PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35456517-11 2022 In the presence of tunicamycin, an ER stress inducer, DDIT3 expression increased in Pcsk6-deficient H9c2 cells but reduced in PCSK6-overexpressing cells. Tunicamycin 19-30 DNA-damage inducible transcript 3 Rattus norvegicus 54-59 34533126-5 2021 Compared with the control group and treatment group with DMSO, the treatment group with 1 mug/mL of tunicamycin had no significant change in cell proliferation, but the expression of alpha-SMA was up-regulated with the apoptosis increased, the proportion of G1 phase cells was significantly increased and that of S phase cells decreased, the ERS induced apoptosis related signal proteins CHOP and caspase-12 were significantly up-regulated, and the expression of cyclin D1 was significantly down-regulated. Tunicamycin 100-111 DNA-damage inducible transcript 3 Rattus norvegicus 388-392 31689455-9 2020 Furthermore, ER stress-mediated apoptosis, determined by the protein levels of CCAAT/enhancer-binding protein-homologous protein and cleaved caspase 12, was increased in tunicamycin or calcification media-treated VSMCs, but the increased effect was reversed in EPO-treated groups. Tunicamycin 170-181 DNA-damage inducible transcript 3 Rattus norvegicus 79-128 33908217-12 2021 T-6 cells transfected with miR-125b mimic and treated with Tunicamycin caused decrease in levels of cleaved caspase-3, sXBP1, CHOP, and LC3. Tunicamycin 59-70 DNA-damage inducible transcript 3 Rattus norvegicus 126-130 33922129-3 2021 While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM. Tunicamycin 37-39 DNA-damage inducible transcript 3 Rattus norvegicus 167-200 33922129-3 2021 While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM. Tunicamycin 37-39 DNA-damage inducible transcript 3 Rattus norvegicus 202-207 28397086-8 2017 Our findings indicate that exposure to tunicamycin (0.5 mug/mL) for 2 h induces the expression of GRP78 and CHOP, and apoptotic markers (caspase-3 and caspase-12) and causes a significant reduction in renal cell viability. Tunicamycin 39-50 DNA-damage inducible transcript 3 Rattus norvegicus 108-112 29291402-4 2018 Tunicamycin (Tm) was employed to excite CHOP expression, and two CHOP small interfering RNAs (siRNAs) were used to inhibit CHOP expression. Tunicamycin 0-11 DNA-damage inducible transcript 3 Rattus norvegicus 40-44 28397086-9 2017 Pre-treatment of cells with piperine and its cyclohexylamino analog decreased the tunicamycin-induced upregulation of GRP78 and CHOP and cell death. Tunicamycin 82-93 DNA-damage inducible transcript 3 Rattus norvegicus 128-132 28399139-5 2017 RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells. Tunicamycin 22-33 DNA-damage inducible transcript 3 Rattus norvegicus 233-237 26151415-9 2015 Molecularly, tunicamycin (100 ng/ml) increased the levels of GRP78 and CHOP 6 h after administration. Tunicamycin 13-24 DNA-damage inducible transcript 3 Rattus norvegicus 71-75 28230089-5 2017 Tunicamycin treatment similarly increased cortical ER stress markers in both rat genotypes; however, only ETB def rats showed a 14-24 fold increase from baseline for medullary GRP78, sXBP-1, and CHOP. Tunicamycin 0-11 DNA-damage inducible transcript 3 Rattus norvegicus 195-199 19567124-6 2009 The GRP78 expression level of the tunicamycin group was 4.9 times as high as that of the control group, and the CHOP expression level of the tunicamycin group was 3.1 times as high as hat of the control group. Tunicamycin 141-152 DNA-damage inducible transcript 3 Rattus norvegicus 112-116 25996208-4 2015 In addition, the compound decreased tunicamycin-induced GRP78 promoter activity in a dose dependent manner without inducing significant inhibition of luciferase activity and cell growth for 6 and 12 h. Moreover, the compound decreased the expression of GRP78, CHOP, XBP-1, and suppressed XBP-1, and reduced phosphorylation of IRE1alpha in FaO rat liver cells. Tunicamycin 36-47 DNA-damage inducible transcript 3 Rattus norvegicus 260-264 24520378-8 2014 Molecularly, baicalin ameliorated tunicamycin-induced ER stress by downregulation of CHOP. Tunicamycin 34-45 DNA-damage inducible transcript 3 Rattus norvegicus 85-89 24520378-9 2014 In addition, baicalin inverted tunicamycin-induced decreases of eNOS mRNA and protein levels, phospho eNOS and NO production through CHOP pathway. Tunicamycin 31-42 DNA-damage inducible transcript 3 Rattus norvegicus 133-137 23999590-7 2013 Moreover, icariin inhibited upregulation of endoplasmic reticulum markers, GRP78, GRP94 and CHOP, elicited by tunicamycin. Tunicamycin 110-121 DNA-damage inducible transcript 3 Rattus norvegicus 92-96 21590646-8 2011 After LY294002 administration in non-TN-treated cells, cell viability was reduced, and CHOP and Bax protein levels were elevated, and Bcl-2 protein levels were reduced. Tunicamycin 37-39 DNA-damage inducible transcript 3 Rattus norvegicus 87-91 24813659-3 2014 Gemigliptin significantly decreased the tunicamycin-mediated increase in glucose regulated protein 78 (GRP78) expression and ER stress-mediated signaling molecules such as protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C-EBP homologous protein (CHOP) and inositol-requiring enzyme 1alpha (IRE1alpha)/c-Jun N-terminal kinase (JNK)-p38. Tunicamycin 40-51 DNA-damage inducible transcript 3 Rattus norvegicus 232-256 24813659-3 2014 Gemigliptin significantly decreased the tunicamycin-mediated increase in glucose regulated protein 78 (GRP78) expression and ER stress-mediated signaling molecules such as protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C-EBP homologous protein (CHOP) and inositol-requiring enzyme 1alpha (IRE1alpha)/c-Jun N-terminal kinase (JNK)-p38. Tunicamycin 40-51 DNA-damage inducible transcript 3 Rattus norvegicus 258-262 24813659-6 2014 The reduction in tunicamycin-induced GRP78 level and PERK/CHOP pathway activity by gemigliptin was reversed after treatment with Akt inhibitor. Tunicamycin 17-28 DNA-damage inducible transcript 3 Rattus norvegicus 58-62 21490406-6 2011 Ghrelin suppressed tunicamycin- or thapsigargin-induced upregulation and nuclear translocation of C/EBP homologous protein (CHOP). Tunicamycin 19-30 DNA-damage inducible transcript 3 Rattus norvegicus 98-122 21490406-6 2011 Ghrelin suppressed tunicamycin- or thapsigargin-induced upregulation and nuclear translocation of C/EBP homologous protein (CHOP). Tunicamycin 19-30 DNA-damage inducible transcript 3 Rattus norvegicus 124-128 19567124-9 2009 Compared with the tunicamycin group, the protein expression levels of GRP78 and CHOP of the SERCA2a overexpression + tunicamycin group were significantly lower by 50.4% and 66.1% respectively, the apoptotic rate was significantly lower by 54.0%, and the cardiomyocyte survival rate was significantly higher by 6.7% (all P < 0.05). Tunicamycin 18-29 DNA-damage inducible transcript 3 Rattus norvegicus 80-84 19567124-9 2009 Compared with the tunicamycin group, the protein expression levels of GRP78 and CHOP of the SERCA2a overexpression + tunicamycin group were significantly lower by 50.4% and 66.1% respectively, the apoptotic rate was significantly lower by 54.0%, and the cardiomyocyte survival rate was significantly higher by 6.7% (all P < 0.05). Tunicamycin 117-128 DNA-damage inducible transcript 3 Rattus norvegicus 80-84 18094145-4 2008 ORP150 expression was found to be regulated by the anti-C/enhancer-binding protein homologous protein (CHOP)/GADD153 transcription factor and ORP150 levels increased in the mitochondria and ER of COS-7 cells after diverse stresses, including hypoxia, serum starvation, prolyl hydroxylase inhibition with dimethyloxaloylglycine, and exposure to tunicamycin, ethidium, bromide, and 2-deoxyglucose. Tunicamycin 344-355 DNA-damage inducible transcript 3 Rattus norvegicus 103-107 18801901-4 2009 Our results demonstrated that tribbles-related protein 3 (TRB3), which is a target gene of CHOP, was responsible for tunicamycin (an ER stress inducer)-induced apoptosis. Tunicamycin 117-128 DNA-damage inducible transcript 3 Rattus norvegicus 91-95 18094145-4 2008 ORP150 expression was found to be regulated by the anti-C/enhancer-binding protein homologous protein (CHOP)/GADD153 transcription factor and ORP150 levels increased in the mitochondria and ER of COS-7 cells after diverse stresses, including hypoxia, serum starvation, prolyl hydroxylase inhibition with dimethyloxaloylglycine, and exposure to tunicamycin, ethidium, bromide, and 2-deoxyglucose. Tunicamycin 344-355 DNA-damage inducible transcript 3 Rattus norvegicus 109-116