis through the BAX and BCL2 pathway. ros 57-60 BCL2 associated X, apoptosis regulator Homo sapiens 117-120 29960166-10 2018 Studies in Bax-Bak knock-out cell model indicated that TDZ trigger both the Bax-Bak dependent and independent apoptosis through ROS. ros 128-131 BCL2 associated X, apoptosis regulator Homo sapiens 11-14 29960166-10 2018 Studies in Bax-Bak knock-out cell model indicated that TDZ trigger both the Bax-Bak dependent and independent apoptosis through ROS. ros 128-131 BCL2 associated X, apoptosis regulator Homo sapiens 76-79 29960166-12 2018 Both Bax-Bak dependent and independent apoptosis were significantly inhibited by ROS inhibitor NAC. ros 81-84 BCL2 associated X, apoptosis regulator Homo sapiens 5-8 29960166-13 2018 Conclusively, TDZ induced Bax-Bak dependent and independent apoptosis by enhancing ROS production followed by ER stress. ros 83-86 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 30048924-5 2018 The intracellular localization assay confirmed that the complex 1 was effectively distributed into mitochondria as well as endoplasmic reticulum (ER), and executed a ROS-mediated calcium and Bax/Bak dependent intrinsic apoptosis. ros 166-169 BCL2 associated X, apoptosis regulator Homo sapiens 191-194 29251335-7 2018 It was observed that marmesin treatment triggered upregulation of Bax and downregulation of Bcl-2 causing significant increase in the Bax/Bcl-2 ratio, marmesin could also induce ROS mediated alterations in mitochondrial membrane potential. ros 178-181 BCL2 associated X, apoptosis regulator Homo sapiens 134-137 29729479-9 2018 Mitochondrial ROS permeation into the cytosol and palmitate-induced ER stress activated JNK and p38, culminating in Bim and Bax overexpression, factors known to increase the outer mitochondrial membrane permeability. ros 14-17 BCL2 associated X, apoptosis regulator Homo sapiens 124-127 26472167-7 2016 Furthermore, ROS generation and subsequent activation of JNK and ERK might be involved in PM2.5 -induced apoptosis and G0/G1 phase arrest by downregulating Bcl-2/Bax protein ratio and upregulating p15INK4B , p16INK4A , and p21WAF1/CIP1 transcription level. ros 13-16 BCL2 associated X, apoptosis regulator Homo sapiens 162-165 29383185-0 2017 GPER-independent inhibition of adrenocortical cancer growth by G-1 involves ROS/Egr-1/BAX pathway. ros 76-79 BCL2 associated X, apoptosis regulator Homo sapiens 86-89 29383185-9 2017 The identified ROS/MAPK/Egr-1/BAX pathway as a potential off-target effect of the G-1 could be useful in implementing the pharmacological approach for ACC therapy. ros 15-18 BCL2 associated X, apoptosis regulator Homo sapiens 30-33 28591670-10 2017 Furthermore, altered levels of ROS triggers intrinsic apoptotic cascade, as evidenced by dissipated mitochondrial membrane potential (psi), decrease in Bcl-2/Bax ratio, cytochrome c release and cleavage of procaspase-3. ros 31-34 BCL2 associated X, apoptosis regulator Homo sapiens 158-161 29088756-7 2017 The ROS, produced by DHS activated the p38 and JNK MAPKs to augment the BAX activity and BID-cleavage, and induce LMP and MMP in the cells. ros 4-7 BCL2 associated X, apoptosis regulator Homo sapiens 72-75 29416349-0 2018 ROS-dependent Bax/Bcl2 and caspase 3 pathway-mediated apoptosis induced by zineb in human keratinocyte cells. ros 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 14-17 27748761-8 2017 We observed that HDACi induced ROS accumulation in cells and apoptosis via promotion of the CFL-1 interaction with Bax and CFL-1 translocation to the mitochondria, resulting in cytochrome C release. ros 31-34 BCL2 associated X, apoptosis regulator Homo sapiens 115-118 27891207-8 2016 These results reveal that GAS has the cytoprotection in HepG2 cells during ROS exposure by inhibiting the caspase activity in the mitochondria and influencing apoptogenic factors of the expression of Bax and Bcl-2. ros 75-78 BCL2 associated X, apoptosis regulator Homo sapiens 200-203 26086416-7 2016 Blockage of ROS production totally reversed WZ26-induced JNK activation, Bcl-2/Bax decrease, ER stress activation, and final cell apoptosis in SGC-7901 cells. ros 12-15 BCL2 associated X, apoptosis regulator Homo sapiens 79-82 26612416-8 2016 Moreover, Se@LDH-pooled siRNAs could induce cell apoptosis, change cell morphology and increase cellular ROS levels through change the expression of Bcl-2/Bax, activation of caspase-3, PI3K/AKT/mTOR and MAPK/ERK pathways. ros 105-108 BCL2 associated X, apoptosis regulator Homo sapiens 155-158 27378626-7 2016 Biochemical evidence of apoptosis came from elevating the intracellular ROS level that was accompanied by mitochondrial membrane potential loss, decreasing the expression profile of anti-apoptotic protein Bcl-2, whereas it augments cleavage of caspase-3 and PARP-1, activates caspase-8 and 9 with concomitant increase in expression of proapoptotic protein Bax in a dose dependent manner. ros 72-75 BCL2 associated X, apoptosis regulator Homo sapiens 356-359 25547582-9 2014 As the glucose concentration increased and duration prolonged, the expression of anti-apoptotic protein Bcl-2 was decreased and pro-apoptotic protein Bax was increased.Intracellular ROS and MDA induced by high glucose were increased significantly with dose-and time-dependence. ros 182-185 BCL2 associated X, apoptosis regulator Homo sapiens 150-153 23769964-11 2013 In conclusion, the study highlights ROS mediated DNA damage, lysosomal and mitochondrial destabilization via upregulation of Bax and activation of caspase-3 which further leads to apoptosis. ros 36-39 BCL2 associated X, apoptosis regulator Homo sapiens 125-128 23732520-4 2013 Consequently, cellular ROS is elevated, leading to the activation of FOXO3a, which contributes to Bim upregulation in Bax/Bak-deficient cells. ros 23-26 BCL2 associated X, apoptosis regulator Homo sapiens 118-121 19113979-3 2009 ROS production induced by complex 1 treatment activated apoptosis through mitochondrial membrane depolarization in all prostate cancer cells, with up-regulation of Bax and down-regulation of Bcl-2 proteins. ros 0-3 BCL2 associated X, apoptosis regulator Homo sapiens 164-167 22848731-8 2012 TSA activated a ROS triggered, p53 independent and caspase dependent mitochondria apoptotic cell death pathway that is characterized with increased ratio of Bax to Bcl-xl, mitochondrial membrane potential disruption, cytochrome c release, and subsequent caspase activation and PARP-1 cleavage. ros 16-19 BCL2 associated X, apoptosis regulator Homo sapiens 157-160 21998736-12 2011 When NQO1(+) cells are treated with combination of IR and beta-lap, positive feedback regulation between ERK and ROS leads to ER stress causing JNK activation and mitochondrial translocation of cleaved Bax. ros 113-116 BCL2 associated X, apoptosis regulator Homo sapiens 202-205 19439215-6 2009 Importantly, we show that the two conserved cysteine residues of Bax seem to be critical for sensing the intracellular ROS to initiate Bax conformational changes and subsequent apoptosis. ros 119-122 BCL2 associated X, apoptosis regulator Homo sapiens 65-68 19439215-6 2009 Importantly, we show that the two conserved cysteine residues of Bax seem to be critical for sensing the intracellular ROS to initiate Bax conformational changes and subsequent apoptosis. ros 119-122 BCL2 associated X, apoptosis regulator Homo sapiens 135-138 21549799-5 2011 Meanwhile, the data showed that olaquindox triggered ROS-mediated apoptosis in HepG2 cells correlated with both the mitochondrial DNA damage and nuclear DNA damage, collapse of Deltapsi(m), opening of mPTP, down-regulation of Bcl-2 and up-regulation of Bax. ros 53-56 BCL2 associated X, apoptosis regulator Homo sapiens 253-256 34403740-11 2021 Moreover, insufficient expression of Bax/Bak counteracted hypoxia-mediated downregulation of mitochondrial function, thereby adding to DHA-induced ROS production and lipid peroxidation in hypoxia. ros 147-150 BCL2 associated X, apoptosis regulator Homo sapiens 37-40 18771651-7 2008 Both BAX(oligo)- and alamethicin-induced cytochrome c releases were accompanied by inhibition of ROS generation, which was assessed by measuring mitochondrial H(2)O(2) release with an Amplex Red assay. ros 97-100 BCL2 associated X, apoptosis regulator Homo sapiens 5-8 18771651-8 2008 The mPT inhibitors antagonized suppression of ROS generation caused by BAX(oligo) but not by alamethicin. ros 46-49 BCL2 associated X, apoptosis regulator Homo sapiens 71-81 18695917-9 2008 These results indicate that activation of p38 MAPK is specifically required for translocation of Bax to the mitochondria, and both JNK and p38 MAPK are involved in phosphorylation of Bcl-2 in response to combination treatment with gamma-radiation and As2O3, and that ROS is a critical regulator of p38 MAPK and JNK activations. ros 267-270 BCL2 associated X, apoptosis regulator Homo sapiens 97-100 34060394-5 2022 Moreover, this agent induced ROS-mediated apoptosis by altering the expression of Bax, Bim, Caspase3, Bcl2, and XIAP. ros 29-32 BCL2 associated X, apoptosis regulator Homo sapiens 82-85