PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30692634-5 2019 Overexpression of RUNX3 increased DR5 expression via induction of the reactive oxygen species (ROS)-endoplasmic reticulum (ER) stress-effector CHOP. Reactive Oxygen Species 70-93 DNA damage inducible transcript 3 Homo sapiens 143-147 30692634-5 2019 Overexpression of RUNX3 increased DR5 expression via induction of the reactive oxygen species (ROS)-endoplasmic reticulum (ER) stress-effector CHOP. Reactive Oxygen Species 95-98 DNA damage inducible transcript 3 Homo sapiens 143-147 30798142-6 2019 Furthermore, luteolin increases levels of intracellular reactive oxygen species (ROS) by activation of lethal endoplasmic reticulum stress response and mitochondrial dysfunction in glioblastoma cells, and by activation of ER stress-associated proteins expressions, including phosphorylation of eIF2alpha, PERK, CHOP, ATF4, and cleaved-caspase 12. Reactive Oxygen Species 56-79 DNA damage inducible transcript 3 Homo sapiens 311-315 30798142-6 2019 Furthermore, luteolin increases levels of intracellular reactive oxygen species (ROS) by activation of lethal endoplasmic reticulum stress response and mitochondrial dysfunction in glioblastoma cells, and by activation of ER stress-associated proteins expressions, including phosphorylation of eIF2alpha, PERK, CHOP, ATF4, and cleaved-caspase 12. Reactive Oxygen Species 81-84 DNA damage inducible transcript 3 Homo sapiens 311-315 29964331-0 2018 Inhibition of euchromatin histone-lysine N-methyltransferase 2 sensitizes breast cancer cells to tumor necrosis factor-related apoptosis-inducing ligand through reactive oxygen species-mediated activating transcription factor 4-C/EBP homologous protein-death receptor 5 pathway activation. Reactive Oxygen Species 161-184 DNA damage inducible transcript 3 Homo sapiens 228-252 30300626-8 2018 Reactive oxygen species (ROS) overproduction by chrysophanol resulted in endoplasmic reticulum (ER) stress, leading to an increase in PERK, eIF2alpha, GADD153, and IRE1alpha levels in BT-474 and MCF-7 cells. Reactive Oxygen Species 0-23 DNA damage inducible transcript 3 Homo sapiens 151-158 30300626-8 2018 Reactive oxygen species (ROS) overproduction by chrysophanol resulted in endoplasmic reticulum (ER) stress, leading to an increase in PERK, eIF2alpha, GADD153, and IRE1alpha levels in BT-474 and MCF-7 cells. Reactive Oxygen Species 25-28 DNA damage inducible transcript 3 Homo sapiens 151-158 30871017-4 2019 Capsazepine can modulate Janus activated kinase (JAK)/signal transducer and activator of the transcription (STAT) pathway, intracellular Ca2+ concentration, and reactive oxygen species (ROS)-JNK-CCAAT/enhancer-binding protein homologous protein (CHOP) pathways. Reactive Oxygen Species 186-189 DNA damage inducible transcript 3 Homo sapiens 246-250 29964331-7 2018 Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL. Reactive Oxygen Species 24-47 DNA damage inducible transcript 3 Homo sapiens 145-149 29433671-8 2018 The three phytochemicals activated the ROS-p38-p53 apoptotic pathway by increasing the level of phosphorylated p38 MAPK and p53, and they activated the ER stress-mediated apoptotic pathway by increasing the level of phosphorylated eIF2alpha and C/EBP homologous protein (CHOP). Reactive Oxygen Species 39-42 DNA damage inducible transcript 3 Homo sapiens 245-269 29964331-8 2018 These findings suggest that BIX-01294 sensitizes breast cancer cells to TRAIL by upregulating ATF4/CHOP-dependent DR5 expression with a reactive oxygen species-dependent manner. Reactive Oxygen Species 136-159 DNA damage inducible transcript 3 Homo sapiens 99-103 29167125-8 2018 Expression of Bnip3 and CHOP, two proapoptotic targets of HIF-1alpha and ROS pathways, respectively, was suppressed by hMSC-CM, while Bcl-2 expression was restored. Reactive Oxygen Species 73-76 DNA damage inducible transcript 3 Homo sapiens 24-28 29328423-7 2018 Cisplatin and cetuximab demonstrated a combinatorial effect on increasing the levels of CHOP, caspase-3 activity and apoptosis, which was largely eliminated by overexpression of TXNDC5 or a reactive oxygen species (ROS) scavenger/antagonist. Reactive Oxygen Species 190-213 DNA damage inducible transcript 3 Homo sapiens 88-92 29433671-8 2018 The three phytochemicals activated the ROS-p38-p53 apoptotic pathway by increasing the level of phosphorylated p38 MAPK and p53, and they activated the ER stress-mediated apoptotic pathway by increasing the level of phosphorylated eIF2alpha and C/EBP homologous protein (CHOP). Reactive Oxygen Species 39-42 DNA damage inducible transcript 3 Homo sapiens 271-275 29164887-10 2017 Overall, our results showed that PTER potentiated TRAIL-induced apoptosis via ROS-mediated CHOP activation leading to the expression of DR4 and DR5. Reactive Oxygen Species 78-81 DNA damage inducible transcript 3 Homo sapiens 91-95 28630460-11 2017 Interestingly, CHOP was positively correlated with TNFalpha and total ROS production and GRP78 was negatively correlated with glutathione levels. Reactive Oxygen Species 70-73 DNA damage inducible transcript 3 Homo sapiens 15-19 28668332-6 2017 Ethanol stimulated reactive oxygen species (ROS) production, which induced CHOP expression and eIF2alpha phosphorylation. Reactive Oxygen Species 19-42 DNA damage inducible transcript 3 Homo sapiens 75-79 28668332-6 2017 Ethanol stimulated reactive oxygen species (ROS) production, which induced CHOP expression and eIF2alpha phosphorylation. Reactive Oxygen Species 44-47 DNA damage inducible transcript 3 Homo sapiens 75-79 27895312-3 2016 Mechanistically, LZ-205 triggers reactive oxygen species (ROS)-induced endoplasmic reticulum (ER) stress and unfolded protein response, which could be reversed by silencing CHOP, a mediator of the ER stress-associated apoptosis. Reactive Oxygen Species 33-56 DNA damage inducible transcript 3 Homo sapiens 173-177 28412728-7 2017 Andrographolide-induced cell death, UPR signaling, and CHOP, Bax, and caspase 3 apoptosis elements were all inhibited in the presence of the ROS scavenger NAC. Reactive Oxygen Species 141-144 DNA damage inducible transcript 3 Homo sapiens 55-59 28573788-9 2017 Increased production of ROS was accompanied by upregulation of CHOP and Noxa. Reactive Oxygen Species 24-27 DNA damage inducible transcript 3 Homo sapiens 63-67 28402965-6 2017 Blocking ROS production attenuated the expression of two markers of ER stress: binding of immunoglobulin protein (BIP) and CCAAT/enhancer-binding protein homologous protein (CHOP). Reactive Oxygen Species 9-12 DNA damage inducible transcript 3 Homo sapiens 123-172 28402965-6 2017 Blocking ROS production attenuated the expression of two markers of ER stress: binding of immunoglobulin protein (BIP) and CCAAT/enhancer-binding protein homologous protein (CHOP). Reactive Oxygen Species 9-12 DNA damage inducible transcript 3 Homo sapiens 174-178 28402965-7 2017 Blocking CHOP expression using RNA interference also inhibited ROS generation. Reactive Oxygen Species 63-66 DNA damage inducible transcript 3 Homo sapiens 9-13 28642847-5 2017 Bax is essential for endoplasmic reticulum (ER) stress-triggered apoptosis, and our RNAi experiments showed that the PERK-eIF2-CHOP pathway and reactive oxygen species (ROS) are also main participants in this process. Reactive Oxygen Species 169-172 DNA damage inducible transcript 3 Homo sapiens 127-131 28642847-6 2017 LT-induced ROS generation was decreased in CHOP-knockdown HCT-8 cells compared to that in control cells. Reactive Oxygen Species 11-14 DNA damage inducible transcript 3 Homo sapiens 43-47 28642847-7 2017 Moreover, pretreatment with the ROS inhibitor NAC down-regulated GRP78, CHOP, Bim, and cleaved caspase-3 expression, resulting in a reduction in the apoptosis rate from 36.2 to 20.3% in LT-treated HCT-8 cells. Reactive Oxygen Species 32-35 DNA damage inducible transcript 3 Homo sapiens 72-76 28323103-7 2017 Moreover, inhibition of C/EBA homologous protein (CHOP) expression by siRNA partially prevented Cr(VI)-induced cell apoptosis, mitochondrial dysfunction and ROS generation. Reactive Oxygen Species 157-160 DNA damage inducible transcript 3 Homo sapiens 24-48 28323103-7 2017 Moreover, inhibition of C/EBA homologous protein (CHOP) expression by siRNA partially prevented Cr(VI)-induced cell apoptosis, mitochondrial dysfunction and ROS generation. Reactive Oxygen Species 157-160 DNA damage inducible transcript 3 Homo sapiens 50-54 28282786-4 2017 Promoted expression of CHOP, a down-streaming transcription factor for endoplasmic reticulum stress (ER stress), enhanced death factor 4 (DR4) activity and accelerated reactive oxygen species (ROS) as well as cell death. Reactive Oxygen Species 168-191 DNA damage inducible transcript 3 Homo sapiens 23-27 28282786-4 2017 Promoted expression of CHOP, a down-streaming transcription factor for endoplasmic reticulum stress (ER stress), enhanced death factor 4 (DR4) activity and accelerated reactive oxygen species (ROS) as well as cell death. Reactive Oxygen Species 193-196 DNA damage inducible transcript 3 Homo sapiens 23-27 27895312-3 2016 Mechanistically, LZ-205 triggers reactive oxygen species (ROS)-induced endoplasmic reticulum (ER) stress and unfolded protein response, which could be reversed by silencing CHOP, a mediator of the ER stress-associated apoptosis. Reactive Oxygen Species 58-61 DNA damage inducible transcript 3 Homo sapiens 173-177 27634458-6 2016 Treatments of SH-SY5Y cells with the chemical chaperone, 4-phenylbutyric acid and the ROS scavenger, N-acetyl-cysteine reduced the AA-induced expression of ATF4 protein and CHOP mRNA, and resulted in the suppression of apoptosis. Reactive Oxygen Species 86-89 DNA damage inducible transcript 3 Homo sapiens 173-177 27573888-9 2016 Elevated expression of spliced X-box binding protein 1 (XBP1) and CCAAT/enhancer-binding protein homologous protein (CHOP) further confirmed that ROS generated by NTGP induces apoptosis through the ER stress signaling pathway. Reactive Oxygen Species 146-149 DNA damage inducible transcript 3 Homo sapiens 66-115 27573888-9 2016 Elevated expression of spliced X-box binding protein 1 (XBP1) and CCAAT/enhancer-binding protein homologous protein (CHOP) further confirmed that ROS generated by NTGP induces apoptosis through the ER stress signaling pathway. Reactive Oxygen Species 146-149 DNA damage inducible transcript 3 Homo sapiens 117-121 27432061-4 2016 In addition, ECH suppressed the ROS and MPP(+)-induced expression of apoptotic genes (ATF3, CHOP, and SCNA). Reactive Oxygen Species 32-35 DNA damage inducible transcript 3 Homo sapiens 92-96 27432061-9 2016 Taken together, these data suggest that the ROS/ATF3/CHOP pathway plays a critical role in mechanisms by which ECH protects against MPP(+)-induced apoptosis in PD. Reactive Oxygen Species 44-47 DNA damage inducible transcript 3 Homo sapiens 53-57 26847145-7 2016 Moreover, Lico B promoted the generation of reactive oxygen species (ROS), which, in turn, can induce CHOP, death receptor (DR) 4 and DR5. Reactive Oxygen Species 44-67 DNA damage inducible transcript 3 Homo sapiens 102-106 27262990-8 2016 As CHOP is an endoplasmic reticulum (ER)-stress related apoptosis marker of which production is induced by ROS, it was considered that these CS components induce apoptosis of SW620 cells by increasing ROS synthesis and ER-stress. Reactive Oxygen Species 107-110 DNA damage inducible transcript 3 Homo sapiens 3-7 27262990-8 2016 As CHOP is an endoplasmic reticulum (ER)-stress related apoptosis marker of which production is induced by ROS, it was considered that these CS components induce apoptosis of SW620 cells by increasing ROS synthesis and ER-stress. Reactive Oxygen Species 201-204 DNA damage inducible transcript 3 Homo sapiens 3-7 26847145-7 2016 Moreover, Lico B promoted the generation of reactive oxygen species (ROS), which, in turn, can induce CHOP, death receptor (DR) 4 and DR5. Reactive Oxygen Species 69-72 DNA damage inducible transcript 3 Homo sapiens 102-106 24525405-5 2014 Consequently, the integrated ER stress signals, such as eIF2alpha, ATF4, BiP, and CHOP are altered accordingly to induce ER-Ca2+ release, reactive oxygen species (ROS) overproduction, and cell death in HLECs treated with VPA. Reactive Oxygen Species 138-161 DNA damage inducible transcript 3 Homo sapiens 82-86 26284193-7 2015 The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1alpha in SKOV-3) in response to ROS accumulation induced by PEITC (5 muM). Reactive Oxygen Species 260-263 DNA damage inducible transcript 3 Homo sapiens 45-49 26284193-7 2015 The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1alpha in SKOV-3) in response to ROS accumulation induced by PEITC (5 muM). Reactive Oxygen Species 260-263 DNA damage inducible transcript 3 Homo sapiens 50-57 26284193-8 2015 ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the effect of PEITC on UPR signatures (P-PERK, IRE1alpha, CHOP/GADD153, and BiP/GRP78), suggesting the involvement of ROS in UPR-mediated apoptosis. Reactive Oxygen Species 0-3 DNA damage inducible transcript 3 Homo sapiens 111-115 26284193-8 2015 ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the effect of PEITC on UPR signatures (P-PERK, IRE1alpha, CHOP/GADD153, and BiP/GRP78), suggesting the involvement of ROS in UPR-mediated apoptosis. Reactive Oxygen Species 0-3 DNA damage inducible transcript 3 Homo sapiens 116-123 26009870-1 2015 BACKGROUND: Previously we have reported that generation of reactive oxygen species is the prime event responsible for calcium mediated activation of PERK-eIF2alpha-CHOP pathway and apoptosis in UV-B irradiated human skin fibroblasts (Hs68). Reactive Oxygen Species 59-82 DNA damage inducible transcript 3 Homo sapiens 164-168 25872712-4 2015 Moreover, the antioxidant N-acetylcysteine (NAC) and pro-apoptotic transcription factor CHOP knockdown were used to clarify the precise interplay between reactive oxygen species (ROS), ER stress and their roles in NaF-induced apoptosis in Sertoli cells. Reactive Oxygen Species 154-177 DNA damage inducible transcript 3 Homo sapiens 88-92 25023940-0 2014 Piperlongumine induces cell death through ROS-mediated CHOP activation and potentiates TRAIL-induced cell death in breast cancer cells. Reactive Oxygen Species 42-45 DNA damage inducible transcript 3 Homo sapiens 55-59 25023940-8 2014 Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation. Reactive Oxygen Species 22-25 DNA damage inducible transcript 3 Homo sapiens 96-100 25023940-8 2014 Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation. Reactive Oxygen Species 22-25 DNA damage inducible transcript 3 Homo sapiens 174-178 25023940-8 2014 Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation. Reactive Oxygen Species 156-159 DNA damage inducible transcript 3 Homo sapiens 96-100 25023940-8 2014 Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation. Reactive Oxygen Species 156-159 DNA damage inducible transcript 3 Homo sapiens 174-178 25023940-11 2014 CONCLUSIONS: Overall, our data suggest a new mechanism for the PL-induced cell death in which ROS mediates CHOP activation, and combination treatment with PL and TRAIL could be a potential strategy for breast cancer therapy. Reactive Oxygen Species 94-97 DNA damage inducible transcript 3 Homo sapiens 107-111 25788268-0 2015 Piperlongumine selectively kills hepatocellular carcinoma cells and preferentially inhibits their invasion via ROS-ER-MAPKs-CHOP. Reactive Oxygen Species 111-114 DNA damage inducible transcript 3 Homo sapiens 124-128 25412307-7 2014 Our study demonstrates a pivotal role of ROS/VSOR in mediating ER stress and functional impairment of cardiomyocytes via the CHOP-Wnt pathway, and suggests the therapeutic values of VSOR Cl(-) channel blockers against ER stress-associated cardiac anomalies. Reactive Oxygen Species 41-44 DNA damage inducible transcript 3 Homo sapiens 125-129 25104093-5 2014 ROS, the expression levels of glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the combination of the two elements. Reactive Oxygen Species 0-3 DNA damage inducible transcript 3 Homo sapiens 74-98 24612139-0 2014 Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway. Reactive Oxygen Species 135-158 DNA damage inducible transcript 3 Homo sapiens 174-223 24612139-0 2014 Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway. Reactive Oxygen Species 135-158 DNA damage inducible transcript 3 Homo sapiens 225-229 24612139-0 2014 Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway. Reactive Oxygen Species 160-163 DNA damage inducible transcript 3 Homo sapiens 174-223 24612139-0 2014 Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway. Reactive Oxygen Species 160-163 DNA damage inducible transcript 3 Homo sapiens 225-229 24612139-6 2014 Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins. Reactive Oxygen Species 93-96 DNA damage inducible transcript 3 Homo sapiens 159-163 24612139-8 2014 Overall, our data suggest that quercetin enhances apoptotic death of ovarian cancer cells to TRAIL through upregulation of CHOP-induced DR5 expression following ROS mediated endoplasmic reticulum-stress. Reactive Oxygen Species 161-164 DNA damage inducible transcript 3 Homo sapiens 123-127 24213373-9 2014 In addition, indomethacin-induced reactive oxygen species (ROS) production preceded upregulation of CHOP and DR5, and consequent sensitization of cells to TRAIL. Reactive Oxygen Species 34-57 DNA damage inducible transcript 3 Homo sapiens 100-104 24213373-9 2014 In addition, indomethacin-induced reactive oxygen species (ROS) production preceded upregulation of CHOP and DR5, and consequent sensitization of cells to TRAIL. Reactive Oxygen Species 59-62 DNA damage inducible transcript 3 Homo sapiens 100-104 24525405-5 2014 Consequently, the integrated ER stress signals, such as eIF2alpha, ATF4, BiP, and CHOP are altered accordingly to induce ER-Ca2+ release, reactive oxygen species (ROS) overproduction, and cell death in HLECs treated with VPA. Reactive Oxygen Species 163-166 DNA damage inducible transcript 3 Homo sapiens 82-86 24078627-8 2013 Up-regulation of DRs was mediated through the generation of reactive oxygen species (ROS) as ROS scavengers reduced the effect of azadirone on ERK activation, CHOP up-regulation, DR induction, and TRAIL sensitization. Reactive Oxygen Species 60-83 DNA damage inducible transcript 3 Homo sapiens 159-163 24551210-9 2014 Conversely, blocking ER stress using CHOP siRNA decreased AMP-induced ROS production and cell apoptosis. Reactive Oxygen Species 70-73 DNA damage inducible transcript 3 Homo sapiens 37-41 24078627-8 2013 Up-regulation of DRs was mediated through the generation of reactive oxygen species (ROS) as ROS scavengers reduced the effect of azadirone on ERK activation, CHOP up-regulation, DR induction, and TRAIL sensitization. Reactive Oxygen Species 85-88 DNA damage inducible transcript 3 Homo sapiens 159-163 24078627-8 2013 Up-regulation of DRs was mediated through the generation of reactive oxygen species (ROS) as ROS scavengers reduced the effect of azadirone on ERK activation, CHOP up-regulation, DR induction, and TRAIL sensitization. Reactive Oxygen Species 93-96 DNA damage inducible transcript 3 Homo sapiens 159-163 24078627-12 2013 Overall, this study indicates that azadirone can sensitize cancer cells to TRAIL through ROS-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival proteins, and up-regulation of proapoptotic proteins. Reactive Oxygen Species 89-92 DNA damage inducible transcript 3 Homo sapiens 97-101 22676837-7 2013 Furthermore, knocking down CHOP by RNA interference decreased ROS generation, increased glutathione level and induced glutathione peroxidase mRNA expression in alpha-TOS-treated cells, whereas catalase and superoxide dismutases mRNA expression were not altered. Reactive Oxygen Species 62-65 DNA damage inducible transcript 3 Homo sapiens 27-31 23554101-6 2013 In conclusion, HDMC induces apoptosis in human nonsmall cell lung cancer cells via activation of DR5 signaling pathway, and ROS-mediated ATF4-CHOP axis is involved in the process. Reactive Oxygen Species 124-127 DNA damage inducible transcript 3 Homo sapiens 142-146 23333652-7 2013 Finally, we showed that CHOP induction by t10,c12 CLA was dependent on ROS production and that the anti-oxidant N-acetyl-cysteine reduced CHOP induction-dependent cell death. Reactive Oxygen Species 71-74 DNA damage inducible transcript 3 Homo sapiens 24-28 22922338-0 2012 Capsazepine, a TRPV1 antagonist, sensitizes colorectal cancer cells to apoptosis by TRAIL through ROS-JNK-CHOP-mediated upregulation of death receptors. Reactive Oxygen Species 98-101 DNA damage inducible transcript 3 Homo sapiens 106-110 23533616-10 2013 Reactive oxygen species (ROS) scavenging also decreased the expression of GRP78, phospho-PERK, CHOP, and BIM. Reactive Oxygen Species 0-23 DNA damage inducible transcript 3 Homo sapiens 95-99 23533616-10 2013 Reactive oxygen species (ROS) scavenging also decreased the expression of GRP78, phospho-PERK, CHOP, and BIM. Reactive Oxygen Species 25-28 DNA damage inducible transcript 3 Homo sapiens 95-99 22922338-11 2012 Together, our results indicate that capsazepine potentiates the apoptotic effects of TRAIL through downregulation of cell survival proteins and upregulation of death receptors via the ROS-JNK-CHOP-mediated pathway. Reactive Oxygen Species 184-187 DNA damage inducible transcript 3 Homo sapiens 192-196 22982206-12 2013 We concluded that VA triggers TRAIL-induced apoptosis by eIF2alpha/CHOP-dependent DR5 induction via ROS generation. Reactive Oxygen Species 100-103 DNA damage inducible transcript 3 Homo sapiens 67-71 23339468-0 2013 Cadmium induces neuronal cell death through reactive oxygen species activated by GADD153. Reactive Oxygen Species 44-67 DNA damage inducible transcript 3 Homo sapiens 81-88 23339468-12 2013 The generation of ROS result in the induction of GADD153 is causative of cadmium-induced apoptosis. Reactive Oxygen Species 18-21 DNA damage inducible transcript 3 Homo sapiens 49-56 23339468-14 2013 Therefore, we conclude that GADD153 sensitizes cells to ROS through mechanisms that involve up-regulation of BAK and enhanced oxidant injury. Reactive Oxygen Species 56-59 DNA damage inducible transcript 3 Homo sapiens 28-35 23536831-9 2013 Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production. Reactive Oxygen Species 232-235 DNA damage inducible transcript 3 Homo sapiens 22-71 23536831-9 2013 Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production. Reactive Oxygen Species 232-235 DNA damage inducible transcript 3 Homo sapiens 73-77 23536831-12 2013 CONCLUSION/SIGNIFICANCE: Casticin enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-ER stress-CHOP pathway. Reactive Oxygen Species 181-184 DNA damage inducible transcript 3 Homo sapiens 195-199 22922338-7 2012 CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL. Reactive Oxygen Species 24-47 DNA damage inducible transcript 3 Homo sapiens 0-4 22922338-7 2012 CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL. Reactive Oxygen Species 24-47 DNA damage inducible transcript 3 Homo sapiens 206-210 22922338-7 2012 CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL. Reactive Oxygen Species 49-52 DNA damage inducible transcript 3 Homo sapiens 0-4 22922338-7 2012 CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL. Reactive Oxygen Species 49-52 DNA damage inducible transcript 3 Homo sapiens 206-210 22922338-7 2012 CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL. Reactive Oxygen Species 109-112 DNA damage inducible transcript 3 Homo sapiens 0-4 22922338-7 2012 CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL. Reactive Oxygen Species 109-112 DNA damage inducible transcript 3 Homo sapiens 0-4 22328338-8 2012 Moreover, orlistat induced reactive oxygen species (ROS), and a ROS scavenger diminished the sensitivity to TRAIL through the suppression of CHOP and DR5 expression in both cell lines. Reactive Oxygen Species 76-79 DNA damage inducible transcript 3 Homo sapiens 165-169 22328338-9 2012 These results suggest that there are two pathways of upregulation of DR5 by orlistat, which are the ROS-CHOP pathway and the ROS-direct pathway. Reactive Oxygen Species 112-115 DNA damage inducible transcript 3 Homo sapiens 116-120 22004570-0 2012 Zyflamend sensitizes tumor cells to TRAIL-induced apoptosis through up-regulation of death receptors and down-regulation of survival proteins: role of ROS-dependent CCAAT/enhancer-binding protein-homologous protein pathway. Reactive Oxygen Species 151-154 DNA damage inducible transcript 3 Homo sapiens 165-214 22004570-13 2012 CONCLUSION: Zyflamend potentiates TRAIL-induced apoptosis through the ROS-CHOP-mediated up-regulation of DRs, increase in pro-apoptotic protein and down-regulation of cell survival proteins. Reactive Oxygen Species 70-73 DNA damage inducible transcript 3 Homo sapiens 74-78 21472292-7 2010 The protein expression of GADD153 and Caspase-3 was increased, but the proto-oncogene bcl-2 was notably decreased in H146 cells treated with Tan-IIA (5 microg/ml) for 24 h. FACS showed that Tan-IIA may increase the production of ROS and Ca2+, but decreases MMP. Reactive Oxygen Species 229-232 DNA damage inducible transcript 3 Homo sapiens 26-33 21797841-13 2012 CONCLUSIONS AND IMPLICATIONS: Cardamonin potentiates TRAIL-induced apoptosis through ROS-CHOP-mediated up-regulation of DRs, decreased expression of decoy receptor and cell survival proteins. Reactive Oxygen Species 85-88 DNA damage inducible transcript 3 Homo sapiens 89-93 22281495-9 2012 Altogether, these observations suggest that Aldo induces apoptosis via ROS-mediated, CHOP-dependent activation in renal tubular epithelial cells. Reactive Oxygen Species 71-74 DNA damage inducible transcript 3 Homo sapiens 85-89 21660448-12 2012 CONCLUSION: The present study demonstrates that DMF selectively enhances TRAIL-induced apoptosis by ROS-stimulated ER-stress triggering CHOP-mediated DR5 upregulation in HCC. Reactive Oxygen Species 100-103 DNA damage inducible transcript 3 Homo sapiens 136-140 21703327-14 2011 These results suggest that O(2)(-) and ONOO(-) are selectively involved in CSE-triggered induction of CHOP and that the PERK-eIF2alpha pathway plays a crucial role in the induction of CHOP and apoptosis downstream of the particular reactive oxygen species. Reactive Oxygen Species 232-255 DNA damage inducible transcript 3 Homo sapiens 184-188 21709020-4 2011 Loss-of-function studies show that ECM detachment activates a canonical PERK-eukaryotic translation initiation factor 2alpha (eIF2alpha)-ATF4-CHOP pathway that coordinately induces the autophagy regulators ATG6 and ATG8, sustains ATP levels, and reduces ROS levels to delay anoikis. Reactive Oxygen Species 254-257 DNA damage inducible transcript 3 Homo sapiens 142-146 22046282-3 2011 Activated gadd153 can generate oxidative damage and reactive oxygen species (ROS), increase beta-amyloid (Abeta) levels, disturb iron homeostasis and induce inflammation as well as cell death, which are all pathological hallmarks of AD. Reactive Oxygen Species 52-75 DNA damage inducible transcript 3 Homo sapiens 10-17 22046282-3 2011 Activated gadd153 can generate oxidative damage and reactive oxygen species (ROS), increase beta-amyloid (Abeta) levels, disturb iron homeostasis and induce inflammation as well as cell death, which are all pathological hallmarks of AD. Reactive Oxygen Species 77-80 DNA damage inducible transcript 3 Homo sapiens 10-17 22046282-9 2011 Additionally, 27-OHC-induced tau phosphorylation, ROS generation, TNF-alpha activation, and iron and apoptosis-regulatory protein levels alteration were also markedly reduced by siRNA to gadd153. Reactive Oxygen Species 50-53 DNA damage inducible transcript 3 Homo sapiens 187-194 20837473-0 2010 Gossypol induces death receptor-5 through activation of the ROS-ERK-CHOP pathway and sensitizes colon cancer cells to TRAIL. Reactive Oxygen Species 60-63 DNA damage inducible transcript 3 Homo sapiens 68-72 20459685-10 2010 Cd2+ also induced reactive oxygen species dependent expression of the pro-apoptotic ER stress marker and Wnt suppressor CHOP/GADD153 which, however, did not abolish Wnt response and cell viability. Reactive Oxygen Species 18-41 DNA damage inducible transcript 3 Homo sapiens 120-124 20559423-5 2010 Oxidative stress was found to be dependent on the upregulation of NAD(P)H oxidase 4 (Nox4), a reactive oxygen species (ROS) Nox homologue, triggering endoplasmic reticulum (ER) stress, as assessed by the ER stress-induced apoptosis marker Growth Arrest and DNA Damage-inducible gene 153 (GADD153). Reactive Oxygen Species 94-117 DNA damage inducible transcript 3 Homo sapiens 239-286 20559423-5 2010 Oxidative stress was found to be dependent on the upregulation of NAD(P)H oxidase 4 (Nox4), a reactive oxygen species (ROS) Nox homologue, triggering endoplasmic reticulum (ER) stress, as assessed by the ER stress-induced apoptosis marker Growth Arrest and DNA Damage-inducible gene 153 (GADD153). Reactive Oxygen Species 94-117 DNA damage inducible transcript 3 Homo sapiens 288-295 20559423-5 2010 Oxidative stress was found to be dependent on the upregulation of NAD(P)H oxidase 4 (Nox4), a reactive oxygen species (ROS) Nox homologue, triggering endoplasmic reticulum (ER) stress, as assessed by the ER stress-induced apoptosis marker Growth Arrest and DNA Damage-inducible gene 153 (GADD153). Reactive Oxygen Species 119-122 DNA damage inducible transcript 3 Homo sapiens 239-286 20559423-5 2010 Oxidative stress was found to be dependent on the upregulation of NAD(P)H oxidase 4 (Nox4), a reactive oxygen species (ROS) Nox homologue, triggering endoplasmic reticulum (ER) stress, as assessed by the ER stress-induced apoptosis marker Growth Arrest and DNA Damage-inducible gene 153 (GADD153). Reactive Oxygen Species 119-122 DNA damage inducible transcript 3 Homo sapiens 288-295 20559423-6 2010 We demonstrated that 3DG-collagen activated GADD153 via phosphorylation of p38 mitogen activated protein kinase (MAPK), and this was dependent on upstream ROS. Reactive Oxygen Species 155-158 DNA damage inducible transcript 3 Homo sapiens 44-51 20459685-10 2010 Cd2+ also induced reactive oxygen species dependent expression of the pro-apoptotic ER stress marker and Wnt suppressor CHOP/GADD153 which, however, did not abolish Wnt response and cell viability. Reactive Oxygen Species 18-41 DNA damage inducible transcript 3 Homo sapiens 125-132 18852146-6 2008 A mechanistic study showed the contributions of reactive oxygen species (ROS) and intracellular calcium in CHOP and DR5 gene up-regulation. Reactive Oxygen Species 48-71 DNA damage inducible transcript 3 Homo sapiens 107-111 20198322-7 2010 ROS induced by 9-HPbD-PDT directly led to downregulated expression of Bcl-2, loss of mitochondrial membrane potential, release of cytochrome c from mitochondria, elevation of intracellular calcium due to ER stress, as well as induction of CHOP and activation of caspase-3, -8, -9 and -12. Reactive Oxygen Species 0-3 DNA damage inducible transcript 3 Homo sapiens 239-243 19345731-5 2009 Interestingly, a Wit A-induced increase in ROS levels preceded the up-regulation of CHOP and DR5. Reactive Oxygen Species 43-46 DNA damage inducible transcript 3 Homo sapiens 84-88 19345731-6 2009 The involvement of ROS in CHOP-mediated DR5 up-regulation was confirmed by the result that pretreatment with an antioxidant, NAC or catalase, inhibited Wit A-induced up-regulation of both CHOP and DR5. Reactive Oxygen Species 19-22 DNA damage inducible transcript 3 Homo sapiens 26-30 19345731-6 2009 The involvement of ROS in CHOP-mediated DR5 up-regulation was confirmed by the result that pretreatment with an antioxidant, NAC or catalase, inhibited Wit A-induced up-regulation of both CHOP and DR5. Reactive Oxygen Species 19-22 DNA damage inducible transcript 3 Homo sapiens 188-192 20154087-8 2010 We found that celastrol also induced reactive oxygen species (ROS) generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL. Reactive Oxygen Species 83-86 DNA damage inducible transcript 3 Homo sapiens 143-147 20154087-9 2010 Overall, our results demonstrate that celastrol can potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and up-regulation of death receptors via the ROS-mediated up-regulation of CHOP pathway. Reactive Oxygen Species 189-192 DNA damage inducible transcript 3 Homo sapiens 219-223 18852146-6 2008 A mechanistic study showed the contributions of reactive oxygen species (ROS) and intracellular calcium in CHOP and DR5 gene up-regulation. Reactive Oxygen Species 73-76 DNA damage inducible transcript 3 Homo sapiens 107-111 18852146-11 2008 In summary, the effect of up-regulation of DR5 by 15dPGJ(2) in colon cancer cells is independent of PPAR-gamma and p53 but relies on CHOP induction through gene transcription involving ROS and calcium. Reactive Oxygen Species 185-188 DNA damage inducible transcript 3 Homo sapiens 133-137 14635187-8 2003 The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species. Reactive Oxygen Species 225-248 DNA damage inducible transcript 3 Homo sapiens 23-30 16400006-10 2006 Our data suggest that CHOP-via increased ROS generation-regulates cell-matrix adhesion of podocytes in glomerular disease. Reactive Oxygen Species 41-44 DNA damage inducible transcript 3 Homo sapiens 22-26 18630529-4 2008 The ROS caused endoplasmic reticulum (ER) stress, confirmed by the increase of GADD153 and GRP78 in the examined cells. Reactive Oxygen Species 4-7 DNA damage inducible transcript 3 Homo sapiens 79-86 16972258-7 2006 In addition, the increase in the expression of heme oxygenase-1 (HO-1), a stress response protein, and the growth arrest and DNA damage-inducible transcription factor 153 (Gadd153) in response to the ROS generation were also blocked by these receptor antagonists. Reactive Oxygen Species 200-203 DNA damage inducible transcript 3 Homo sapiens 172-179 16386220-10 2006 Indeed, we demonstrated that mitochondrial ROS act as key elements in the control of white adipose tissue development by specific up-regulation of the anti-adipogenic transcription factor CHOP-10/GADD153. Reactive Oxygen Species 43-46 DNA damage inducible transcript 3 Homo sapiens 188-195 16386220-10 2006 Indeed, we demonstrated that mitochondrial ROS act as key elements in the control of white adipose tissue development by specific up-regulation of the anti-adipogenic transcription factor CHOP-10/GADD153. Reactive Oxygen Species 43-46 DNA damage inducible transcript 3 Homo sapiens 196-203 14635187-8 2003 The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species. Reactive Oxygen Species 225-248 DNA damage inducible transcript 3 Homo sapiens 137-144 12880976-6 2003 Therefore, fenretinide induces apoptosis via RAR-dependent and -independent pathways in which the RAR-independent pathway is characterised by the reactive oxygen species-dependent induction of GADD153 and Bak. Reactive Oxygen Species 146-169 DNA damage inducible transcript 3 Homo sapiens 193-200 12907753-6 2003 The use of pharmacological inhibitors indicated that cAMP-induced CHOP expression was dependent on protein kinase A (PKA), mammalian target of rapamycin pathway, and reactive oxygen species. Reactive Oxygen Species 166-189 DNA damage inducible transcript 3 Homo sapiens 66-70 32878253-7 2020 These ROS-mediated responses induce caspase-dependent apoptosis via the activation of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), CCAAT/enhancer-binding protein homologous protein (chop), and phosphoprotein p53 gene expressions. Reactive Oxygen Species 6-9 DNA damage inducible transcript 3 Homo sapiens 145-194 19002820-1 2000 The use of the gadd153promoter to induce expression of a reporter geneunder heat stress conditions was investigated,since the results of previous studies have suggestedthat the gadd153promoter is likely to be activated by the indirecteffects of hyperthermia, that is, by DNA damage thatoccurs when reactive oxygen species are produced byheat stress. Reactive Oxygen Species 298-321 DNA damage inducible transcript 3 Homo sapiens 177-184 35151835-20 2022 CONCLUSION: GLA is a promising therapeutic agent that activates the ROS-mediated ATF4/CHOP/CHAC1 axis in OSCC patients. Reactive Oxygen Species 68-71 DNA damage inducible transcript 3 Homo sapiens 86-90 35427876-8 2022 Further experiments demonstrated that two different signaling pathways were activated by PFOA-induced ER stress and involved in PFOA toxicity: the reactive oxygen species (ROS)-dependent ERK signaling triggered trophoblast proliferation, while the ATF4-dependent C/EBP homologous protein (CHOP) signaling was the trigger of apoptosis. Reactive Oxygen Species 172-175 DNA damage inducible transcript 3 Homo sapiens 289-293 32700751-8 2020 The level of reactive oxygen species (ROS) production was found to induce the hallmark of ER stress GADD153, proapoptotic marker caspase-3, and calpain activity after AITC treatment. Reactive Oxygen Species 13-36 DNA damage inducible transcript 3 Homo sapiens 100-107 32700751-8 2020 The level of reactive oxygen species (ROS) production was found to induce the hallmark of ER stress GADD153, proapoptotic marker caspase-3, and calpain activity after AITC treatment. Reactive Oxygen Species 38-41 DNA damage inducible transcript 3 Homo sapiens 100-107 11158311-6 2001 Investigation of the mechanisms contributing to this effect revealed that elevated Gadd153 expression results in the down-regulation of Bcl2 expression, depletion of cellular glutathione, and exaggerated production of reactive oxygen species. Reactive Oxygen Species 218-241 DNA damage inducible transcript 3 Homo sapiens 83-90 11158311-7 2001 Restoration of Bcl2 expression in Gadd153-overexpressing cells led to replenishment of glutathione and a reduction in levels of reactive oxygen species, and it protected cells from ER stress-induced cell death. Reactive Oxygen Species 128-151 DNA damage inducible transcript 3 Homo sapiens 34-41 34599545-0 2021 CSC-3436 sensitizes triple negative breast cancer cells to TRAIL-induced apoptosis through ROS-mediated p38/CHOP/death receptor 5 signaling pathways. Reactive Oxygen Species 91-94 DNA damage inducible transcript 3 Homo sapiens 108-112 34599545-7 2021 In addition, the induction of DR5 by CSC-3436 was found to be dependent on the modulation of reactive oxygen species (ROS)/p38/C/EBP-homologous protein (CHOP) signaling pathways. Reactive Oxygen Species 93-116 DNA damage inducible transcript 3 Homo sapiens 153-157 34599545-8 2021 Overall, our results indicated that CSC-3436 could potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and upregulation of DR5 via the ROS-mediated upregulation of CHOP protein. Reactive Oxygen Species 175-178 DNA damage inducible transcript 3 Homo sapiens 204-208 34993544-12 2022 This study demonstrated that TGF-beta1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2alpha/CHOP pathway. Reactive Oxygen Species 101-104 DNA damage inducible transcript 3 Homo sapiens 149-153 34054558-14 2021 Accumulation of ROS caused ER stress through the PERK-eIF2alpha-CHOP and IRE1alpha-CHOP pathways. Reactive Oxygen Species 16-19 DNA damage inducible transcript 3 Homo sapiens 64-68 34054558-14 2021 Accumulation of ROS caused ER stress through the PERK-eIF2alpha-CHOP and IRE1alpha-CHOP pathways. Reactive Oxygen Species 16-19 DNA damage inducible transcript 3 Homo sapiens 83-87 32506763-0 2020 ROS-mediated PERK-eIF2alpha-ATF4 pathway plays an important role in arsenite-induced L-02 cells apoptosis via regulating CHOP-DR5 signaling. Reactive Oxygen Species 0-3 DNA damage inducible transcript 3 Homo sapiens 121-125 32506763-10 2020 Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity. Reactive Oxygen Species 42-45 DNA damage inducible transcript 3 Homo sapiens 184-188 33042407-9 2020 Intriguingly, Chlorin A-PDT promoted autophagy via activation of ROS-induced ERS-related PERK/p-eif2alpha/CHOP axis, and blocked the ensuing autophagy flux by lysosomal damage. Reactive Oxygen Species 65-68 DNA damage inducible transcript 3 Homo sapiens 106-110 32878253-7 2020 These ROS-mediated responses induce caspase-dependent apoptosis via the activation of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), CCAAT/enhancer-binding protein homologous protein (chop), and phosphoprotein p53 gene expressions. Reactive Oxygen Species 6-9 DNA damage inducible transcript 3 Homo sapiens 196-200 32604833-0 2020 TRPV1 Antagonist DWP05195 Induces ER Stress-Dependent Apoptosis through the ROS-p38-CHOP Pathway in Human Ovarian Cancer Cells. Reactive Oxygen Species 76-79 DNA damage inducible transcript 3 Homo sapiens 84-88 31054874-6 2019 Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress. Reactive Oxygen Species 132-135 DNA damage inducible transcript 3 Homo sapiens 110-114 31360107-0 2019 PERK/eIF-2alpha/CHOP Pathway Dependent ROS Generation Mediates Butein-induced Non-small-cell Lung Cancer Apoptosis and G2/M Phase Arrest. Reactive Oxygen Species 39-42 DNA damage inducible transcript 3 Homo sapiens 16-20