PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 118-154 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 156-161 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 98-103 29728739-11 2018 In the cultured renal arteries, tunicamycin and thapsigargin increased the expression of binding immunoglobulin protein (BiP), an ER stress marker. Tunicamycin 32-43 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 89-119 29728739-11 2018 In the cultured renal arteries, tunicamycin and thapsigargin increased the expression of binding immunoglobulin protein (BiP), an ER stress marker. Tunicamycin 32-43 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 121-124 28987725-12 2017 RESULTS: Tunicamycin, 20% mechanical forces and hypoxia (1% O2) all significantly increased chondrocytes apoptosis rates and expression of ERS markers (GRP78, GRP94 and Caspase 12). Tunicamycin 9-20 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 152-157 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 118-123 26711306-3 2016 The hepatic I/R injury, demonstrated by serum aminotransferase level and the ultra-structure of the liver, was alleviated by administration of tunicamycin, which induced ER stress in rat liver by activating inositol-requiring enzyme 1 (IRE1) and upregulating 78 kDa glucose-regulated protein (GRP78). Tunicamycin 143-154 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 293-298 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 117-122 25492867-4 2015 In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78). Tunicamycin 143-154 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 295-323 27582328-6 2016 Tunicamycin increased the expression of BiP in organ-cultured arteries. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 40-43 26548430-5 2016 The ERS model induced by tunicamycin showed significantly increased expression of binding immunoglobulin protein (BIP)/glucose-regulated protein 78 (Grp78), which is a marker for ERS, and the expression of Erp29 was also increased at the mRNA and protein levels. Tunicamycin 25-36 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 82-112 26548430-5 2016 The ERS model induced by tunicamycin showed significantly increased expression of binding immunoglobulin protein (BIP)/glucose-regulated protein 78 (Grp78), which is a marker for ERS, and the expression of Erp29 was also increased at the mRNA and protein levels. Tunicamycin 25-36 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 114-117 26548430-5 2016 The ERS model induced by tunicamycin showed significantly increased expression of binding immunoglobulin protein (BIP)/glucose-regulated protein 78 (Grp78), which is a marker for ERS, and the expression of Erp29 was also increased at the mRNA and protein levels. Tunicamycin 25-36 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 149-154 26151415-9 2015 Molecularly, tunicamycin (100 ng/ml) increased the levels of GRP78 and CHOP 6 h after administration. Tunicamycin 13-24 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 61-66 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 56-61 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 253-258 25492867-4 2015 In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78). Tunicamycin 143-154 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 325-330 23999590-7 2013 Moreover, icariin inhibited upregulation of endoplasmic reticulum markers, GRP78, GRP94 and CHOP, elicited by tunicamycin. Tunicamycin 110-121 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 75-80 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 73-101 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 103-108 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 37-42 23816873-9 2013 Administration of ER stress inducer, tunicamycin along with cold hypoxic stress, caused a discernible increase in protein oxidation and GRP78 expression, along with a significant elevation in proteasome and apoptotic activity. Tunicamycin 37-48 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 136-141 22460328-4 2012 Here hyperphosphorylation of tau, activation of glycogen synthase kinase-3beta (GSK-3beta), and elevation of Bip were induced by ventricular infusion of ER stressors, tunicamycin (TM) and thapsigargin (TG), in rats. Tunicamycin 167-178 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 109-112 22460328-4 2012 Here hyperphosphorylation of tau, activation of glycogen synthase kinase-3beta (GSK-3beta), and elevation of Bip were induced by ventricular infusion of ER stressors, tunicamycin (TM) and thapsigargin (TG), in rats. Tunicamycin 180-182 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 109-112 21970967-5 2011 Annexin V and propidium iodide labeling revealed cells transiently expressing GRP78 prior to injury were protected against high-concentrations of tunicamycin and glutamate within 72 h. Our findings support the hypothesis that GRP78 inhibits cell death associated with ER stress. Tunicamycin 146-157 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 78-83 21970967-3 2011 Using the rat C6 glioma cell line and flow cytometry, we assessed GRP78 expression following tunicamycin- and glutamate-induced ER stress. Tunicamycin 93-104 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 66-71 21970967-5 2011 Annexin V and propidium iodide labeling revealed cells transiently expressing GRP78 prior to injury were protected against high-concentrations of tunicamycin and glutamate within 72 h. Our findings support the hypothesis that GRP78 inhibits cell death associated with ER stress. Tunicamycin 146-157 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 226-231 21360721-5 2011 Treatment of McA-RH7777 cells with 4-phenyl butyric acid, a chemical ER stress inhibitor, prevented glucosamine- and tunicamycin-induced increases in GRP78 and phosphorylated eIF2alpha, rescued newly synthesized [(35) S]-labeled apoB100, and substantially blocked the colocalization of apoB with GFP-LC3. Tunicamycin 117-128 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 150-155 16875701-9 2006 In addition, dithiothreitol and tunicamycin (ER stress inducers), which increased the expression of GRP78 and activated caspase-12, caused gastric mucosal injury and mucosal cell apoptosis in vitro. Tunicamycin 32-43 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 100-105 12969271-3 2003 Tunicamycin, an inhibitor of N-glycosylation, rapidly induced the expression of the ER-resident chaperone Bip/grp78, a known target gene of the unfolded protein response. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 106-109 12969271-3 2003 Tunicamycin, an inhibitor of N-glycosylation, rapidly induced the expression of the ER-resident chaperone Bip/grp78, a known target gene of the unfolded protein response. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 110-115 12770613-2 2003 GRP78/Bip is expressed following ER stress induced by thapsigargin, tunicamycin or chemical factors. Tunicamycin 68-79 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 0-5 12770613-2 2003 GRP78/Bip is expressed following ER stress induced by thapsigargin, tunicamycin or chemical factors. Tunicamycin 68-79 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 6-9 19322020-7 2009 Finally, chemical endoplasmic reticulum (ER) stress inducers, thapsigargin, tunicamycin, and brefeldin A, dose-dependently increased both mRNA and protein expressions of NF-L, and, its expression was specific to BIP-positive rBMSCs. Tunicamycin 76-87 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 212-215 21245056-11 2011 SAM treatment also reduced tumour necrosis factor-alpha-induced reactive oxygen species and tunicamycin-induced GRP78 expression in VSMCs. Tunicamycin 92-103 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 112-117 19367787-2 2009 In the present study we propose that the cytoprotective effects attributed to 17beta-estradiol and tunicamycin in an in vivo rodent model of ischemia are reflected by changes in neuronal tissue levels of m-calpain, HSP70, GRP94 and GRP78. Tunicamycin 99-110 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 232-237 19367787-8 2009 Lastly, a combined treatment in which rats undergoing MCAO were pretreated with both tunicamycin (24 h prior) and 17beta-estradiol (30 min prior) was associated with an attenuated stress response as indicated by reduced expression of GRP78 and GRP94 when compared to saline-treated controls. Tunicamycin 85-96 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 234-239 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 34-45 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 4-9 19567124-7 2009 SERCA2a overexpression was found to relieve the expression of GRP78 induced by hypoxia and tunicamycin (49.1% and 50.4% decrease respectively), and to inhibit the activation of CHOP (52.7% and 66.1% decrease respectively). Tunicamycin 91-102 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 62-67 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 70-75 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 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 70-75 9492298-5 1998 In rat hepatoma cells ERp29 was found to be associated with the abundant molecular chaperone/stress protein BiP/GRP78 and this interaction was significantly enhanced after treatment with tunicamycin and A23187. Tunicamycin 187-198 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 108-111 9492298-5 1998 In rat hepatoma cells ERp29 was found to be associated with the abundant molecular chaperone/stress protein BiP/GRP78 and this interaction was significantly enhanced after treatment with tunicamycin and A23187. Tunicamycin 187-198 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 112-117 8576245-8 1996 In contrast, co-treatment with the classical GRP inducers thapsigargin and tunicamycin produced only simple additive increases in grp78 promoter activity. Tunicamycin 75-86 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 130-135 1624059-3 1992 Deletion analysis of the rat GRP78 promoter revealed that sequences between -154 and -130 were necessary for full tunicamycin-inducible and constitutive expression of the fusion gene. Tunicamycin 114-125 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 29-34 34533126-2 2021 Methods With the expression level of glucose regulated protein 78 (GRP78) as an indicator to explore the optimal concentration and time, a cell model of tunicamycin-induced ERS in HSC-T6 cells was established. Tunicamycin 153-164 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 37-65 34533126-2 2021 Methods With the expression level of glucose regulated protein 78 (GRP78) as an indicator to explore the optimal concentration and time, a cell model of tunicamycin-induced ERS in HSC-T6 cells was established. Tunicamycin 153-164 heat shock protein family A (Hsp70) member 5 Rattus norvegicus 67-72