PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32407927-5 2020 In hepatocyte-derived cells and primary hepatocytes, luteolin significantly decreased Tm- or thapsigargin-mediated C/EBP homologous protein (CHOP) expression. Tunicamycin 86-88 DNA damage inducible transcript 3 Homo sapiens 115-139 32407927-5 2020 In hepatocyte-derived cells and primary hepatocytes, luteolin significantly decreased Tm- or thapsigargin-mediated C/EBP homologous protein (CHOP) expression. Tunicamycin 86-88 DNA damage inducible transcript 3 Homo sapiens 141-145 32040528-4 2020 Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P < 0.05). Tunicamycin 71-82 DNA damage inducible transcript 3 Homo sapiens 311-344 32608212-7 2020 In addition, H2O2 and TM could increase the levels of PGE2, GRP78, CHOP, caspase-12, and reactive oxygen species (ROS), resulting in the degeneration of CHs. Tunicamycin 22-24 DNA damage inducible transcript 3 Homo sapiens 67-71 32035621-5 2020 Tunicamycin treatment upregulated the expression of ER stress markers (DNA damage inducible transcript 3, heat shock protein family A (Hsp70) member 5, and phosphorylated eukaryotic translation initiation factor 2 alpha kinase 3, eukaryotic translation initiation factor 2 subunit alpha, and endoplasmic reticulum to nucleus signaling 1); however, these were decreased in ULK1 and ATG13 KO cells. Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 71-104 32040528-4 2020 Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P < 0.05). Tunicamycin 71-82 DNA damage inducible transcript 3 Homo sapiens 346-351 32040528-4 2020 Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P < 0.05). Tunicamycin 84-86 DNA damage inducible transcript 3 Homo sapiens 311-344 32040528-4 2020 Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P < 0.05). Tunicamycin 84-86 DNA damage inducible transcript 3 Homo sapiens 346-351 32040528-5 2020 Treatment with 1,25D3 (100 nM) inhibited TG (10 nM)- and TM (1 mug/mL)-induced mRNA and/or protein levels of ATF4, ATF6, DDIT3 and HSPA5 in MCF-7 cells (P < 0.05). Tunicamycin 57-59 DNA damage inducible transcript 3 Homo sapiens 121-126 30893871-7 2019 Molecular modulation of endoplasmic reticulum (ER) stress induced by tunicamycin was studied by western blot analysis of the ER stress markers GRP78, CHOP and p-IRE1. Tunicamycin 69-80 DNA damage inducible transcript 3 Homo sapiens 150-154 31974624-5 2020 The present study demonstrated that 3 microM tunicamycin (TM) increased the expression of the ER stress-related proteins protein kinase RNA-like endoplasmic reticulum kinase (PERK), alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) and C/EBP homologous protein (CHOP) in human primary epidermal melanocytes. Tunicamycin 45-56 DNA damage inducible transcript 3 Homo sapiens 258-282 31974624-5 2020 The present study demonstrated that 3 microM tunicamycin (TM) increased the expression of the ER stress-related proteins protein kinase RNA-like endoplasmic reticulum kinase (PERK), alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) and C/EBP homologous protein (CHOP) in human primary epidermal melanocytes. Tunicamycin 45-56 DNA damage inducible transcript 3 Homo sapiens 284-288 31974624-5 2020 The present study demonstrated that 3 microM tunicamycin (TM) increased the expression of the ER stress-related proteins protein kinase RNA-like endoplasmic reticulum kinase (PERK), alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) and C/EBP homologous protein (CHOP) in human primary epidermal melanocytes. Tunicamycin 58-60 DNA damage inducible transcript 3 Homo sapiens 258-282 31974624-5 2020 The present study demonstrated that 3 microM tunicamycin (TM) increased the expression of the ER stress-related proteins protein kinase RNA-like endoplasmic reticulum kinase (PERK), alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) and C/EBP homologous protein (CHOP) in human primary epidermal melanocytes. Tunicamycin 58-60 DNA damage inducible transcript 3 Homo sapiens 284-288 30336657-5 2019 RESULTS: Tunicamycin increased the expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules, including spliced X-box binding protein 1 (XBP-1), transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP), and ATF6. Tunicamycin 9-20 DNA damage inducible transcript 3 Homo sapiens 206-255 30336657-5 2019 RESULTS: Tunicamycin increased the expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules, including spliced X-box binding protein 1 (XBP-1), transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP), and ATF6. Tunicamycin 9-20 DNA damage inducible transcript 3 Homo sapiens 257-261 30336657-7 2019 Furthermore, siRNA knockdowns of XBP-1, CHOP, and ATF6 blocked the tunicamycin-induced mRNA expressions and glycoprotein productions of MUC5AC and MUC5B. Tunicamycin 67-78 DNA damage inducible transcript 3 Homo sapiens 40-44 30770792-7 2019 BV6 consistently abolishes TM-stimulated accumulation of ER stress markers such as glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) and reduces protein kinase RNA-like ER kinase (PERK) phosphorylation and X box-binding protein 1 (XBP1) splicing upon TM treatment. Tunicamycin 27-29 DNA damage inducible transcript 3 Homo sapiens 124-148 30820153-4 2019 The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1. Tunicamycin 14-25 DNA damage inducible transcript 3 Homo sapiens 108-112 30657961-6 2019 We found that ER stress marker GRP78 expression increased with CHOP and TRIB3 expression in normal endometrial stromal cells (NESCs) treated with tunicamycin, and this increase was accompanied by decreased AKT and mTOR activity and cellular invasiveness. Tunicamycin 146-157 DNA damage inducible transcript 3 Homo sapiens 63-67 30389633-10 2019 More importantly, both xanthatin and tunicamycin, an endoplasmic reticulum stress (ERS) inducing compound, increased the levels of CHOP and cleaved-caspase-3 in HepG2 cells, but their effects were significantly abolished by siRNA-mediated knockdown of CHOP. Tunicamycin 37-48 DNA damage inducible transcript 3 Homo sapiens 131-135 30389633-10 2019 More importantly, both xanthatin and tunicamycin, an endoplasmic reticulum stress (ERS) inducing compound, increased the levels of CHOP and cleaved-caspase-3 in HepG2 cells, but their effects were significantly abolished by siRNA-mediated knockdown of CHOP. Tunicamycin 37-48 DNA damage inducible transcript 3 Homo sapiens 252-256 30770792-7 2019 BV6 consistently abolishes TM-stimulated accumulation of ER stress markers such as glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) and reduces protein kinase RNA-like ER kinase (PERK) phosphorylation and X box-binding protein 1 (XBP1) splicing upon TM treatment. Tunicamycin 27-29 DNA damage inducible transcript 3 Homo sapiens 150-154 30567393-3 2018 Tunicamycin (TM) treatment significantly increased mRNA levels of CHOP and GRP78, and induced lipid accumulation in the liver. Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 66-70 30567393-3 2018 Tunicamycin (TM) treatment significantly increased mRNA levels of CHOP and GRP78, and induced lipid accumulation in the liver. Tunicamycin 13-15 DNA damage inducible transcript 3 Homo sapiens 66-70 28951205-4 2017 In cultured VSMC, tunicamycin caused cell death accompanied by an increase in caspase-3 processing and C/EBP homologous protein (CHOP) expression. Tunicamycin 18-29 DNA damage inducible transcript 3 Homo sapiens 103-127 30107908-6 2018 Furthermore, oxicam-NSAIDs suppressed the increases in the ER stress marker CHOP (apoptosis mediator) caused by MPP+ or tunicamycin, beside suppressing eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation and the increase in ATF4 caused by MPP+. Tunicamycin 120-131 DNA damage inducible transcript 3 Homo sapiens 76-80 30146638-7 2018 Treatment with tunicamycin resulted in up-regulation of ER stress genes, such as splicing x-box binding protein-1(sXBP1), activating transcription factor 4(ATF4), glucose-regulated protein 78(GRP78) and C/EBP homologous protein (CHOP). Tunicamycin 15-26 DNA damage inducible transcript 3 Homo sapiens 203-227 30146638-7 2018 Treatment with tunicamycin resulted in up-regulation of ER stress genes, such as splicing x-box binding protein-1(sXBP1), activating transcription factor 4(ATF4), glucose-regulated protein 78(GRP78) and C/EBP homologous protein (CHOP). Tunicamycin 15-26 DNA damage inducible transcript 3 Homo sapiens 229-233 28951205-4 2017 In cultured VSMC, tunicamycin caused cell death accompanied by an increase in caspase-3 processing and C/EBP homologous protein (CHOP) expression. Tunicamycin 18-29 DNA damage inducible transcript 3 Homo sapiens 129-133 28630443-6 2017 Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP. Tunicamycin 25-36 DNA damage inducible transcript 3 Homo sapiens 65-69 28841673-5 2017 Furthermore, CHOP was shown to be significantly upregulated upon treatment with tunicamycin in HCC cells. Tunicamycin 80-91 DNA damage inducible transcript 3 Homo sapiens 13-17 28841673-6 2017 Specific knockdown of CHOP not only enhanced tunicamycin-induced autophagy, but also significantly attenuated ER stress-induced apoptosis in HCC cells. Tunicamycin 45-56 DNA damage inducible transcript 3 Homo sapiens 22-26 28652211-4 2017 Plk2 expression was dramatically decreased under ER stress induced by brefeldin A (BFA), thapsigargin (TG), or tunicamycin (TM), and this down regulation of Plk2 expression was dependent on activating transcription factor 4 (ATF4) and C/EBP homology protein (CHOP). Tunicamycin 124-126 DNA damage inducible transcript 3 Homo sapiens 235-257 28652211-4 2017 Plk2 expression was dramatically decreased under ER stress induced by brefeldin A (BFA), thapsigargin (TG), or tunicamycin (TM), and this down regulation of Plk2 expression was dependent on activating transcription factor 4 (ATF4) and C/EBP homology protein (CHOP). Tunicamycin 124-126 DNA damage inducible transcript 3 Homo sapiens 259-263 28631572-8 2017 With tunicamycin treatment, phosphorylation of PERK and eIF2alpha and CHOP expression increased. Tunicamycin 5-16 DNA damage inducible transcript 3 Homo sapiens 70-74 27603596-0 2017 Tunicamycin enhances human colon cancer cells to TRAIL-induced apoptosis by JNK-CHOP-mediated DR5 upregulation and the inhibition of the EGFR pathway. Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 80-84 28459209-10 2017 In MCF-7 cells treated with tunicamycin, cell viability decreased significantly, but PEAK, eIF2, and CHOP were upregulated markedly and p-PI3K, p-AKT, and p-MTOR were downregulated in dose- and time-dependent manners. Tunicamycin 28-39 DNA damage inducible transcript 3 Homo sapiens 101-105 28460451-5 2017 In addition, tunicamycin caused pronounced endoplasmatic reticulum stress and apoptosis through activation of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and activation of the gene encoding CCAAT-enhancer-binding protein homologous protein (CHOP). Tunicamycin 13-24 DNA damage inducible transcript 3 Homo sapiens 206-255 28460451-5 2017 In addition, tunicamycin caused pronounced endoplasmatic reticulum stress and apoptosis through activation of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and activation of the gene encoding CCAAT-enhancer-binding protein homologous protein (CHOP). Tunicamycin 13-24 DNA damage inducible transcript 3 Homo sapiens 257-261 27603596-7 2017 In summary, tunicamycin effectively enhanced TRAIL-induced apoptosis might through JNK-CHOP-mediated DR5 upregulation and the inhibition of the epidermal growth factor receptor pathway. Tunicamycin 12-23 DNA damage inducible transcript 3 Homo sapiens 87-91 27980366-4 2016 Protein and mRNA levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and ARPE-19 cell viability were measured in the presence of tunicamycin-induced ER stress in control or PTX3 small hairpin RNA (shRNA)-transfected ARPE-19 cells. Tunicamycin 144-155 DNA damage inducible transcript 3 Homo sapiens 78-82 27980366-8 2016 Decreased cell viability and prolonged protein and mRNA expression of CHOP were observed under tunicamycin-induced ER stress in PTX3 shRNA transfected ARPE-19 cells. Tunicamycin 95-106 DNA damage inducible transcript 3 Homo sapiens 70-74 27350212-9 2016 Increased level of spliced XBP-1, ATF6 nuclear translocation and CHOP protein expression were detected in CD44+/CD24- and original MCF7 cells treated with tunicamycin. Tunicamycin 155-166 DNA damage inducible transcript 3 Homo sapiens 65-69 28011957-11 2016 Tunicamycin treatment, as expected, increased the expression of Grp94, PDI, CHOP and inactivated PARP. Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 76-80 26419929-6 2015 Furthermore, CTRP9 decreased palmitate- or tunicamycin-induced ER stress markers, such as eIF2alpha, CHOP and IRE-1, in HepG2 cells. Tunicamycin 43-54 DNA damage inducible transcript 3 Homo sapiens 101-105 26577412-6 2015 Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation. Tunicamycin 25-36 DNA damage inducible transcript 3 Homo sapiens 108-112 27330716-13 2016 The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA. Tunicamycin 87-98 DNA damage inducible transcript 3 Homo sapiens 74-78 27330716-15 2016 CONCLUSIONS: Endoplasmic reticulum stress induced by tunicamycin increased resistin mRNA through the PERK-ATF4-CHOP pathway in THP-1 human monocytes. Tunicamycin 53-64 DNA damage inducible transcript 3 Homo sapiens 111-115 25322957-5 2015 Thapsigargin/tunicamycin treatment induced a significant increase in endoplasmic reticulum stress and of cell death, represented by higher GADD153 and GRP78 expression and propidium iodide flow cytometry, respectively. Tunicamycin 13-24 DNA damage inducible transcript 3 Homo sapiens 139-146 26540043-5 2015 MEAO significantly inhibited tunicamycin-induced ER stress marker expression including GRP78, CHOP, and XBP-1 in tunicamycin-treated Human hepatocellular carcinoma (HepG2) cells and the livers of tunicamycin-injected mice. Tunicamycin 29-40 DNA damage inducible transcript 3 Homo sapiens 94-98 25737469-4 2015 Although NaF and tunicamycin both induced PERK activation followed by eIF2alpha phosphorylation and ATF4 expression, CHOP expression was only induced by tunicamycin. Tunicamycin 153-164 DNA damage inducible transcript 3 Homo sapiens 117-121 25737469-8 2015 The GADD34 siRNA increased CHOP expression, which corresponded to increased ATF4 in tunicamycin-treated cells; however, the increased ATF4 did not induce CHOP expression in NaF-treated cells. Tunicamycin 84-95 DNA damage inducible transcript 3 Homo sapiens 27-31 24962313-7 2014 Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP). Tunicamycin 37-48 DNA damage inducible transcript 3 Homo sapiens 74-98 25231320-6 2014 In human breast cancer MCF-7 cells, ER stress activator tunicamycin increased the expression of CCL5, STAT3 and CHOP in a time- and concentration-dependent manner. Tunicamycin 56-67 DNA damage inducible transcript 3 Homo sapiens 112-116 25360516-2 2014 Here, we show that induction in cell surface GRP78 by doxorubicin and tunicamycin was associated with CHOP/GADD153 upregulation and increase in apoptosis in triple negative breast cancer tumor cells. Tunicamycin 70-81 DNA damage inducible transcript 3 Homo sapiens 102-106 25360516-2 2014 Here, we show that induction in cell surface GRP78 by doxorubicin and tunicamycin was associated with CHOP/GADD153 upregulation and increase in apoptosis in triple negative breast cancer tumor cells. Tunicamycin 70-81 DNA damage inducible transcript 3 Homo sapiens 107-114 25314137-9 2014 Augmentation of miR-615-3p levels, using a precursor molecule, repressed CHOP expression; and under these conditions palmitate- or tunicamycin-induced cell death were significantly reduced. Tunicamycin 131-142 DNA damage inducible transcript 3 Homo sapiens 73-77 25428129-4 2015 Tunicamycin induced the phosphorylation and activation of PERK and eIF2alpha within 2 h in RPTC, which was followed by the induction of GRP78 and CHOP. Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 146-150 25428129-7 2015 Inhibition of mTOR with rapamycin partially suppressed the phosphorylation of PERK and eIF2a and the induction of CHOP and GRP78 induction during tunicamycin treatment. Tunicamycin 146-157 DNA damage inducible transcript 3 Homo sapiens 114-118 24962313-10 2014 Knockdown endogenous BiP with siRNA abolished the suppression of propofol on tunicamycin-mediated activation of CHOP and caspase-3. Tunicamycin 77-88 DNA damage inducible transcript 3 Homo sapiens 112-116 24962313-7 2014 Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP). Tunicamycin 37-48 DNA damage inducible transcript 3 Homo sapiens 100-104 24167719-5 2013 On the other hand, NaF- and tunicamycin-induced ER-stress caused only autophagy in the early stage by ~8 hr with ATF4 expression and without CHOP expression. Tunicamycin 28-39 DNA damage inducible transcript 3 Homo sapiens 141-145 24167719-6 2013 ATF4-siRNA completely inhibited the autophagy induced by NaF or tunicamycin with suppressed ATF4 protein and mRNA expressions, and also inhibited apoptosis by thapsigargin with suppression of both ATF4 and CHOP. Tunicamycin 64-75 DNA damage inducible transcript 3 Homo sapiens 206-210 24416259-0 2014 4-Phenylbutyrate inhibits tunicamycin-induced acute kidney injury via CHOP/GADD153 repression. Tunicamycin 26-37 DNA damage inducible transcript 3 Homo sapiens 75-82 21159733-7 2011 However, tunicamycin (a potent stimulator of ER stress) changed the ER stress response from protective to cytotoxic, as tunicamycin induced the proapoptotic ER stress gene, C/EBP homologous protein-10, and exacerbated apoptosis in GECs adherent to plastic, but not collagen. Tunicamycin 9-20 DNA damage inducible transcript 3 Homo sapiens 173-200 23665024-9 2013 From a mechanistic stand point, fasudil inhibited expression of activating transcription factor (ATF)4 and subsequent C/EBP homologous protein (CHOP) induction by tunicamycin. Tunicamycin 163-174 DNA damage inducible transcript 3 Homo sapiens 118-142 23665024-9 2013 From a mechanistic stand point, fasudil inhibited expression of activating transcription factor (ATF)4 and subsequent C/EBP homologous protein (CHOP) induction by tunicamycin. Tunicamycin 163-174 DNA damage inducible transcript 3 Homo sapiens 144-148 23658755-9 2013 However, co-pretreatment with tunicamycin and Pae decreased the expression of COX-2 and levels of activation of Akt as well as increasing the levels of CHOP in HCC cells. Tunicamycin 30-41 DNA damage inducible transcript 3 Homo sapiens 152-156 23171849-3 2012 Here we show in U937 cells that the ER stressors tunicamycin and thapsigargin cause increased expression of c-Jun N-terminal kinase 2 (JNK2), which allows regulation of the UPR, whose silencing or pharmacological inhibition delays BiP (immunoglobulin heavy-chain binding protein) upregulation, and causes earlier and greater expression of CCAAT/enhancer-binding protein-homologous protein (CHOP). Tunicamycin 49-60 DNA damage inducible transcript 3 Homo sapiens 339-388 23171849-3 2012 Here we show in U937 cells that the ER stressors tunicamycin and thapsigargin cause increased expression of c-Jun N-terminal kinase 2 (JNK2), which allows regulation of the UPR, whose silencing or pharmacological inhibition delays BiP (immunoglobulin heavy-chain binding protein) upregulation, and causes earlier and greater expression of CCAAT/enhancer-binding protein-homologous protein (CHOP). Tunicamycin 49-60 DNA damage inducible transcript 3 Homo sapiens 390-394 22225575-7 2012 Interestingly, co-treatment with tunicamycin and melatonin also decreased the expression of COX-2 and significantly increased the rate of apoptosis by elevating the levels of CHOP and reducing the Bcl-2/Bax ratio. Tunicamycin 33-44 DNA damage inducible transcript 3 Homo sapiens 175-179 22550476-5 2012 Cells subjected to either glucolipotoxicity or tunicamycin exhibited increased ROS generation, gene and protein (PERK, GRP-78, IRE1alpha, and CHOP) expression of ER stress markers. Tunicamycin 47-58 DNA damage inducible transcript 3 Homo sapiens 142-146 23281479-5 2013 We found that metabolic dysregulation was associated with induction of eIF2alpha signaling and CHOP up-regulation during challenge with tunicamycin or Velcade. Tunicamycin 136-147 DNA damage inducible transcript 3 Homo sapiens 95-99 21159733-7 2011 However, tunicamycin (a potent stimulator of ER stress) changed the ER stress response from protective to cytotoxic, as tunicamycin induced the proapoptotic ER stress gene, C/EBP homologous protein-10, and exacerbated apoptosis in GECs adherent to plastic, but not collagen. Tunicamycin 120-131 DNA damage inducible transcript 3 Homo sapiens 173-200 21046477-5 2010 Finally, the pro-apoptotic molecules CHOP and BIM are only induced in the presence of tunicamycin in the culture medium. Tunicamycin 86-97 DNA damage inducible transcript 3 Homo sapiens 37-41 21294793-7 2011 Tunicamycin dose dependently increased CHOP expression and apoptosis of cultured chondrocytes. Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 39-43 22093624-14 2011 In the melanoma cells after exposure to tunicamycin (3 micromol/L) for 6, 12, 24, and 36 hours the transcription factor CHOP at mRNA level were significantly increased and the expressions at protein level were also up-regulated. Tunicamycin 40-51 DNA damage inducible transcript 3 Homo sapiens 120-124 21276850-0 2011 Proteasome inhibitor-I enhances tunicamycin-induced chemosensitization of prostate cancer cells through regulation of NF-kappaB and CHOP expression. Tunicamycin 32-43 DNA damage inducible transcript 3 Homo sapiens 132-136 21168844-10 2011 Nicorandil significantly attenuated tunicamycin-induced CHOP upregulation in cultured THP-1 macrophages. Tunicamycin 36-47 DNA damage inducible transcript 3 Homo sapiens 56-60 20020442-5 2010 Interestingly, in thapsigargin and tunicamycin-stressed chondrocytes induction of the proapoptotic transcription factor CHOP preceded that of the anti-apoptotic BiP by 12 h. Although both of these agents caused sustained Akt and ERK phosphorylation; inhibition of Akt phosphorylation sensitized chondrocytes to ER stress, while blocking ERK signaling by U0126 had no effect. Tunicamycin 35-46 DNA damage inducible transcript 3 Homo sapiens 120-124 18544642-8 2008 In vitro, palmitate, thapsigargin, and tunicamycin but not oleate induced endoplasmic reticulum stress in HepG2 cells, including increased transcripts CHOP, ERN1, GADD34, and PERK, and increased XBP1 splicing along with phosphorylation of eukaryotic initiation factor eIF2alpha, JNK1, and c-jun. Tunicamycin 39-50 DNA damage inducible transcript 3 Homo sapiens 151-155 19773801-8 2010 ER stress agent tunicamycin induced ARMET and CHOP expressions in the primary cultured neurons. Tunicamycin 16-27 DNA damage inducible transcript 3 Homo sapiens 46-50 19007793-5 2009 Furthermore, PACT-induced PKR activation is essential for tunicamycin-induced apoptosis, since PACT as well as PKR null cells are markedly resistant to tunicamycin and show defective eIF2alpha phosphorylation and C/EBP homologous protein (CHOP, also known as GADD153) induction especially at low concentrations of tunicamycin. Tunicamycin 58-69 DNA damage inducible transcript 3 Homo sapiens 213-237 19007793-5 2009 Furthermore, PACT-induced PKR activation is essential for tunicamycin-induced apoptosis, since PACT as well as PKR null cells are markedly resistant to tunicamycin and show defective eIF2alpha phosphorylation and C/EBP homologous protein (CHOP, also known as GADD153) induction especially at low concentrations of tunicamycin. Tunicamycin 58-69 DNA damage inducible transcript 3 Homo sapiens 239-243 19007793-5 2009 Furthermore, PACT-induced PKR activation is essential for tunicamycin-induced apoptosis, since PACT as well as PKR null cells are markedly resistant to tunicamycin and show defective eIF2alpha phosphorylation and C/EBP homologous protein (CHOP, also known as GADD153) induction especially at low concentrations of tunicamycin. Tunicamycin 58-69 DNA damage inducible transcript 3 Homo sapiens 259-266 17455323-0 2007 Brain-derived neurotrophic factor suppresses tunicamycin-induced upregulation of CHOP in neurons. Tunicamycin 45-56 DNA damage inducible transcript 3 Homo sapiens 81-85 17525289-4 2007 Treatment with thapsigargin and tunicamycin led to the activation of all 3 branches of the UPR, with early splicing of XBP1 indicative of IRE1 activation, upregulation of CHOP consistent with ER resident kinase (PERK) activation, and activating transcription factor 6 (ATF6) splicing. Tunicamycin 32-43 DNA damage inducible transcript 3 Homo sapiens 171-175 17217928-5 2007 RESULTS: Compared with control subjects, thapsigargin- and tunicamycin-induced increases in XBP1 and CHOP but not GRP78 messenger RNA levels were significantly lower in BD-I patients. Tunicamycin 59-70 DNA damage inducible transcript 3 Homo sapiens 101-105 18228003-7 2008 Tunicamycin induced a rapid decline of cyclin D1 and cyclin A expression and an early increase of glucose-related protein (GRP) 78 and growth arrest and DNA damage-inducible transcription factor (GADD) 153 levels. Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 135-205 15775988-5 2005 Tunicamycin treatment enhanced the TRB3 promoter activity, while dominant-negative forms of CHOP suppressed the tunicamycin-induced activation. Tunicamycin 112-123 DNA damage inducible transcript 3 Homo sapiens 92-96 16000304-4 2005 Here we report that glucose withdrawal, tunicamycin, and thapsigargin induce up-regulation of GADD153 and caspase-12, two markers of endoplasmic reticulum stress, in both primary chondrocytes and a chondrocyte cell line. Tunicamycin 40-51 DNA damage inducible transcript 3 Homo sapiens 94-101 16024639-8 2005 Tunicamycin increased DR5 promoter activity and this enhanced activity was diminished by mutation of a CHOP-binding site. Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 103-107 16024639-9 2005 In addition, suppression of CHOP expression by small interfering RNA reduced the tunicamycin-mediated induction of DR5. Tunicamycin 81-92 DNA damage inducible transcript 3 Homo sapiens 28-32 16024639-10 2005 Of note, tunicamycin-mediated induction of CHOP and DR5 protein expression was not observed in normal human peripheral blood mononuclear cells. Tunicamycin 9-20 DNA damage inducible transcript 3 Homo sapiens 43-47 15605392-5 2005 Increasing intracellular nitric oxide levels by SNAP treatment or inhibiting protein folding in the ER lumen by tunicamycin induced the ER stress response as evidenced by increased protein and gene expression of GADD153 as well as PERK and eIF2-alpha phosphorylation, and resulted in apoptosis. Tunicamycin 112-123 DNA damage inducible transcript 3 Homo sapiens 212-219 15775988-6 2005 In addition, the tunicamycin response region in the TRB3 promoter contains amino-acid response elements overlapping the CHOP-binding site, and CHOP and ATF4 cooperated to activate this promoter activity. Tunicamycin 17-28 DNA damage inducible transcript 3 Homo sapiens 120-124 15775988-7 2005 Knockdown of endogenous ATF4 or CHOP expression dramatically repressed tunicamycin-induced TRB3 induction. Tunicamycin 71-82 DNA damage inducible transcript 3 Homo sapiens 32-36 9755171-7 1998 Over-expression of a dominant-negative form of Ire1 blocks the induction of GRP78/BiP and CHOP in response to the ER stress induced by tunicamycin treatment. Tunicamycin 135-146 DNA damage inducible transcript 3 Homo sapiens 90-94 11360202-3 2001 In this report, we demonstrate that NF-kappaB inhibits GADD153 activation in breast cancer cells exposed to nutrient deprived media, tunicamycin (which blocks protein folding in ER) or calcium ionopore (which depletes calcium stores in ER). Tunicamycin 133-144 DNA damage inducible transcript 3 Homo sapiens 55-62 9384597-6 1997 The glycosylation inhibitor tunicamycin potently induced expression of both ER chaperones and CHOP in ligand-deprived cells, demonstrating that the UPR pathway remains functionally intact in the absence of growth factor-mediated signaling. Tunicamycin 28-39 DNA damage inducible transcript 3 Homo sapiens 94-98 35104011-7 2022 Nrf2 deficiency enhanced the tunicamycin-mediated induction of CHOP, which was attenuated by Sirt3 overexpression. Tunicamycin 29-40 DNA damage inducible transcript 3 Homo sapiens 63-67 34250248-4 2021 Results: In HEI-OC1 cells, dexamethasone was shown to significantly reduce the tunicamycin-induced expression of ATF4 and CHOP in the context of sustained viability and proliferation, a therapeutic effect that was reversible by co-treatment with a glucocorticoid antagonist. Tunicamycin 79-90 DNA damage inducible transcript 3 Homo sapiens 122-126 35233582-6 2022 Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01). Tunicamycin 0-11 DNA damage inducible transcript 3 Homo sapiens 87-91 34954323-6 2022 Bleomycin and tunicamycin combination models in vivo and in vitro showed that CHOP downregulation rescued alveolar epithelial cell senescence, reduced fibroblast activation mediated by the senescence-associated secretory phenotype, and improved pulmonary fibrosis pathology. Tunicamycin 14-25 DNA damage inducible transcript 3 Homo sapiens 78-82 34775235-4 2022 Pre-treatment with DA-9805 (1 mug/ml) attenuated upregulation of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and cleaved caspase-3 in SH-SY5Y neuroblastoma cells treated with thapsigargin (1 microg/ml) or tunicamycin (2 microg/ml). Tunicamycin 231-242 DNA damage inducible transcript 3 Homo sapiens 103-127 34775235-4 2022 Pre-treatment with DA-9805 (1 mug/ml) attenuated upregulation of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and cleaved caspase-3 in SH-SY5Y neuroblastoma cells treated with thapsigargin (1 microg/ml) or tunicamycin (2 microg/ml). Tunicamycin 231-242 DNA damage inducible transcript 3 Homo sapiens 129-133 34533242-7 2021 Biochemical experiments further discovered that rosamultin could inhibit p38 and JNK activation, and downregulate the levels of CHOP and proteins in its upstream PERK-eIF2alpha-ATF4 signaling pathway stimulated by cisplatin or tunicamycin. Tunicamycin 227-238 DNA damage inducible transcript 3 Homo sapiens 128-132 33904834-5 2021 ER-stress induction using tunicamycin and brefeldin A resulted in increased CHOP (4.6-fold change; P <= 0.001), XBP1 expression (1.7- and 1.3-fold change, respectively; P <= 0.001 and P < 0.05) and XBP1 splicing (7.9- and 12.8-fold change, respectively; P <= 0.001). Tunicamycin 26-37 DNA damage inducible transcript 3 Homo sapiens 76-80 35165522-8 2022 Moreover in vitro experiments, ER stress induced by tunicamycin (TM) not only significantly increased the expression of GRP78 and CHOP, but also caused the epithelial to myofibroblast transformation (EMT) of renal tubular epithelial cells, evidenced by decreased expression of E-cadherin and increased expression of vimentin, and extracellular matrix (ECM) deposition, evidenced by increased expression of fibronectin (FN). Tunicamycin 52-63 DNA damage inducible transcript 3 Homo sapiens 130-134 34033090-5 2021 In this chapter, we describe a quantitative PCR method to detect the upregulation of CHOP and XBP1s mRNA during Tunicamycin-induced UPR. Tunicamycin 112-123 DNA damage inducible transcript 3 Homo sapiens 85-89 32979141-7 2021 In conclusion, this study found that naringin combined with tunicamycin+BAY 11-7082 efficiently induced apoptotic cell death in HT29 colon cancer cells via oxidative stress and the PERK/eIF2alpha/ATF4/CHOP pathway, suggesting that naringin combined with tunicamycin plus BAY 11-7082 could be a new combination therapy strategy for effective colon cancer treatment with minimal side effects on healthy cells. Tunicamycin 60-71 DNA damage inducible transcript 3 Homo sapiens 201-205