PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 34786210-5 2021 Activation of ER stress positively correlated with PKM2 expression both in HCC tissue samples and tunicamycin (TM)-induced HCC cell lines. Tunicamycin 98-109 pyruvate kinase M1/2 Homo sapiens 51-55 34786210-5 2021 Activation of ER stress positively correlated with PKM2 expression both in HCC tissue samples and tunicamycin (TM)-induced HCC cell lines. Tunicamycin 111-113 pyruvate kinase M1/2 Homo sapiens 51-55 34604209-4 2021 In the current study, we demonstrated that tunicamycin (a novel ERS inducer) can induce the apoptosis of HSCs and increase the concentration of intracellular Ca2+ and the expression of ERS protein GRP78, apoptosis protein caspase-12, and Bax, while it can decrease the antiapoptosis protein expression of Bcl-2. Tunicamycin 43-54 heat shock protein family A (Hsp70) member 5 Homo sapiens 197-202 34604209-4 2021 In the current study, we demonstrated that tunicamycin (a novel ERS inducer) can induce the apoptosis of HSCs and increase the concentration of intracellular Ca2+ and the expression of ERS protein GRP78, apoptosis protein caspase-12, and Bax, while it can decrease the antiapoptosis protein expression of Bcl-2. Tunicamycin 43-54 BCL2 associated X, apoptosis regulator Homo sapiens 238-241 34604209-4 2021 In the current study, we demonstrated that tunicamycin (a novel ERS inducer) can induce the apoptosis of HSCs and increase the concentration of intracellular Ca2+ and the expression of ERS protein GRP78, apoptosis protein caspase-12, and Bax, while it can decrease the antiapoptosis protein expression of Bcl-2. Tunicamycin 43-54 BCL2 apoptosis regulator Homo sapiens 305-310 34604209-5 2021 Our findings indicate that tunicamycin can induce HSCs apoptosis through calpain-2/Ca2+-dependent ERS pathway. Tunicamycin 27-38 calpain 2 Homo sapiens 73-82 34077277-4 2021 The current study aimed to investigate the effect of imoxin (IMX), a selective PKR inhibitor, on tunicamycin (TN)-induced promotion of ER stress and suppression of insulin signaling in C2C12 myotubes. Tunicamycin 97-108 eukaryotic translation initiation factor 2-alpha kinase 2 Mus musculus 79-82 34386060-5 2021 Notably, restoration of the ATG5-dependent autophagy in DU145 cells significantly increased the cytotoxic effects of the chemotherapeutic drugs, docetaxel and valproic acid, and the endoplasmic reticulum stress inducers, brefeldin A, tunicamycin and thapsigargin. Tunicamycin 234-245 autophagy related 5 Homo sapiens 28-32 34448454-3 2021 We find that mutants in the intraflagellar transport protein gene osm-3 were significantly protected from tunicamycin-induced ER stress. Tunicamycin 106-117 Osmotic avoidance abnormal protein 3 Caenorhabditis elegans 66-71 34448454-6 2021 Expression of P-glycoprotein (PGP) xenobiotic detoxification genes was elevated in osm-3 mutants and their knockdown or inhibition with verapamil suppressed tunicamycin resistance. Tunicamycin 157-168 Osmotic avoidance abnormal protein 3 Caenorhabditis elegans 83-88 34436503-5 2021 Meanwhile, tunicamycin-induced ER stress blocked the TGF-beta/Smad signaling pathway. Tunicamycin 11-22 transforming growth factor alpha Homo sapiens 53-61 34415333-7 2021 Ex vivo treatment of mesenteric arteries with an AMPK agonist (A769662) or a PPARdelta agonist (GW1516) improved the impaired EDR in DMO and reversed the tunicamycin-induced ER stress, ROS production, and EDR impairment in mesenteric arteries from CMO. Tunicamycin 154-165 protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus 49-53 34521445-10 2021 In addition, overexpression of KCNQ1OT1/XIST partly abolished the inhibitory effects of XBP-1u knockdown or tunicamycin, an activator of endoplasmic reticulum stress, on CRC cell viability loss and apoptosis. Tunicamycin 108-119 KCNQ1 overlapping transcript 1 Mus musculus 31-39 34521445-10 2021 In addition, overexpression of KCNQ1OT1/XIST partly abolished the inhibitory effects of XBP-1u knockdown or tunicamycin, an activator of endoplasmic reticulum stress, on CRC cell viability loss and apoptosis. Tunicamycin 108-119 inactive X specific transcripts Mus musculus 40-44 34378991-6 2021 We further demonstrated that the mTORC1-dependent ATF4 activation is an integral signaling event of unfolded protein response (UPR) as both ATF4 activation and NNMT upregulation by tunicamycin, a well-documented endoplasmic reticulum (ER) stress inducer, are blunted when hepatocytes were pretreated with Torin1. Tunicamycin 181-192 CREB regulated transcription coactivator 1 Mus musculus 33-39 34378991-6 2021 We further demonstrated that the mTORC1-dependent ATF4 activation is an integral signaling event of unfolded protein response (UPR) as both ATF4 activation and NNMT upregulation by tunicamycin, a well-documented endoplasmic reticulum (ER) stress inducer, are blunted when hepatocytes were pretreated with Torin1. Tunicamycin 181-192 activating transcription factor 4 Mus musculus 50-54 34378991-6 2021 We further demonstrated that the mTORC1-dependent ATF4 activation is an integral signaling event of unfolded protein response (UPR) as both ATF4 activation and NNMT upregulation by tunicamycin, a well-documented endoplasmic reticulum (ER) stress inducer, are blunted when hepatocytes were pretreated with Torin1. Tunicamycin 181-192 activating transcription factor 4 Mus musculus 140-144 34378991-6 2021 We further demonstrated that the mTORC1-dependent ATF4 activation is an integral signaling event of unfolded protein response (UPR) as both ATF4 activation and NNMT upregulation by tunicamycin, a well-documented endoplasmic reticulum (ER) stress inducer, are blunted when hepatocytes were pretreated with Torin1. Tunicamycin 181-192 nicotinamide N-methyltransferase Mus musculus 160-164 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 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 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 caspase 12 Rattus norvegicus 397-407 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 cyclin D1 Rattus norvegicus 463-472 34077277-4 2021 The current study aimed to investigate the effect of imoxin (IMX), a selective PKR inhibitor, on tunicamycin (TN)-induced promotion of ER stress and suppression of insulin signaling in C2C12 myotubes. Tunicamycin 110-112 eukaryotic translation initiation factor 2-alpha kinase 2 Mus musculus 79-82 34077277-11 2021 These findings suggest that IMX may protect against TN-induced skeletal muscle ER stress and insulin resistance, which are potentially mediated by PKR. Tunicamycin 52-54 eukaryotic translation initiation factor 2-alpha kinase 2 Mus musculus 147-150 34260993-9 2021 CAE suppressed the bleomycin or TM-induced increases in ER-stress biomarker, BiP, and PERK pathway proteins, resulting in a decrease in ER stress in mouse lung tissues and A549 cells, respectively. Tunicamycin 32-34 heat shock protein 5 Mus musculus 77-80 34260993-9 2021 CAE suppressed the bleomycin or TM-induced increases in ER-stress biomarker, BiP, and PERK pathway proteins, resulting in a decrease in ER stress in mouse lung tissues and A549 cells, respectively. Tunicamycin 32-34 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 86-90 34260993-10 2021 Additionally, CAE treatment suppressed the bleomycin or TM-induced increase in the ER-stress downstream proteins, activating ATF3 and increased the levels of PINK1 in AEC IIs, both in vivo and in vitro. Tunicamycin 56-58 activating transcription factor 3 Mus musculus 125-129 34260993-10 2021 Additionally, CAE treatment suppressed the bleomycin or TM-induced increase in the ER-stress downstream proteins, activating ATF3 and increased the levels of PINK1 in AEC IIs, both in vivo and in vitro. Tunicamycin 56-58 PTEN induced putative kinase 1 Mus musculus 158-163 34336161-0 2021 Tunicamycin-Induced Endoplasmic Reticulum Stress Promotes Breast Cancer Cell MDA-MB-231 Apoptosis through Inhibiting Wnt/beta-Catenin Signaling Pathway. Tunicamycin 0-11 catenin beta 1 Homo sapiens 121-133 34336161-8 2021 Besides, tunicamycin dose dependently inhibited both Wnt/beta-catenin pathway and cells viability. Tunicamycin 9-20 catenin beta 1 Homo sapiens 57-69 34237462-12 2021 The mutant AGR2 showed reduced capacity to bind MUC2 and alleviate tunicamycin-induced ER stress. Tunicamycin 67-78 anterior gradient 2, protein disulphide isomerase family member Homo sapiens 11-15 34299151-8 2021 In conclusion, PAR2-induced TF synthesis in HTECs is enhanced by culture in high concentrations of glucose and suppressed by inhibiting either PAR2 activation (I-191), glycolysis (2DOG) or glycosylation (tunicamycin). Tunicamycin 204-215 F2R like trypsin receptor 1 Homo sapiens 15-19 34322380-12 2021 Besides, some compounds (such as the Acetaminophen, Urethane and Tunicamycin) were predicted for curing breast cancer via targeting MRPL12, MRPL13 and POP1 simultaneously. Tunicamycin 65-76 mitochondrial ribosomal protein L12 Homo sapiens 132-138 34322380-12 2021 Besides, some compounds (such as the Acetaminophen, Urethane and Tunicamycin) were predicted for curing breast cancer via targeting MRPL12, MRPL13 and POP1 simultaneously. Tunicamycin 65-76 mitochondrial ribosomal protein L13 Homo sapiens 140-146 34322380-12 2021 Besides, some compounds (such as the Acetaminophen, Urethane and Tunicamycin) were predicted for curing breast cancer via targeting MRPL12, MRPL13 and POP1 simultaneously. Tunicamycin 65-76 POP1 homolog, ribonuclease P/MRP subunit Homo sapiens 151-155 34322482-5 2021 Pharmacological ER stress inducers (tunicamycin (TCN) and thapsigargin) and hyperglycemia robustly increase the expression of miR-494 in vitro. Tunicamycin 36-47 epiregulin Homo sapiens 16-18 34322482-5 2021 Pharmacological ER stress inducers (tunicamycin (TCN) and thapsigargin) and hyperglycemia robustly increase the expression of miR-494 in vitro. Tunicamycin 36-47 microRNA 494 Homo sapiens 126-133 34322482-5 2021 Pharmacological ER stress inducers (tunicamycin (TCN) and thapsigargin) and hyperglycemia robustly increase the expression of miR-494 in vitro. Tunicamycin 49-52 epiregulin Homo sapiens 16-18 34322482-5 2021 Pharmacological ER stress inducers (tunicamycin (TCN) and thapsigargin) and hyperglycemia robustly increase the expression of miR-494 in vitro. Tunicamycin 49-52 microRNA 494 Homo sapiens 126-133 34322482-7 2021 Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to TCN in endothelial cells and increases cell viability. Tunicamycin 99-102 microRNA 494 Homo sapiens 14-21 34322482-7 2021 Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to TCN in endothelial cells and increases cell viability. Tunicamycin 99-102 epiregulin Homo sapiens 74-76 34229656-5 2021 METHODS: To investigate changes in ER stress response genes, we treated LRRK2-wild type and LRRK2-G2019S astrocytes with tunicamycin, an ER stress-inducing agent, and performed gene expression profiling with microarrays. Tunicamycin 121-132 leucine-rich repeat kinase 2 Mus musculus 72-77 34229656-5 2021 METHODS: To investigate changes in ER stress response genes, we treated LRRK2-wild type and LRRK2-G2019S astrocytes with tunicamycin, an ER stress-inducing agent, and performed gene expression profiling with microarrays. Tunicamycin 121-132 leucine-rich repeat kinase 2 Mus musculus 92-97 34143952-7 2021 Furthermore, analysis of the unfolded protein response showed a reduced increase in EIF2AK3 (PERK) expression upon stimulation with tunicamycin as compared to controls, suggesting an impaired unfolded protein response. Tunicamycin 132-143 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 84-91 34143952-7 2021 Furthermore, analysis of the unfolded protein response showed a reduced increase in EIF2AK3 (PERK) expression upon stimulation with tunicamycin as compared to controls, suggesting an impaired unfolded protein response. Tunicamycin 132-143 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 93-97 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 34086738-5 2021 In MIN6 beta cells, HSPGs, HS and HPSE were reduced following treatment with pharmacological inducers of ER stress (thapsigargin or tunicamycin). Tunicamycin 132-143 heparanase Mus musculus 34-38 34199510-4 2021 Downregulation of microtubule acetylation using shRNA or CRSIPR/Cas9 techniques targeting ATAT1, which encodes alpha-tubulin N-acetyltransferase (alphaTAT1), resulted in the upregulation of ER stress markers, changes in ER morphology, and enhanced tunicamycin-induced UPR signaling in cancer cells. Tunicamycin 248-259 alpha tubulin acetyltransferase 1 Homo sapiens 90-95 34199510-4 2021 Downregulation of microtubule acetylation using shRNA or CRSIPR/Cas9 techniques targeting ATAT1, which encodes alpha-tubulin N-acetyltransferase (alphaTAT1), resulted in the upregulation of ER stress markers, changes in ER morphology, and enhanced tunicamycin-induced UPR signaling in cancer cells. Tunicamycin 248-259 alpha tubulin acetyltransferase 1 Homo sapiens 146-155 34199510-5 2021 A set of genes involved in cancer progression, especially focal adhesion genes, were downregulated in both ATAT1-knockout and tunicamycin-treated cells, whereas ATAT1 overexpression restored the gene expression inhibited by tunicamycin. Tunicamycin 224-235 alpha tubulin acetyltransferase 1 Homo sapiens 161-166 34139004-4 2021 We also find an attenuation of glucose induced increase of alpha-E catenin when hexosamine biosynthesis pathway is inhibited either with glutamine depletion or with the drugs azaserine and tunicamycin. Tunicamycin 189-200 catenin alpha 1 Homo sapiens 59-74 34121978-10 2021 Cell viability and apoptosis in STF-083010 and Tunicamycin (Tm) co-treated cells were evaluated using BrdU, MTT, Annexin V-FITC/PI staining, and caspase-12 and -3 activities assays. Tunicamycin 47-58 annexin A5 Homo sapiens 113-122 34121978-10 2021 Cell viability and apoptosis in STF-083010 and Tunicamycin (Tm) co-treated cells were evaluated using BrdU, MTT, Annexin V-FITC/PI staining, and caspase-12 and -3 activities assays. Tunicamycin 47-58 caspase 3 Homo sapiens 145-162 34121978-10 2021 Cell viability and apoptosis in STF-083010 and Tunicamycin (Tm) co-treated cells were evaluated using BrdU, MTT, Annexin V-FITC/PI staining, and caspase-12 and -3 activities assays. Tunicamycin 60-62 annexin A5 Homo sapiens 113-122 34121978-10 2021 Cell viability and apoptosis in STF-083010 and Tunicamycin (Tm) co-treated cells were evaluated using BrdU, MTT, Annexin V-FITC/PI staining, and caspase-12 and -3 activities assays. Tunicamycin 60-62 caspase 3 Homo sapiens 145-162 35421744-4 2022 Using ET receptor Never ripe (Nr) mutants, a significant role of ET in tunicamycin (Tm)-induced ER stress sensing and signaling was confirmed based on the changes in the expression levels of SlIRE1b and SlBiP. Tunicamycin 71-82 BEL1-like homeodomain protein 2 Solanum lycopersicum 203-208 35421744-4 2022 Using ET receptor Never ripe (Nr) mutants, a significant role of ET in tunicamycin (Tm)-induced ER stress sensing and signaling was confirmed based on the changes in the expression levels of SlIRE1b and SlBiP. Tunicamycin 84-86 BEL1-like homeodomain protein 2 Solanum lycopersicum 203-208 35398613-7 2022 The cells treated with A23187 or tunicamycin exhibited the activation of calpain-5 and truncation of caspase-4. Tunicamycin 33-44 calpain 5 Homo sapiens 73-82 35398613-7 2022 The cells treated with A23187 or tunicamycin exhibited the activation of calpain-5 and truncation of caspase-4. Tunicamycin 33-44 caspase 4 Homo sapiens 101-110 35304860-4 2022 Control and IRE1alpha knockout (KO) GECs were incubated with tunicamycin to induce ER stress and subjected to proteomic analysis. Tunicamycin 61-72 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 12-21 35304860-6 2022 Tunicamycin enhanced expression of Sec23B and the reticulophagy adaptor reticulon-3-long (RTN3L) in control, but not IRE1alpha KO GECs. Tunicamycin 0-11 SEC23 homolog B, COPII coat complex component Mus musculus 35-41 35304860-10 2022 Degradation of RTN3L and collagen IV increased in response to tunicamycin, and the turnover was blocked by deletion of IRE1alpha; thus, the IRE1alpha pathway promotes RTN3L-mediated reticulophagy and collagen IV may be an IRE1alpha-dependent reticulophagy substrate. Tunicamycin 62-73 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 222-231 35304860-6 2022 Tunicamycin enhanced expression of Sec23B and the reticulophagy adaptor reticulon-3-long (RTN3L) in control, but not IRE1alpha KO GECs. Tunicamycin 0-11 reticulon 3 Mus musculus 72-83 35304860-8 2022 Tunicamycin stimulated colocalization of autophagosomes with Sec23B and RTN3L in an IRE1alpha-dependent manner. Tunicamycin 0-11 SEC23 homolog B, COPII coat complex component Mus musculus 61-67 35304860-8 2022 Tunicamycin stimulated colocalization of autophagosomes with Sec23B and RTN3L in an IRE1alpha-dependent manner. Tunicamycin 0-11 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 84-93 35304860-10 2022 Degradation of RTN3L and collagen IV increased in response to tunicamycin, and the turnover was blocked by deletion of IRE1alpha; thus, the IRE1alpha pathway promotes RTN3L-mediated reticulophagy and collagen IV may be an IRE1alpha-dependent reticulophagy substrate. Tunicamycin 62-73 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 140-149 35339509-13 2022 Importin alpha4 expression was increased in the nuclear insoluble fraction after incubation with tunicamycin or hydrogen peroxide. Tunicamycin 97-108 karyopherin (importin) alpha 3 Mus musculus 0-15 35194770-3 2022 METHODS: IL-1beta and two additional ER stress activators, palmitate and tunicamycin were applied to evaluate the expression level miR-25 by Taqman RT-PCR. Tunicamycin 73-84 microRNA 25 Homo sapiens 131-137 35194770-8 2022 Expression levels of miR-25 were significantly upregulated with the treatment of IL-1beta, palmitate or tunicamycin in both INS-1 cells and human islets. Tunicamycin 104-115 microRNA 25 Rattus norvegicus 21-27 35344886-6 2022 After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75). Tunicamycin 21-32 heat shock protein 1B Mus musculus 183-188 35325747-8 2022 Moreover, this method is competent to monitor changed states of PTK7-specific sialylation induced by tunicamycin. Tunicamycin 101-112 protein tyrosine kinase 7 (inactive) Homo sapiens 64-68 34079010-6 2021 Hence, although levels of spliced XBP1 and CHOP mRNA and ATF4 protein increase with Ipom-F, the accompanying increase in the levels of ER lumenal BiP and GRP94 seen with tunicamycin are not observed. Tunicamycin 170-181 X-box binding protein 1 Homo sapiens 34-38 34079010-6 2021 Hence, although levels of spliced XBP1 and CHOP mRNA and ATF4 protein increase with Ipom-F, the accompanying increase in the levels of ER lumenal BiP and GRP94 seen with tunicamycin are not observed. Tunicamycin 170-181 heat shock protein family A (Hsp70) member 5 Homo sapiens 146-149 34079010-6 2021 Hence, although levels of spliced XBP1 and CHOP mRNA and ATF4 protein increase with Ipom-F, the accompanying increase in the levels of ER lumenal BiP and GRP94 seen with tunicamycin are not observed. Tunicamycin 170-181 heat shock protein 90 beta family member 1 Homo sapiens 154-159 35603939-11 2022 In HCT116 cells, tunicamycin increased the expression of Grp78, Gro-alpha and IL-8 in a concentration-dependent manner. Tunicamycin 17-28 heat shock protein family A (Hsp70) member 5 Homo sapiens 57-62 35603939-11 2022 In HCT116 cells, tunicamycin increased the expression of Grp78, Gro-alpha and IL-8 in a concentration-dependent manner. Tunicamycin 17-28 C-X-C motif chemokine ligand 1 Homo sapiens 64-73 35603939-11 2022 In HCT116 cells, tunicamycin increased the expression of Grp78, Gro-alpha and IL-8 in a concentration-dependent manner. Tunicamycin 17-28 C-X-C motif chemokine ligand 8 Homo sapiens 78-82 35603939-12 2022 Furthermore, p38 MAPK inhibitor significantly inhibited the upregulation of Gro-alpha and IL-8 induced by tunicamycin. Tunicamycin 106-117 C-X-C motif chemokine ligand 1 Homo sapiens 76-85 35603939-12 2022 Furthermore, p38 MAPK inhibitor significantly inhibited the upregulation of Gro-alpha and IL-8 induced by tunicamycin. Tunicamycin 106-117 C-X-C motif chemokine ligand 8 Homo sapiens 90-94 35597864-0 2022 The yeast two-component SLN1 branch of the HOG pathway and the scaffolding activity of Pbs2 modulate the response to endoplasmic reticulum stress induced by tunicamycin. Tunicamycin 157-168 histidine kinase Saccharomyces cerevisiae S288C 24-28 35597864-0 2022 The yeast two-component SLN1 branch of the HOG pathway and the scaffolding activity of Pbs2 modulate the response to endoplasmic reticulum stress induced by tunicamycin. Tunicamycin 157-168 mitogen-activated protein kinase kinase PBS2 Saccharomyces cerevisiae S288C 87-91 35594368-0 2022 Concise Synthesis of Tunicamycin V and Discovery of a Cytostatic DPAGT1 Inhibitor. Tunicamycin 21-32 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 65-71 35579911-6 2022 We discovered that PD patients with high amounts of PDIA6 and HYOU1 proteins were more sensitive to endoplasmic reticulum stress, in particular to tunicamycin. Tunicamycin 147-158 protein disulfide isomerase family A member 6 Homo sapiens 52-57 35579911-6 2022 We discovered that PD patients with high amounts of PDIA6 and HYOU1 proteins were more sensitive to endoplasmic reticulum stress, in particular to tunicamycin. Tunicamycin 147-158 hypoxia up-regulated 1 Homo sapiens 62-67 35344886-6 2022 After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75). Tunicamycin 21-32 heat shock protein 5 Mus musculus 207-212 35344886-6 2022 After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75). Tunicamycin 21-32 heat shock protein 9 Mus musculus 219-224 35344886-6 2022 After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75). Tunicamycin 21-32 heat shock protein family A (Hsp70) member 9 Rattus norvegicus 226-231 35344886-6 2022 After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75). Tunicamycin 34-36 heat shock protein 1B Mus musculus 183-188 35344886-6 2022 After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75). Tunicamycin 34-36 heat shock protein 5 Mus musculus 207-212 35344886-6 2022 After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75). Tunicamycin 34-36 heat shock protein 9 Mus musculus 219-224 35344886-6 2022 After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75). Tunicamycin 34-36 heat shock protein family A (Hsp70) member 9 Rattus norvegicus 226-231 35390453-8 2022 Tunicamycin, an ER stress inducer, increased ERdj5 levels. Tunicamycin 0-11 DnaJ heat shock protein family (Hsp40) member C10 Mus musculus 45-50 35513574-6 2022 Sptlc2 was upregulated and ceramide levels were elevated by tunicamycin in the livers of C57BL/6J wild-type mice. Tunicamycin 60-71 serine palmitoyltransferase, long chain base subunit 2 Mus musculus 0-6 35500653-7 2022 Furthermore, ablation of IRE1alpha phosphorylation at Ser724 exacerbated ER stress-induced hepatic steatosis in Tunicamycin-treated Ern1S724A/S724A mice. Tunicamycin 112-123 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 25-34 35500653-7 2022 Furthermore, ablation of IRE1alpha phosphorylation at Ser724 exacerbated ER stress-induced hepatic steatosis in Tunicamycin-treated Ern1S724A/S724A mice. Tunicamycin 112-123 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 132-136 35514983-4 2022 We found that microglia release nanomolar levels of calreticulin when inflammatory-activated with lipopolysaccharide, when endoplasmic reticulum stress was induced by tunicamycin, or when cell death was induced by staurosporine, and that neurons release calreticulin when crushed. Tunicamycin 167-178 calreticulin Homo sapiens 52-64 35348185-5 2022 After treating with the ER-stress inducer tunicamycin, cell viability was investigated by performing Cell Counting Kit-8, TUNEL and western blotting assays, which revealed that CTRP9 increased the activity of HTR8/SVneo cells induced by HG through the alleviation of ER stress. Tunicamycin 42-53 C1q and TNF related 9 Homo sapiens 177-182 35467485-4 2022 Top six better performing drugs, binding affinity for dpagt1 at the range of -17.63 to -20.40 kcal/mol, than the reference ligand (tunicamycin; -14.86 kcal/mol) were obtained at the end of structure-based-pharmacophore- and virtual-screening and "induced fit" docking calculations. Tunicamycin 131-142 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 54-60 35019714-7 2022 Tunicamycin treatment confirmed p44 as glycosylated form of p41. Tunicamycin 0-11 erythrocyte membrane protein band 4.1 Homo sapiens 60-63 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 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 proprotein convertase subtilisin/kexin type 6 Rattus norvegicus 84-89 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 proprotein convertase subtilisin/kexin type 6 Rattus norvegicus 126-131 35428325-4 2022 RESULTS: Palmitate- or tunicamycin-induced ER stress resulted in PGC-1alpha downregulation and enhanced expression of activating transcription factor 4 (ATF4) in human myotubes and mouse skeletal muscle. Tunicamycin 23-34 PPARG coactivator 1 alpha Homo sapiens 65-75 35428325-4 2022 RESULTS: Palmitate- or tunicamycin-induced ER stress resulted in PGC-1alpha downregulation and enhanced expression of activating transcription factor 4 (ATF4) in human myotubes and mouse skeletal muscle. Tunicamycin 23-34 activating transcription factor 4 Homo sapiens 118-151 35428325-4 2022 RESULTS: Palmitate- or tunicamycin-induced ER stress resulted in PGC-1alpha downregulation and enhanced expression of activating transcription factor 4 (ATF4) in human myotubes and mouse skeletal muscle. Tunicamycin 23-34 activating transcription factor 4 Homo sapiens 153-157 35428325-5 2022 Overexpression of ATF4 decreased basal PCG-1alpha expression, whereas ATF4 knockdown abrogated the reduction of PCG-1alpha caused by tunicamycin in myotubes. Tunicamycin 133-144 activating transcription factor 4 Mus musculus 70-74 35428325-8 2022 Moreover, siRNA against S6 kinase, an mTORC1 downstream target, prevented the reduction in the expression of CRTC2 and PGC-1alpha caused by the ER stressor tunicamycin. Tunicamycin 156-167 CREB regulated transcription coactivator 2 Homo sapiens 109-114 35428325-8 2022 Moreover, siRNA against S6 kinase, an mTORC1 downstream target, prevented the reduction in the expression of CRTC2 and PGC-1alpha caused by the ER stressor tunicamycin. Tunicamycin 156-167 PPARG coactivator 1 alpha Homo sapiens 119-129 35492579-5 2022 Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets. Tunicamycin 110-112 tumor necrosis factor Sus scrofa 74-83 35492579-5 2022 Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets. Tunicamycin 110-112 interleukin 6 Sus scrofa 88-92 35492579-5 2022 Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets. Tunicamycin 110-112 interleukin 6 Sus scrofa 161-165 35492579-5 2022 Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets. Tunicamycin 110-112 C-reactive protein Sus scrofa 170-173 35492579-5 2022 Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets. Tunicamycin 237-239 interleukin 6 Sus scrofa 161-165 35454076-9 2022 We tested a small biological molecule, Tunicamycin, that blocks a specific step of the protein N-glycosylation pathway in the endoplasmic reticulum (ER), i.e., the catalytic activity of N-acetylglusosaminyl 1-phosphate transferase (GPT). Tunicamycin 39-50 glutamic--pyruvic transaminase Homo sapiens 232-235 35273242-6 2022 In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2. Tunicamycin 13-24 C-X-C motif chemokine ligand 8 Homo sapiens 65-68 35273242-6 2022 In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2. Tunicamycin 13-24 C-X-C motif chemokine ligand 1 Homo sapiens 70-75 35273242-6 2022 In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2. Tunicamycin 13-24 C-X-C motif chemokine ligand 2 Homo sapiens 81-86 35273242-6 2022 In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2. Tunicamycin 13-24 valosin containing protein Homo sapiens 125-128 35273242-6 2022 In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2. Tunicamycin 13-24 nucleotide binding oligomerization domain containing 2 Homo sapiens 222-226 35233582-0 2022 The role of GRP78 in oxidative stress induced by tunicamycin in trabecular meshwork cells. Tunicamycin 49-60 heat shock protein family A (Hsp70) member 5 Homo sapiens 12-17 35233582-1 2022 OBJECTIVE: To clarify the regulatory effect of GRP-78 induced by tunicamycin on endoplasmic reticulum (ER) stress. Tunicamycin 65-76 heat shock protein family A (Hsp70) member 5 Homo sapiens 47-53 35233582-2 2022 METHODS: Tunicamycin was used to induce ER stress in trabecular meshwork cells (HTMC and GTM3). Tunicamycin 9-20 glutathione S-transferase mu 3 Homo sapiens 89-93 35233582-4 2022 RESULTS: Tunicamycin could significantly increase the ROS content and the apoptosis rate in HTMC and GTM3 (p<0.01). Tunicamycin 9-20 glutathione S-transferase mu 3 Homo sapiens 101-105 35233582-6 2022 Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01). Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 51-56 35233582-6 2022 Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01). Tunicamycin 0-11 voltage dependent anion channel 1 Homo sapiens 57-62 35233582-6 2022 Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01). Tunicamycin 0-11 activating transcription factor 4 Homo sapiens 64-68 35233582-6 2022 Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01). Tunicamycin 0-11 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 70-74 35233582-6 2022 Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01). Tunicamycin 0-11 eukaryotic translation initiation factor 2 subunit alpha Homo sapiens 76-81 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 35233582-10 2022 CONCLUSION: Tunicamycin induces oxidative stress in trabecular meshwork cells, and the increase in GRP78 expression can protect the cells during ER stress by regulating eIF2. Tunicamycin 12-23 heat shock protein family A (Hsp70) member 5 Homo sapiens 99-104 35233582-10 2022 CONCLUSION: Tunicamycin induces oxidative stress in trabecular meshwork cells, and the increase in GRP78 expression can protect the cells during ER stress by regulating eIF2. Tunicamycin 12-23 eukaryotic translation initiation factor 2 subunit alpha Homo sapiens 169-173 35104011-6 2022 In tunicamycin-induced ER stress conditions and liver injury animal models following ER stress, NRF2 levels were highly correlated with SIRT3. Tunicamycin 3-14 NFE2 like bZIP transcription factor 2 Homo sapiens 96-100 35104011-7 2022 Nrf2 deficiency enhanced the tunicamycin-mediated induction of CHOP, which was attenuated by Sirt3 overexpression. Tunicamycin 29-40 NFE2 like bZIP transcription factor 2 Homo sapiens 0-4 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 35104011-7 2022 Nrf2 deficiency enhanced the tunicamycin-mediated induction of CHOP, which was attenuated by Sirt3 overexpression. Tunicamycin 29-40 sirtuin 3 Homo sapiens 93-98 35330105-6 2022 Tunicamycin treatment significantly increased the levels of serum ALT and AST and hepatic triglycerides. Tunicamycin 0-11 glutamic pyruvic transaminase, soluble Mus musculus 66-69 35330105-6 2022 Tunicamycin treatment significantly increased the levels of serum ALT and AST and hepatic triglycerides. Tunicamycin 0-11 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 74-77 35222844-6 2022 Remarkably, the nucleoside antibiotic tunicamycin, which targets UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosaminephosphotransferase (ALG7) and N-glycosylation in other organisms, induces a delayed-death effect and inhibits parasite growth during the second IDC after treatment. Tunicamycin 38-49 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 147-151 35104011-8 2022 Further, Sirt3 delivery to hepatocytes in Nrf2 knockout mice prevented tunicamycin from increasing mortality by decreasing ER stress. Tunicamycin 71-82 sirtuin 3 Mus musculus 9-14 35104011-8 2022 Further, Sirt3 delivery to hepatocytes in Nrf2 knockout mice prevented tunicamycin from increasing mortality by decreasing ER stress. Tunicamycin 71-82 nuclear factor, erythroid derived 2, like 2 Mus musculus 42-46 2514095-7 1989 Incubation of NS-1 cells with tunicamycin resulted in a shift in the apparent molecular mass of the transferrin receptor from 96 kDa and 94 kDa to approximately 82 kDa. Tunicamycin 30-41 transferrin Mus musculus 100-111 35159364-7 2022 Furthermore, tunicamycin suppresses the association of C53 with the centrosome. Tunicamycin 13-24 CDK5 regulatory subunit associated protein 3 Homo sapiens 55-58 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 vimentin Homo sapiens 316-324 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 fibronectin 1 Homo sapiens 406-417 35162959-7 2022 We also find that, in response to tunicamycin-induced ER stress, miR-16-5p suppression decreases apoptosis, inflammation and cardiac damage via activating the ATF6-mediated cytoprotective pathway. Tunicamycin 34-45 activating transcription factor 6 Homo sapiens 159-163 35053376-9 2022 LCN2 knockout cells showed enhanced and sustained activation of unfolded protein response proteins when treated with tunicamycin or cultured under glucose deprivation. Tunicamycin 117-128 lipocalin 2 Homo sapiens 0-4 35370192-5 2022 The usefulness of tunicamycin as antibacterial agents is limited by off-target inhibition of human UDP-N-acetylglucosamine (GlcNAc): polyprenol phosphate translocase (GPT). Tunicamycin 18-29 glutamic--pyruvic transaminase Homo sapiens 167-170 35370192-7 2022 Next, the minimum structural requirements for tunicamycin V for MraY inhibition were established by systematic structure-activity relationship studies with truncated analogs of tunicamycin V. Our collaborative study elucidated a crystal structure of human GPT in complex with tunicamycin. Tunicamycin 46-57 glutamic--pyruvic transaminase Homo sapiens 256-259 35370192-7 2022 Next, the minimum structural requirements for tunicamycin V for MraY inhibition were established by systematic structure-activity relationship studies with truncated analogs of tunicamycin V. Our collaborative study elucidated a crystal structure of human GPT in complex with tunicamycin. Tunicamycin 177-188 glutamic--pyruvic transaminase Homo sapiens 256-259 35370192-7 2022 Next, the minimum structural requirements for tunicamycin V for MraY inhibition were established by systematic structure-activity relationship studies with truncated analogs of tunicamycin V. Our collaborative study elucidated a crystal structure of human GPT in complex with tunicamycin. Tunicamycin 276-287 glutamic--pyruvic transaminase Homo sapiens 256-259 2514095-2 1989 We have investigated the structural and functional properties of the transferrin receptor from murine plasmacytoma cells (NS-1 cells) treated with the glycosylation inhibitor, tunicamycin and the glycosylation-processing inhibitors, swainsonine and castanospermine. Tunicamycin 176-187 transferrin Mus musculus 69-80 2513184-5 1989 Inhibition of N-linked glycosylation by treatment with tunicamycin, 2-deoxy-D-glucose or glucosamine stimulated the synthesis of non-ADP-ribosylated GRP78 up to sixfold with relatively little effect on its ADP-ribosylation. Tunicamycin 55-66 heat shock protein 5 Mus musculus 149-154 2590385-5 1989 Neuraminidase and tunicamycin treatment demonstrated that the GH receptor on F442A preadipocytes is a sialo-glycoprotein with N-linked carbohydrate chains. Tunicamycin 18-29 growth hormone receptor Mus musculus 62-73 35350536-6 2022 Pak2 overexpression enhances the XBP1-Hrd1 UPR axis and ameliorates tunicamycin induced cardiac apoptosis and dysfunction in mice. Tunicamycin 68-79 p21 (RAC1) activated kinase 2 Mus musculus 0-4 35226981-10 2022 In addition, the expression of TGF-betaRII and Smad2/3, and mRNAs of TGF-betaRII and Smad3 were also decreased by the TM treatment. Tunicamycin 118-120 transforming growth factor beta receptor 2 Homo sapiens 31-42 35226981-10 2022 In addition, the expression of TGF-betaRII and Smad2/3, and mRNAs of TGF-betaRII and Smad3 were also decreased by the TM treatment. Tunicamycin 118-120 SMAD family member 2 Homo sapiens 47-54 35226981-10 2022 In addition, the expression of TGF-betaRII and Smad2/3, and mRNAs of TGF-betaRII and Smad3 were also decreased by the TM treatment. Tunicamycin 118-120 transforming growth factor beta receptor 2 Homo sapiens 69-80 35226981-10 2022 In addition, the expression of TGF-betaRII and Smad2/3, and mRNAs of TGF-betaRII and Smad3 were also decreased by the TM treatment. Tunicamycin 118-120 SMAD family member 3 Homo sapiens 85-90 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 120-125 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 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 cadherin 1 Homo sapiens 277-287 2481822-8 1989 Analysis of biosynthetically labeled CD6 in the presence of tunicamycin revealed a reduction in mol. Tunicamycin 60-71 CD6 molecule Homo sapiens 37-40 2789018-5 1989 In the presence of tunicamycin, IL-6 is secreted exclusively in the O-glycosylated form, whereas in the presence of cycloheximide the pathway leading to both N- and O-glycosylation is dominant. Tunicamycin 19-30 interleukin 6 Homo sapiens 32-36 2570611-9 1989 Cells treated with tunicamycin produced a 120 kDa form of P-glycoprotein which was no longer processed but showed stability similar to that of the mature 140-150 kDa form. Tunicamycin 19-30 ATP binding cassette subfamily B member 1 Homo sapiens 58-72 2514095-17 1989 The non-glycosylated receptor from tunicamycin-treated cells appears to bind transferrin as demonstrated by interaction with transferrin-Sepharose. Tunicamycin 35-46 transferrin Mus musculus 77-88 2514095-17 1989 The non-glycosylated receptor from tunicamycin-treated cells appears to bind transferrin as demonstrated by interaction with transferrin-Sepharose. Tunicamycin 35-46 transferrin Mus musculus 125-136 16666984-7 1989 The molecular weight of these polypeptides is reduced by treatment with glycopeptidase F but not with endoglycosidase H. Treatment of the suspension cultures with tunicamycin also leads to reduction in the molecular weight of the chitinase bands. Tunicamycin 163-174 endochitinase A Nicotiana tabacum 230-239 2692828-5 1989 Tunicamycin blocked the appearance of such accumulations, suggesting that glycosylation is involved in the transport of nascent BuChE molecules to the oocyte"s surface. Tunicamycin 0-11 butyrylcholinesterase like L homeolog Xenopus laevis 128-133 2474541-2 1989 In the presence of tunicamycin, keratinocytes incorporated [3H]glucosamine into a vitamin A-regulated acidic 53-kDa component of the cytoskeleton which was identified as cytokeratin 13 by one- and two-dimensional immunoblotting with specific monoclonal antibodies. Tunicamycin 19-30 keratin 13 Homo sapiens 170-184 2760068-13 1989 Furthermore, tunicamycin shifted the synthesis of PLP-A by placental explants from the Mr 29,000 and 33,000 forms to the Mr 25,000 species. Tunicamycin 13-24 prolactin family 4, subfamily A, member 1 Rattus norvegicus 50-55 2677679-2 1989 Tunicamycin, a nucleoside antibiotic which prevents the formation of the dolichol intermediate necessary for oligosaccharide addition of the nascent polypeptide chain, appeared to block secretory exit and led to an increase in the cellular associated, nonglycosylated pro-TGF-beta 1 form. Tunicamycin 0-11 transforming growth factor beta-1 proprotein Cricetulus griseus 272-282 2525840-4 1989 In experiments in which infected cells were treated with tunicamycin it was shown that the glycosylation of NS1 was not required for either the dimerization or the membrane association. Tunicamycin 57-68 influenza virus NS1A binding protein Homo sapiens 108-111 2722854-7 1989 This nonglycosylated receptor was also capable of dimer formation; however, much less of it reached the cell surface than the fully glycosylated form, although both untreated and tunicamycin-grown cells appeared to synthesize transferrin receptors at similar rates. Tunicamycin 179-190 transferrin Homo sapiens 226-237 2722854-8 1989 Although the number of receptor molecules/cell was similar in control and tunicamycin-treated cells, the nonglycosylated receptors exhibited a much lower affinity for transferrin than those of untreated cells; in contrast, when receptors were purified by immunoprecipitation and digested with bacterial alkaline phosphatase, no difference was observed between the affinity of these receptors and undigested immunoprecipitated receptors. Tunicamycin 74-85 transferrin Homo sapiens 167-178 2498325-9 1989 Studies with tunicamycin indicated that this apoE was N-glycosylated at Asn194. Tunicamycin 13-24 apolipoprotein E Homo sapiens 45-49 2722801-1 1989 Tunicamycin, a specific inhibitor of N-glycosylation, was used to study the function of asparagine-linked oligosaccharides of the low density lipoprotein (LDL) receptor in cultured human skin fibroblasts. Tunicamycin 0-11 low density lipoprotein receptor Homo sapiens 130-168 2722801-7 1989 However, the LDL receptor produced in tunicamycin-treated cells was smaller in molecular size, and it exhibited an about 50% lower binding capacity when compared with its counterpart synthesized in control cells. Tunicamycin 38-49 low density lipoprotein receptor Homo sapiens 13-25 2471524-1 1989 Previous studies in this laboratory (1) have shown that tunicamycin-treatment inhibits the secretion of three secretory glycoproteins--alpha 2-macroglobulin, ceruloplasmin, and alpha 1-protease inhibitor in human hepatoma (Hep G2) cell cultures. Tunicamycin 56-67 alpha-2-macroglobulin Homo sapiens 135-156 2471524-1 1989 Previous studies in this laboratory (1) have shown that tunicamycin-treatment inhibits the secretion of three secretory glycoproteins--alpha 2-macroglobulin, ceruloplasmin, and alpha 1-protease inhibitor in human hepatoma (Hep G2) cell cultures. Tunicamycin 56-67 ceruloplasmin Homo sapiens 158-171 2471524-1 1989 Previous studies in this laboratory (1) have shown that tunicamycin-treatment inhibits the secretion of three secretory glycoproteins--alpha 2-macroglobulin, ceruloplasmin, and alpha 1-protease inhibitor in human hepatoma (Hep G2) cell cultures. Tunicamycin 56-67 serpin family A member 1 Homo sapiens 177-203 2471524-3 1989 Using percoll density gradient centrifugation, we found that tunicamycin-treatment markedly inhibited the transport of alpha 2-macroglobulin, ceruloplasmin and alpha 1-protease inhibitor from the rough endoplasmic reticulum. Tunicamycin 61-72 alpha-2-macroglobulin Homo sapiens 119-140 2471524-3 1989 Using percoll density gradient centrifugation, we found that tunicamycin-treatment markedly inhibited the transport of alpha 2-macroglobulin, ceruloplasmin and alpha 1-protease inhibitor from the rough endoplasmic reticulum. Tunicamycin 61-72 ceruloplasmin Homo sapiens 142-155 2471524-3 1989 Using percoll density gradient centrifugation, we found that tunicamycin-treatment markedly inhibited the transport of alpha 2-macroglobulin, ceruloplasmin and alpha 1-protease inhibitor from the rough endoplasmic reticulum. Tunicamycin 61-72 serpin family A member 1 Homo sapiens 160-186 2523818-8 1989 Incubation of monocytes with tunicamycin and 1-deoxymynnojirimycin and treatment of IL-6 with endoglucosaminidase H suggested that the 27.5 kDa form of IL-6 carries at least one N-linked complex-type oligosaccharide chain. Tunicamycin 29-40 interleukin 6 Homo sapiens 152-156 2676595-4 1989 In addition, labeling of the wild-type yeast cells with [3H]palmitate in the presence of tunicamycin revealed the incorporation of [3H]palmitate into the same five bands as found in the alg1 and alg2 mutants at the non-permissive temperature without tunicamycin. Tunicamycin 89-100 chitobiosyldiphosphodolichol beta-1,4 mannosyltransferase Saccharomyces cerevisiae S288C 186-190 2676595-4 1989 In addition, labeling of the wild-type yeast cells with [3H]palmitate in the presence of tunicamycin revealed the incorporation of [3H]palmitate into the same five bands as found in the alg1 and alg2 mutants at the non-permissive temperature without tunicamycin. Tunicamycin 89-100 GDP-Man:Man(1)GlcNAc(2)-PP-dolichol alpha-1,3-mannosyltransferase Saccharomyces cerevisiae S288C 195-199 2676595-4 1989 In addition, labeling of the wild-type yeast cells with [3H]palmitate in the presence of tunicamycin revealed the incorporation of [3H]palmitate into the same five bands as found in the alg1 and alg2 mutants at the non-permissive temperature without tunicamycin. Tunicamycin 250-261 chitobiosyldiphosphodolichol beta-1,4 mannosyltransferase Saccharomyces cerevisiae S288C 186-190 2676595-4 1989 In addition, labeling of the wild-type yeast cells with [3H]palmitate in the presence of tunicamycin revealed the incorporation of [3H]palmitate into the same five bands as found in the alg1 and alg2 mutants at the non-permissive temperature without tunicamycin. Tunicamycin 250-261 GDP-Man:Man(1)GlcNAc(2)-PP-dolichol alpha-1,3-mannosyltransferase Saccharomyces cerevisiae S288C 195-199 2644281-5 1989 When cells were cultured in the presence of tunicamycin, a 49-kDa form of LPL was synthesized by the cells but was not secreted. Tunicamycin 44-55 lipoprotein lipase Rattus norvegicus 74-77 2538234-9 1989 As a result of inhibition of glycosylation by the antibiotic tunicamycin, a fourth intracellular TAP (P58) and a third extracellular TAP (P60) were found. Tunicamycin 61-72 sequestosome 1 Homo sapiens 138-141 2644281-6 1989 In addition, LPL activity was reduced by 90% when glycosylation was blocked by either tunicamycin or glucose deprivation. Tunicamycin 86-97 lipoprotein lipase Rattus norvegicus 13-16 2564824-6 1989 mAb 12-15 was also reactive with the tunicamycin-treated form of the CD2 antigen suggesting that the cross-reactive epitope was of protein nature. Tunicamycin 37-48 CD2 antigen Mus musculus 69-72 2463989-10 1989 Tunicamycin-treated HEL cells synthesized three to four precursors of 80-92 kDa, suggesting the possibility of heterogeneity of GMP-140 at the protein level. Tunicamycin 0-11 selectin P Homo sapiens 128-135 2545067-0 1989 Tunicamycin modulates binding of 125I-erythropoietin to Friend erythroleukemia cells. Tunicamycin 0-11 erythropoietin Mus musculus 38-52 2545067-2 1989 Neuraminidase treatment of B8 cells did not affect the specific binding of erythropoietin, but tunicamycin treatment caused a 2.5 to 4-fold increase in the amount of 125I-erythropoietin binding. Tunicamycin 95-106 erythropoietin Mus musculus 171-185 3366781-0 1988 Characterization of the transferrin receptor in tunicamycin-treated A431 cells. Tunicamycin 48-59 transferrin receptor Homo sapiens 24-44 2536232-0 1989 Effects of lectins and tunicamycin on cAMP response to parathyroid hormone. Tunicamycin 23-34 parathyroid hormone Rattus norvegicus 55-74 2492635-6 1989 The carbohydrate side-chains are essential for the stability of fibroblast PS beta G, because PS beta G synthesis in these fibroblasts could not be detected in the presence of tunicamycin, a protein glycosylation inhibitor which did not affect PS beta G mRNA expression. Tunicamycin 176-187 protein S (beta) pseudogene Homo sapiens 75-82 2494430-9 1989 Treatment of Sf9 cells with tunicamycin, but not with inhibitors of oligosaccharide processing, prevented the appearance of t-PA in the extracellular medium. Tunicamycin 28-39 chromosome 20 open reading frame 181 Homo sapiens 124-128 2718627-4 1989 The calculated molecular mass (64 kDa) of the protein is in good agreement with that of the unglycosylated HN protein (63 kDa) identified in tunicamycin treated mumps virus infected cells (Herrler and Compans, 1983). Tunicamycin 141-152 hemagglutinin-neuraminidase Mumps orthorubulavirus 107-109 2848842-2 1988 The first step in the assembly of the dolichol-linked oligosaccharides required for asparagine-linked glycosylation in eukaryotes is catalyzed by a tunicamycin-sensitive, dolichol phosphate-dependent N-acetylglucosamine-1-phosphate transferase (GPT). Tunicamycin 148-159 alanine aminotransferase 1 Cricetulus griseus 245-248 3198612-1 1988 A protein doublet (Mr = 135,000/130,000) was found to coprecipitate with an unglycosylated form of the transferrin receptor in tunicamycin-treated A431 cells. Tunicamycin 127-138 transferrin receptor Homo sapiens 103-123 3063258-5 1988 The extent of co-translational glycosylation was measured by treating the cells with tunicamycin; in the presence of this inhibitor, a 74 kDa aglyco-CEA was produced and was still recognized by the antibody. Tunicamycin 85-96 CEA cell adhesion molecule 3 Homo sapiens 149-152 3262613-6 1988 Treatment with either tunicamycin or N-glycanase resulted in IL-3 running as one band with Mr 16,000, corresponding to its 140-amino acid polypeptide chain. Tunicamycin 22-33 interleukin 3 Mus musculus 61-65 3141784-1 1988 The importance of carbohydrate in the secretion of immunoglobulin A (IgA) has previously been suggested by results of studies with tunicamycin, which prevents N-linked glycosylation of all cell glycoproteins. Tunicamycin 131-142 immunoglobulin heavy constant alpha Mus musculus 51-73 3047151-7 1988 Glycosylation of Sec12p during biogenesis is indicated by an electrophoretic mobility shift of the protein that is influenced by tunicamycin and by imposition of an independent secretory pathway block. Tunicamycin 129-140 Sar family guanine nucleotide exchange factor SEC12 Saccharomyces cerevisiae S288C 17-23 3042455-1 1988 Tyrosine sulfation of entactin was studied by labeling of 3T3-L1 adipocytes with [35S]methionine or H2 35SO4 in the presence or absence of tunicamycin or monensin. Tunicamycin 139-150 nidogen 1 Homo sapiens 22-30 3042455-4 1988 Inhibition of co-translational transfer of N-linked oligosaccharides by tunicamycin produced EN1 and EN3 as intracellular species, and EN3 was sulfated and secreted. Tunicamycin 72-83 engrailed homeobox 1 Homo sapiens 93-96 3177093-1 1988 We have investigated the effect of tunicamycin-C2, which specifically inhibits glycosylation of proteins but not their synthesis, in the induction of crystal-induced chemotactic factor (CCF) in human neutrophils by monosodium urate crystals. Tunicamycin 35-46 paired like homeodomain 1 Homo sapiens 150-184 3177093-1 1988 We have investigated the effect of tunicamycin-C2, which specifically inhibits glycosylation of proteins but not their synthesis, in the induction of crystal-induced chemotactic factor (CCF) in human neutrophils by monosodium urate crystals. Tunicamycin 35-46 paired like homeodomain 1 Homo sapiens 186-189 3046935-7 1988 The in vitro phenotype of sec53 could be mimicked by isolating rough microsomes from wild-type cells that had been grown for 1 h in the presence of tunicamycin. Tunicamycin 148-159 phosphomannomutase SEC53 Saccharomyces cerevisiae S288C 26-31 3150971-4 1988 Like others (Volpe & Goldberg, 1983), we found that tunicamycin inhibited the activity of 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMG-CoA), which constitutes the ratelimiting step in the biosynthesis of cholesterol and isoprenoid derivatives, by catalysing the reduction of HMG-CoA to mevalonate, and it has been suggested that it plays a role in the control of cell proliferation and in tumour transformation. Tunicamycin 56-67 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 94-141 3150971-4 1988 Like others (Volpe & Goldberg, 1983), we found that tunicamycin inhibited the activity of 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMG-CoA), which constitutes the ratelimiting step in the biosynthesis of cholesterol and isoprenoid derivatives, by catalysing the reduction of HMG-CoA to mevalonate, and it has been suggested that it plays a role in the control of cell proliferation and in tumour transformation. Tunicamycin 56-67 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 143-150 3150971-4 1988 Like others (Volpe & Goldberg, 1983), we found that tunicamycin inhibited the activity of 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMG-CoA), which constitutes the ratelimiting step in the biosynthesis of cholesterol and isoprenoid derivatives, by catalysing the reduction of HMG-CoA to mevalonate, and it has been suggested that it plays a role in the control of cell proliferation and in tumour transformation. Tunicamycin 56-67 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 287-294 3382684-0 1988 Tunicamycin-treated rat heart cell cultures synthesize an inactive nonreleasable lipoprotein lipase. Tunicamycin 0-11 lipoprotein lipase Rattus norvegicus 81-99 3382684-3 1988 Treatment of the cultures with 5 micrograms/ml tunicamycin caused almost complete loss of lipoprotein lipase activity in all three compartments. Tunicamycin 47-58 lipoprotein lipase Rattus norvegicus 90-108 2618551-4 1989 PAA of HL-60 cells pre-cultured in the presence of tunicamycin (0.1-1.0 microgram/ml) to inhibit glycosylation decreased after neuraminidase treatment. Tunicamycin 51-62 neuraminidase 1 Homo sapiens 127-140 2531019-3 1989 This rapidly excreted fraction exhibits a low density on rubidium chloride gradients characteristic of poorly sialylated and poorly iodinated thyroglobulin, comigrating on rubidium chloride gradients with thyroglobulin isolated from tunicamycin treated glands. Tunicamycin 233-244 thyroglobulin Homo sapiens 142-155 2531019-3 1989 This rapidly excreted fraction exhibits a low density on rubidium chloride gradients characteristic of poorly sialylated and poorly iodinated thyroglobulin, comigrating on rubidium chloride gradients with thyroglobulin isolated from tunicamycin treated glands. Tunicamycin 233-244 thyroglobulin Homo sapiens 205-218 2903742-1 1988 Tunicamycin, a known inhibitor of the lipid-dependent glycosylation of proteins, was used in vivo to study the biosynthesis of rat intestinal brush border membrane aminopeptidase N and dipeptidyl aminopeptidase IV. Tunicamycin 0-11 alanyl aminopeptidase, membrane Rattus norvegicus 164-180 2903742-5 1988 In addition, there were decreased levels of assayable aminopeptidase N, dipeptidyl aminopeptidase IV and disaccharidase activity in intestinal mucosal cell homogenates and brush border membranes of tunicamycin-treated rats. Tunicamycin 198-209 alanyl aminopeptidase, membrane Rattus norvegicus 54-70 2903742-6 1988 Though tunicamycin decreased incorporation of newly synthesized aminopeptidase N and dipeptidyl aminopeptidase IV protein into brush border membranes by 70-75%, the newly synthesized enzyme that was incorporated was indistinguishable from that of controls. Tunicamycin 7-18 alanyl aminopeptidase, membrane Rattus norvegicus 64-80 2905169-6 1988 Tunicamycin treatment blocks the conversion of the precursor to the mature form, and removal of N-linked oligosaccharides with Endo F reduces the relative molecular weight of P-glycoprotein to 140K. Tunicamycin 0-11 ATP binding cassette subfamily B member 1 Homo sapiens 175-189 2844594-1 1988 (Na,K)ATPase from Torpedo californica was expressed in Xenopus laevis oocytes in the presence of tunicamycin by injecting mRNAs for the alpha- and beta-subunits derived from the cloned cDNAs into the oocytes. Tunicamycin 97-108 ATPase Na+/K+ transporting subunit beta 1 L homeolog Xenopus laevis 1-12 3149275-2 1988 The EGF receptor of NA cells synthesized in the presence of tunicamycin had an apparent molecular weight of 130,000. Tunicamycin 60-71 epidermal growth factor receptor Homo sapiens 4-16 3137261-3 1988 The induction of ICAM-1 by these cytokines was neutralized by cytokine-specific antisera as well as some steroids and the glycosylation inhibitor, tunicamycin. Tunicamycin 147-158 intercellular adhesion molecule 1 Homo sapiens 17-23 2456347-4 1988 Therefore, we examined the effect of tunicamycin (TM), an inhibitor of asparagine-linked glycosylation and ganglioside biosynthesis, on the expression of Hh-1 determinants in H-2b/Hh-1b lymphomas. Tunicamycin 37-48 hemopoietic histocompatibility Mus musculus 154-158 2456347-4 1988 Therefore, we examined the effect of tunicamycin (TM), an inhibitor of asparagine-linked glycosylation and ganglioside biosynthesis, on the expression of Hh-1 determinants in H-2b/Hh-1b lymphomas. Tunicamycin 50-52 hemopoietic histocompatibility Mus musculus 154-158 3259951-4 1988 Under conditions where treatment of CD4+ human acute lymphoblastic leukemia cells (CEM-CM3 cells) with the glycosylation inhibitor tunicamycin decreased surface expression of CD4 in a time- and concentration-dependent manner, the surface expression of several other glycoproteins was unaffected. Tunicamycin 131-142 CD4 molecule Homo sapiens 36-39 3259951-4 1988 Under conditions where treatment of CD4+ human acute lymphoblastic leukemia cells (CEM-CM3 cells) with the glycosylation inhibitor tunicamycin decreased surface expression of CD4 in a time- and concentration-dependent manner, the surface expression of several other glycoproteins was unaffected. Tunicamycin 131-142 CD4 molecule Homo sapiens 175-178 3259951-5 1988 Incubation with tunicamycin for 48 h inhibited mannose incorporation by 98%, caused a 76% decrease in CD4 surface expression as judged by flow cytometry, and had little effect on methionine incorporation. Tunicamycin 16-27 CD4 molecule Homo sapiens 102-105 3259951-6 1988 Scatchard analysis showed a decrease in the total number of CD4 molecules on the cell surface from 17,000 to 8,900 after 24 h of tunicamycin treatment. Tunicamycin 129-140 CD4 molecule Homo sapiens 60-63 3259951-7 1988 Immunoprecipitation of metabolically labeled CD4 revealed the presence of an unglycosylated precursor in tunicamycin-treated cells. Tunicamycin 105-116 CD4 molecule Homo sapiens 45-48 3366781-2 1988 In this study, the functional and structural properties of the transferrin receptor from tunicamycin-treated A431 cells were examined. Tunicamycin 89-100 transferrin Homo sapiens 63-74 2452086-12 1988 The inhibition of N-glycosylation by tunicamycin abolished the effect of interleukin-6 on the secretion of alpha 2-macroglobulin, indicating a possible role of interleukin-6 on N-glycosylation. Tunicamycin 37-48 interleukin 6 Homo sapiens 73-86 3234361-4 1988 The SP-A synthesized under these conditions showed a shift in apparent molecular weight to 27,000 and 29,000 compared to 29,000 and 31,000 for SP-A synthesized in the presence of tunicamycin alone. Tunicamycin 179-190 surfactant protein A2 Homo sapiens 4-8 3234361-4 1988 The SP-A synthesized under these conditions showed a shift in apparent molecular weight to 27,000 and 29,000 compared to 29,000 and 31,000 for SP-A synthesized in the presence of tunicamycin alone. Tunicamycin 179-190 surfactant protein A2 Homo sapiens 143-147 2452086-12 1988 The inhibition of N-glycosylation by tunicamycin abolished the effect of interleukin-6 on the secretion of alpha 2-macroglobulin, indicating a possible role of interleukin-6 on N-glycosylation. Tunicamycin 37-48 alpha-2-macroglobulin Homo sapiens 107-128 3258589-7 1988 P3.58 molecules precipitated from tunicamycin-treated cells were identical in all cell types, suggesting that the variation observed is due to variable N-glycosylation. Tunicamycin 34-45 intercellular adhesion molecule 1 Homo sapiens 0-5 3339713-2 1988 Pulse-chase, tunicamycin treatment, and carbohydrate trimming experiments revealed that VGF is synthesized as a 19-kilodalton (kDa) precursor which is rapidly modified to a high-mannose-type 22-kDa protein. Tunicamycin 13-24 VGF nerve growth factor inducible Homo sapiens 88-91 3367907-7 1988 Unglycosylated NB, expressed either in influenza B virus-infected cells treated with tunicamycin or in cells expressing the NB mutant lacking both N-linked glycosylation sites, was expressed at the cell surface, indicating that NB does not require carbohydrate addition for transport. Tunicamycin 85-96 NUBP iron-sulfur cluster assembly factor 1, cytosolic Homo sapiens 15-17 3131023-3 1988 In addition, the processing of the EGF receptor and its intracellular transport was analyzed by distinguishing cell surface receptors from intracellular receptors and by treating cells with inhibitors such as tunicamycin, monensin and brefeldin A. Tunicamycin 209-220 epidermal growth factor receptor Homo sapiens 35-47 3131023-7 1988 In A431 cells, the truncated EGF receptor was generated from a protein of Mr 60,000 through tunicamycin- and monensin-sensitive glycosylation. Tunicamycin 92-103 epidermal growth factor receptor Homo sapiens 29-41 2968956-6 1988 When the FcE receptor-positive RPMI-1788 cells are treated with tunicamycin and then with papain, a suppressor factor(s) for human IgE synthesis is released. Tunicamycin 64-75 ferrochelatase Homo sapiens 9-12 3372529-14 1988 We identified two putative precursors of hsp47 using an in vitro translation/processing system and tunicamycin: one is a 42-kDa primary translation product and the second is a 41-kDa polypeptide lacking signal peptide and carbohydrate moieties. Tunicamycin 99-110 serpin family H member 1 Gallus gallus 41-46 3128509-3 1988 NCA components synthesized by three tumor cell lines, QGP-1 (pancreas), HLC-1 (lung) and CAOV-2 (ovary) showed slightly different migration patterns on SDS-PAGE, but the molecular weights of their unglycosylated peptides synthesized in the presence of tunicamycin were all found to be 35K. Tunicamycin 252-263 CEA cell adhesion molecule 3 Homo sapiens 0-3 3445230-4 1987 Optimal transport of TF to the plasma membrane and shedding in membrane vesicles required glycosylation as judged by partial inhibition of this process by the tunicamycin homologues B2 and C2. Tunicamycin 159-170 coagulation factor III, tissue factor Homo sapiens 21-23 2823941-4 1987 In addition it was found that the secretion of erythropoietin was almost completely abrogated by tunicamycin, an inhibitor of N-linked glycosylation. Tunicamycin 97-108 erythropoietin Homo sapiens 47-61 2823941-5 1987 This effect of tunicamycin was also observed in a permanently transfected cell line that secretes erythropoietin in large quantities. Tunicamycin 15-26 erythropoietin Homo sapiens 98-112 3121640-7 1987 Tunicamycin could in fact mimic the effect of a temperature shift on the biosynthesis of EGF receptor, but it did not have the same rapid effect on DNA synthesis and cell cycle progression. Tunicamycin 0-11 epidermal growth factor receptor Homo sapiens 89-101 3681266-8 1987 The glycosylated E1 (gp26, gp25) proteins arose as a result of O-linked glycosylation of p23/E1 as indicated by the resistance of these species to tunicamycin. Tunicamycin 147-158 prostaglandin E synthase 3 Homo sapiens 89-95 2443498-4 1987 In tunicamycin-treated cells, the initial precursor is similar in size (Mr = 24,000) to deglycosylated GPA from human erythrocytes. Tunicamycin 3-14 glycophorin A (MNS blood group) Homo sapiens 103-106 3057191-2 1988 As in normal fibroblasts the EGF receptor from MDA-MB-231 cells was synthesized from a Mr = 160,000 precursor and tunicamycin treatment of cells resulted in accumulation of a Mr = 130,000 polypeptide. Tunicamycin 114-125 epidermal growth factor receptor Homo sapiens 29-41 3040864-4 1987 All three forms of the Ki-1 antigen possess a tunicamycin-sensitive 6-kDa N-linked carbohydrate moiety. Tunicamycin 46-57 TNF receptor superfamily member 8 Homo sapiens 23-35 2822343-0 1987 Effect of tunicamycin on the biosynthesis of human fibroblast collagenase. Tunicamycin 10-21 matrix metallopeptidase 1 Homo sapiens 51-73 2440862-4 1987 Tunicamycin prevents approximately 50% of the phosphate from being incorporated into FRTL-5 cell thyroglobulin. Tunicamycin 0-11 thyroglobulin Rattus norvegicus 97-110 3499144-12 1987 In the presence of tunicamycin an unglycosylated alpha 1-inhibitor3 with an apparent Mr of 154,000 was found in cells and in the medium. Tunicamycin 19-30 alpha-1-inhibitor III Rattus norvegicus 49-67 3499144-13 1987 In a pulse-chase experiment it was shown that inhibition of glycosylation by tunicamycin resulted in a marked delay of secretion of alpha 1-inhibitor3. Tunicamycin 77-88 alpha-1-inhibitor III Rattus norvegicus 132-150 3671295-7 1987 Tunicamycin, an inhibitor of glycosylation of proteins, blocked the glycosylation of nascent ovalbumin molecules at a concentration of 5 micrograms/mL in the medium. Tunicamycin 0-11 ovalbumin Coturnix japonica 93-102 3115291-4 1987 Experiments with tunicamycin and endoglycosidase H demonstrated that sialophorin contains N-linked carbohydrate (approximately two units per molecule) and is therefore an N,O-glycoprotein. Tunicamycin 17-28 sialophorin Homo sapiens 69-80 3115291-5 1987 Pulse-labeling of tunicamycin-treated CEM cells together with immunoprecipitation provided the means to isolate the [35S]-methionine-labeled polypeptide core of sialophorin and determine its molecular weight (58,000). Tunicamycin 18-29 sialophorin Homo sapiens 161-172 3108266-8 1987 The glycosylation of GPIIb-IIIa was examined in megakaryocytes by metabolic labeling in the presence of tunicamycin, monensin, or treatment with endoglycosidase H. The polypeptide backbones of the GPIIb and the GPIIIa have molecular masses of 120 and 90 kD, respectively. Tunicamycin 104-115 integrin subunit alpha 2b Homo sapiens 21-26 3104330-10 1987 A 47,000-dalton form of hepatic lipase was immunoisolated from cell lysates only after tunicamycin treatment and could be generated from the secreted 59,000-dalton enzyme by prolonged endoglycosidase digestion. Tunicamycin 87-98 lipase C, hepatic type Rattus norvegicus 24-38 2438387-6 1987 Quantitative electroimmunoblotting for myelin basic protein (MBP) in the CNS of tunicamycin-treated young adult rats indicated that, as in acute EAE, no extensive demyelination had occurred. Tunicamycin 80-91 myelin basic protein Rattus norvegicus 39-59 2438387-6 1987 Quantitative electroimmunoblotting for myelin basic protein (MBP) in the CNS of tunicamycin-treated young adult rats indicated that, as in acute EAE, no extensive demyelination had occurred. Tunicamycin 80-91 myelin basic protein Rattus norvegicus 61-64 2435722-9 1987 In a pulse-chase experiment using tunicamycin to block N-glycosylation, alpha 1-macroglobulin secretion was totally inhibited. Tunicamycin 34-45 pregnancy-zone protein Rattus norvegicus 72-93 3104330-12 1987 Further, an intracellular 47,000-dalton precursor peptide can be identified after tunicamycin treatment, which may represent the hepatic lipase polypeptide, presumably after removal of its signal sequence; a 53,000-dalton partially glycosylated peptide exists as a major precursor form in the cell; and the mature 59,000-dalton hepatic lipase is present in the hepatocyte, but it is rapidly secreted. Tunicamycin 82-93 lipase C, hepatic type Rattus norvegicus 129-143 3104330-12 1987 Further, an intracellular 47,000-dalton precursor peptide can be identified after tunicamycin treatment, which may represent the hepatic lipase polypeptide, presumably after removal of its signal sequence; a 53,000-dalton partially glycosylated peptide exists as a major precursor form in the cell; and the mature 59,000-dalton hepatic lipase is present in the hepatocyte, but it is rapidly secreted. Tunicamycin 82-93 lipase C, hepatic type Rattus norvegicus 328-342 2950522-4 1987 Tunicamycin-resistant cells contain amplified DNA, which hybridizes in proportion to the cells" degree of drug resistance with Alg 7, a cloned DNA probe apparently encoding yeast N-acetylglucosaminyltransferase. Tunicamycin 0-11 UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase Saccharomyces cerevisiae S288C 127-132 3803451-4 1987 Peptide mapping analysis and pulse-chase experiments revealed that p45 A is a precursor of polypeptides p45 B, C, D. Tunicamycin treatment inhibits the synthesis of all four polypeptides but a new related protein appears, p-p45, the unglycosylated precursor. Tunicamycin 117-128 nuclear factor, erythroid derived 2 Mus musculus 67-70 3803451-4 1987 Peptide mapping analysis and pulse-chase experiments revealed that p45 A is a precursor of polypeptides p45 B, C, D. Tunicamycin treatment inhibits the synthesis of all four polypeptides but a new related protein appears, p-p45, the unglycosylated precursor. Tunicamycin 117-128 nuclear factor, erythroid derived 2 Mus musculus 104-107 3803451-4 1987 Peptide mapping analysis and pulse-chase experiments revealed that p45 A is a precursor of polypeptides p45 B, C, D. Tunicamycin treatment inhibits the synthesis of all four polypeptides but a new related protein appears, p-p45, the unglycosylated precursor. Tunicamycin 117-128 nuclear factor, erythroid derived 2 Mus musculus 104-107 3803451-5 1987 In the presence of tunicamycin, p-p45 is also found in the medium, demonstrating that glycosylation is not essential for the secretion. Tunicamycin 19-30 nuclear factor, erythroid derived 2 Mus musculus 34-37 3301649-2 1987 Cell-surface expression of transfected H-2Db in the B2m deficient cell line R1E was completely abolished by the drug tunicamycin (Tm). Tunicamycin 117-128 beta-2 microglobulin Mus musculus 52-55 3305909-3 1987 Tunicamycin, an inhibitor of N-linked oligosaccharide addition, blocks acquisition of both EGF and insulin binding activity. Tunicamycin 0-11 insulin Homo sapiens 99-106 3497327-6 1987 In contrast, T cells treated with tunicamycin released IgE-suppressing factors capable of inhibiting the IgE-potentiating activity of TCS derived from untreated T cells. Tunicamycin 34-45 immunoglobulin heavy constant epsilon Homo sapiens 55-58 3497327-6 1987 In contrast, T cells treated with tunicamycin released IgE-suppressing factors capable of inhibiting the IgE-potentiating activity of TCS derived from untreated T cells. Tunicamycin 34-45 immunoglobulin heavy constant epsilon Homo sapiens 105-108 3039288-8 1986 Furthermore, non-glycosylated t-PA synthesized in the presence of tunicamycin was secreted efficiently and was indistinguishable in specific activity from glycosylated t-PAs. Tunicamycin 66-77 plasminogen activator, tissue type Homo sapiens 30-34 3475645-1 1987 The activity and intracellular distribution of catalase was studied in culture human myeloid leukemia cells before and after induction of differentiation with tunicamycin. Tunicamycin 159-170 catalase Homo sapiens 47-55 3475645-5 1987 Induction of differentiation with tunicamycin decreased high activity of catalase in cultured leukemic cells. Tunicamycin 34-45 catalase Homo sapiens 73-81 3535799-8 1986 Specific 125I-insulin binding was increased by glucose refeeding of glucose-starved cells and this change in binding was inhibited by tunicamycin and cycloheximide. Tunicamycin 134-145 insulin Homo sapiens 14-21 3771139-3 1986 Incubation of Xenopus retinas with tunicamycin has been shown to block the glycosylation of opsin, the rod visual pigment apoglycoprotein, with concomitant accumulation of vesicular membrane material in the compartment between the rod inner and outer segments (i.e., the intersegmental space) (Fliesler et al, J Cell Biol 100:574-587, 1985). Tunicamycin 35-46 rhodopsin, gene2 L homeolog Xenopus laevis 92-97 3490480-9 1986 Activation is blocked by tunicamycin and is markedly slowed (t 1/2 = 120 min) by 1-deoxynojirimycin, an inhibitor of glucosidase I. Tunicamycin 25-36 mannosyl-oligosaccharide glucosidase Homo sapiens 117-130 2946699-2 1986 Tunicamycin was used to produce carbohydrate-depleted fibronectin; it was synthesized by cultured fibroblasts. Tunicamycin 0-11 fibronectin 1 Homo sapiens 54-65 3021451-5 1986 Culturing the cells in the presence of varying concentrations of tunicamycin, an inhibitor of N-glycosylation, revealed six species of 5"-nucleotidase after sodium dodecyl sulfate/polyacrylamide electrophoresis. Tunicamycin 65-76 5' nucleotidase, ecto Rattus norvegicus 135-150 3771140-3 1986 Tunicamycin (TM), a selective inhibitor of dolichylphosphate-dependent oligosaccharide biosynthesis, effectively blocks glycosylation, but not synthesis, of opsin, the rod visual pigment apoglycoprotein. Tunicamycin 0-11 rhodopsin, gene2 L homeolog Xenopus laevis 157-162 3771140-3 1986 Tunicamycin (TM), a selective inhibitor of dolichylphosphate-dependent oligosaccharide biosynthesis, effectively blocks glycosylation, but not synthesis, of opsin, the rod visual pigment apoglycoprotein. Tunicamycin 13-15 rhodopsin, gene2 L homeolog Xenopus laevis 157-162 3768962-2 1986 To study the role of the sugar moieties of this adhesion molecule, we tested the effect of tunicamycin on aggregation mediated by E-cadherin of teratocarcinoma cells. Tunicamycin 91-102 cadherin 1 Homo sapiens 130-140 2874833-7 1986 Tunicamycin also reduced lysyl oxidase activity in the medium and to a lesser extent in the cell layer, but the effective dose, 1-10 micrograms/ml, also inhibited the incorporation of [3H]leucine into total protein. Tunicamycin 0-11 lysyl oxidase Homo sapiens 25-38 3753016-8 1986 Pulse-labeling in the presence of tunicamycin yielded a 42,000-Da form of LAMP-1, which was converted within 30 min to a 43,000-Da molecule. Tunicamycin 34-45 lysosomal-associated membrane protein 1 Mus musculus 74-80 3768962-3 1986 Immunoblot analysis using a monoclonal antibody to E-cadherin showed that in cells treated with tunicamycin this adhesion molecule is converted into two forms with MW of 118,000 and 131,000. Tunicamycin 96-107 cadherin 1 Homo sapiens 51-61 3768962-4 1986 The smaller one was exposed on the cell surface and showed a trypsin sensitivity characteristic to E-cadherin, suggesting that this is the peptide moiety of E-cadherin whose glycosylation with N-linked oligosaccharides was blocked by tunicamycin. Tunicamycin 234-245 cadherin 1 Homo sapiens 99-109 3768962-4 1986 The smaller one was exposed on the cell surface and showed a trypsin sensitivity characteristic to E-cadherin, suggesting that this is the peptide moiety of E-cadherin whose glycosylation with N-linked oligosaccharides was blocked by tunicamycin. Tunicamycin 234-245 cadherin 1 Homo sapiens 157-167 3768962-6 1986 These tunicamycin-treated cells aggregated in a Ca2+-dependent manner, and the aggregation was inhibited by a monoclonal antibody to E-cadherin. Tunicamycin 6-17 cadherin 1 Homo sapiens 133-143 3541907-10 1986 Cell-surface immunodetectable lipoprotein lipase amounts were decreased significantly when cells were incubated in the presence of either colchicine or tunicamycin. Tunicamycin 152-163 lipoprotein lipase Homo sapiens 30-48 2427577-7 1986 All three forms of DAF were approximately 3000 lower in Mr in the presence of tunicamycin. Tunicamycin 78-89 CD55 molecule (Cromer blood group) Homo sapiens 19-22 3733260-0 1986 Effect of tunicamycin on synthesis and secretion of carcinoembryonic antigen by human colonic adenocarcinoma cells. Tunicamycin 10-21 CEA cell adhesion molecule 3 Homo sapiens 52-76 3733260-1 1986 The effect of the glycosylation inhibitor, tunicamycin, on synthesis and secretion of the membrane-associated glycoprotein carcinoembryonic antigen (CEA), was studied in the LS174T human colon cancer cell line. Tunicamycin 43-54 CEA cell adhesion molecule 3 Homo sapiens 123-147 3733260-1 1986 The effect of the glycosylation inhibitor, tunicamycin, on synthesis and secretion of the membrane-associated glycoprotein carcinoembryonic antigen (CEA), was studied in the LS174T human colon cancer cell line. Tunicamycin 43-54 CEA cell adhesion molecule 3 Homo sapiens 149-152 3733260-4 1986 However, in the tunicamycin-treated cells several forms of CEA with lower MWs and representing molecules with decreased glycosylation could be detected in addition to the original CEA molecule of 200 kDa present in control cells. Tunicamycin 16-27 CEA cell adhesion molecule 3 Homo sapiens 59-62 3733260-4 1986 However, in the tunicamycin-treated cells several forms of CEA with lower MWs and representing molecules with decreased glycosylation could be detected in addition to the original CEA molecule of 200 kDa present in control cells. Tunicamycin 16-27 CEA cell adhesion molecule 3 Homo sapiens 180-183 3733260-5 1986 The rates of synthesis, secretion and turnover of the lower-molecular-weight forms of poorly glycosylated CEA that appear after tunicamycin treatment are similar to those of CEA in control cells. Tunicamycin 128-139 CEA cell adhesion molecule 3 Homo sapiens 106-109 2429661-0 1986 Inhibition of overall protein and RNA synthesis as a mechanism for the tunicamycin induced decrease in cytochrome P-450 in rat hepatocytes. Tunicamycin 71-82 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 103-119 2429661-1 1986 In rat hepatocytes maintained in culture, cytochrome P-450 and NADPH cytochrome c reductase activities were decreased by tunicamycin in a dose and time dependent fashion. Tunicamycin 121-132 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 42-58 2429661-3 1986 Tunicamycin decreased L-[35S] methionine incorporation into many proteins, including a 52 kDa cytochrome P-450 isozyme. Tunicamycin 0-11 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 94-110 2429661-5 1986 These results indicate that tunicamycin decreased cytochrome P-450 levels in hepatocytes by inhibiting protein and RNA synthesis. Tunicamycin 28-39 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 50-66 3522736-5 1986 The glycosylation of Mac-1 was examined by both translation in vitro in the presence of dog pancreas microsomes and by biosynthesis in vivo and treatment with tunicamycin, endoglycosidase H, and the deglycosylating agent trifluoromethane sulfonic acid. Tunicamycin 159-170 integrin alpha M Mus musculus 21-26 3016293-5 1986 When PRV-infected Vero cells were incubated in the presence of tunicamycin, the gp50 that was produced had an identical molecular weight to that produced in the absence of drug. Tunicamycin 63-74 tumor associated calcium signal transducer 2 Homo sapiens 80-84 3800894-5 1986 We show here that two-dimensional gel patterns of PSP-A similar to that of the primary translation products are obtained by incorporation of [35S]methionine in the presence of tunicamycin or by N-glycanase digestion of the 32-36 kDa group. Tunicamycin 176-187 surfactant protein A2 Homo sapiens 50-55 3099750-6 1986 In the presence of tunicamycin, a compound that blocks the formation of N-asparagine-linked oligosaccharide chains, a decrease in Mr of both secreted and intracellular major forms is observed, indicating that secreted and intracellular C1 Inh contain N-linked oligosaccharide units. Tunicamycin 19-30 serpin family G member 1 Homo sapiens 236-242 3099750-11 1986 The underglycosylated C1 Inh secreted in presence of tunicamycin is still reactive with purified C1s. Tunicamycin 53-64 serpin family G member 1 Homo sapiens 22-28 3000457-4 1985 Thus, treatment of 3T3-L1 adipocytes with tunicamycin caused the loss of cellular insulin binding activity and the accumulation of an inactive aglyco-proreceptor. Tunicamycin 42-53 insulin Homo sapiens 82-89 3094838-1 1986 Effects of the intraocular injection of three inhibitors of glycosylation (tunicamycin, castanospermine, and swainsonine) on the rhodopsin content and the integrity of disc membranes in frog retina were studied. Tunicamycin 75-86 rhodopsin Homo sapiens 129-138 3094838-2 1986 The administration of 10 or 100 micrograms of tunicamycin resulted in a 78% loss of rhodopsin in the frog retina which also exhibited a significant reduction in the length of photoreceptor outer segments (as examined under light microscope). Tunicamycin 46-57 rhodopsin Homo sapiens 84-93 3094838-3 1986 This suggests that the synthesis and/or insertion of rhodopsin into the disc membrane is inhibited by tunicamycin. Tunicamycin 102-113 rhodopsin Homo sapiens 53-62 2878363-8 1986 p185 and the EGF receptor had distinct electrophoretic mobilities when synthesized under normal culture conditions or in the presence of tunicamycin. Tunicamycin 137-148 epidermal growth factor receptor Rattus norvegicus 13-25 3081330-11 1986 In contrast, in the presence of tunicamycin, the predominant intracellular form of TBG had an apparent mol wt of 44K (TBG3). Tunicamycin 32-43 serpin family A member 7 Homo sapiens 83-86 3086086-9 1986 Synaptophysin is N-glycosylated, since cultivation of the rat phaeochromocytoma cell line PC12 in the presence of tunicamycin reduced its mol. Tunicamycin 114-125 synaptophysin Rattus norvegicus 0-13 2422549-7 1986 When macrophages were induced in the presence of tunicamycin, only one activity of a molecular weight of about 19,000 dalton was found which again was neutralized by anti-interferon-beta. Tunicamycin 49-60 interferon beta 1, fibroblast Mus musculus 171-186 3905815-6 1985 The post-translational modification which, despite the removal of signal peptide, resulted in an increase in apparent Mr, reflects the glycosylation as examined using Xenopus oocytes microinjected with renin mRNA in the presence of tunicamycin, an inhibitor of protein glycosylation. Tunicamycin 232-243 LOW QUALITY PROTEIN: renin Oryctolagus cuniculus 202-207 3937276-5 1985 The possible role of N-linked oligosaccharides for the biological activity of t-PA was studied using t-PA secreted by melanoma cells in the presence of tunicamycin, an inhibitor of N-glycosylation. Tunicamycin 152-163 plasminogen activator, tissue type Homo sapiens 78-82 4066700-4 1985 The biosynthesis of PP63 was studied in vitro in a cell-free system and in intact hepatocytes incubated with or without tunicamycin. Tunicamycin 120-131 alpha-2-HS-glycoprotein Rattus norvegicus 20-24 4066700-12 1985 PP63 secretion was altered by tunicamycin. Tunicamycin 30-41 alpha-2-HS-glycoprotein Rattus norvegicus 0-4 4052441-0 1985 Importance of the different steps of glycosylation for the activity and secretion of lipoprotein lipase in rat preadipocytes studied with monensin and tunicamycin. Tunicamycin 151-162 lipoprotein lipase Rattus norvegicus 85-103 4052441-5 1985 Addition of tunicamycin (5 micrograms/ml) for 24 h caused a 30-50% reduction in immunoadsorbable lipoprotein lipase, but the enzyme activity was reduced by 90%. Tunicamycin 12-23 lipoprotein lipase Rattus norvegicus 97-115 4052441-9 1985 The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium. Tunicamycin 121-132 lipoprotein lipase Rattus norvegicus 169-187 4052441-9 1985 The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium. Tunicamycin 121-132 lipoprotein lipase Rattus norvegicus 198-216 4052441-9 1985 The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium. Tunicamycin 121-132 lipoprotein lipase Rattus norvegicus 198-216 4052441-9 1985 The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium. Tunicamycin 121-132 lipoprotein lipase Rattus norvegicus 198-216 3936778-5 1985 Proliferation of the IL 2-dependent CTLL cells was normal in the presence of Swainsonine but strongly impaired in the presence of Tunicamycin. Tunicamycin 130-141 interleukin 2 Mus musculus 21-25 3934016-4 1985 N-Glycosylation of secreted angiotensinogen was inhibited using tunicamycin. Tunicamycin 64-75 angiotensinogen Homo sapiens 28-43 4046741-0 1985 Inhibition of protein synthesis: a basis for tunicamycin-induced decrease in rat liver cytochrome P-450. Tunicamycin 45-56 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 87-103 4046741-1 1985 Tunicamycin caused a dose and time dependent decrease in cytochrome P-450 in rat liver. Tunicamycin 0-11 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 57-73 4046741-6 1985 A decrease in cytochrome P-450 was also observed in cultured rat hepatocytes treated with tunicamycin. Tunicamycin 90-101 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 14-30 4046741-8 1985 This indicates that a decrease in protein synthesis may be responsible for the tunicamycin-induced decrease in cytochrome P-450 and drug metabolism. Tunicamycin 79-90 cytochrome P450, family 2, subfamily g, polypeptide 1 Rattus norvegicus 111-127 3093061-8 1986 Tunicamycin-treated B16-F10 cells exhibited poor adhesion to substrate-adsorbed fibronectin and laminin, whereas both castanospermine- and swainsonine-treated cells possessed near normal adhesive capacity; furthermore, the initial rate of loss of tunicamycin-treated cells from the lungs of mice was substantially greater than either control, castanospermine- or swainsonine-treated cells. Tunicamycin 0-11 fibronectin 1 Mus musculus 80-91 2939068-8 1986 In the presence of tunicamycin, each of the CR1 allelic products is 25,000 lower in Mr than the glycosylated receptor. Tunicamycin 19-30 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 44-47 2939068-11 1986 Nonglycosylated CR1 synthesized in the presence of tunicamycin had twice the turnover rate of glycosylated CR1. Tunicamycin 51-62 complement C3b/C4b receptor 1 (Knops blood group) Homo sapiens 16-19 3011561-0 1986 Tunicamycin sensitivity of prolactin, insulin and epidermal growth factor receptors in rat liver plasmalemma. Tunicamycin 0-11 prolactin Rattus norvegicus 27-36 3011561-0 1986 Tunicamycin sensitivity of prolactin, insulin and epidermal growth factor receptors in rat liver plasmalemma. Tunicamycin 0-11 epidermal growth factor like 1 Rattus norvegicus 50-73 3011561-1 1986 We have used the glycosylation inhibitor tunicamycin to assess the stability of the receptors for prolactin, insulin and epidermal growth factor (EGF) in rat liver cell membrane. Tunicamycin 41-52 prolactin Rattus norvegicus 98-107 3011561-2 1986 Direct binding studies on liver plasmalemma fractions which were isolated from tunicamycin-treated rats revealed a rapid loss of prolactin receptors (t1/2 approximately 35 min) with a more prolonged half-life for insulin (10 h) and EGF receptors (8 h). Tunicamycin 79-90 prolactin Rattus norvegicus 129-138 3011561-2 1986 Direct binding studies on liver plasmalemma fractions which were isolated from tunicamycin-treated rats revealed a rapid loss of prolactin receptors (t1/2 approximately 35 min) with a more prolonged half-life for insulin (10 h) and EGF receptors (8 h). Tunicamycin 79-90 epidermal growth factor like 1 Rattus norvegicus 232-235 3955081-3 1986 In the presence of tunicamycin, an inhibitor of N-glycosylation, the secretion of angiotensinogen as well as total protein and albumin secretion were diminished. Tunicamycin 19-30 angiotensinogen Rattus norvegicus 82-97 3082891-2 1986 Treatment of human umbilical vein endothelial cells with tunicamycin inhibited N-linked glycosylation of nascent vWf and the resulting pro-vWf monomers failed to dimerize. Tunicamycin 57-68 von Willebrand factor Homo sapiens 113-116 3082891-2 1986 Treatment of human umbilical vein endothelial cells with tunicamycin inhibited N-linked glycosylation of nascent vWf and the resulting pro-vWf monomers failed to dimerize. Tunicamycin 57-68 von Willebrand factor Homo sapiens 139-142 3510667-5 1986 The repletion of lipoprotein lipase content was studied in these cells maintained in the presence of tunicamycin after cycloheximide removal. Tunicamycin 101-112 lipoprotein lipase Mus musculus 17-35 3510667-10 1986 An inactive form of lipoprotein lipase from tunicamycin-treated cells was detected by competition experiments with mature active lipoprotein lipase for the binding to immobilized antilipoprotein lipase antibodies, as well as by immunofluorescence staining. Tunicamycin 44-55 lipoprotein lipase Mus musculus 20-38 3510667-10 1986 An inactive form of lipoprotein lipase from tunicamycin-treated cells was detected by competition experiments with mature active lipoprotein lipase for the binding to immobilized antilipoprotein lipase antibodies, as well as by immunofluorescence staining. Tunicamycin 44-55 lipoprotein lipase Mus musculus 129-147 3510667-13 1986 Despite this lack of activation, the lipoprotein lipase molecule was able to migrate intracellularily and to undergo secretion after heparin stimulation of the tunicamycin-treated cells. Tunicamycin 160-171 lipoprotein lipase Mus musculus 37-55 2418827-3 1986 When the cells were treated with tunicamycin the unglycosylated alpha 2-macroglobulin subunit exhibited a molecular weight of 160,000. Tunicamycin 33-44 alpha-2-macroglobulin Homo sapiens 64-85 3510136-3 1986 Insulin receptor turnover was estimated by measurement of insulin binding after inhibition of synthesis of functional receptors with tunicamycin (0.5 micrograms/ml). Tunicamycin 133-144 insulin receptor Homo sapiens 0-16 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 83-94 insulin Homo sapiens 42-49 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 83-94 insulin Homo sapiens 118-125 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 83-94 insulin Homo sapiens 118-125 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 150-161 insulin Homo sapiens 42-49 3510136-6 1986 The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1). Tunicamycin 150-161 ectonucleotide pyrophosphatase/phosphodiesterase 3 Homo sapiens 214-217 3007151-8 1986 Results from digestion with endoglycosidase H, incubation with tunicamycin and metabolic labelling with [3H]mannose indicated that myeloperoxidase contained high mannose oligosaccharide side chains. Tunicamycin 63-74 myeloperoxidase Homo sapiens 131-146 3023826-2 1986 When grown in the presence of tunicamycin, both cells expressed a receptor-related species p135, the presumptive aglycosylated form of the biosynthetic precursor, gp145, of the mature form of the receptor, gp165, expressed at the cell surface. Tunicamycin 30-41 dynactin subunit 1 Homo sapiens 91-95 3023826-3 1986 Two additional receptor-related species, p115 and p70, were detected when A431, but not Hep 3B, cells were treated with tunicamycin. Tunicamycin 120-131 USO1 vesicle transport factor Homo sapiens 41-45 3023826-3 1986 Two additional receptor-related species, p115 and p70, were detected when A431, but not Hep 3B, cells were treated with tunicamycin. Tunicamycin 120-131 ubiquitin associated and SH3 domain containing B Homo sapiens 50-53 3161943-5 1985 The Ly-m20.2 molecules of tissues and clonal cell lines exhibit size and charge heterogeneity that can be eliminated by the complete removal of N-linked sugars with the enzyme endo-F or by inhibiting glycosylation with tunicamycin. Tunicamycin 219-230 Fc receptor, IgG, low affinity IIb Mus musculus 4-10 4079938-5 1985 The BW5147 T200 molecule is 3000 daltons larger than the molecule expressed by the transfected L-cell, a size difference due to glycosylation moieties, since treatment of the molecules with Endoglycosidase F or treatment of cells with tunicamycin yields T200 molecules of the same size from the 2 cell sources. Tunicamycin 235-246 protein tyrosine phosphatase, receptor type, C Mus musculus 11-15 3931637-3 1985 The predominant intracellular form was not susceptible to digestion by neuraminidase but was sensitive to endoglycosidase treatment, which digested it to a species with a molecular weight comparable to that of the sole hemopexin species produced by tunicamycin-treated hepatocytes and that produced by in vitro translation. Tunicamycin 249-260 hemopexin Rattus norvegicus 219-228 4031826-6 1985 Tunicamycin treatment results in the synthesis of a 70K protein (p70) which incorporates [3H]glucosamine and [3H]fucose but not [3H]mannose. Tunicamycin 0-11 ubiquitin associated and SH3 domain containing B Homo sapiens 65-68 3894594-8 1985 If the cultures are treated with tunicamycin, the astrocytes produce fibronectin that is unglycosylated, as shown by [3H]glucosamine labeling, and is neither sulfated nor phosphorylated as indicated by [35S]O4 and [32P]O4 labeling studies. Tunicamycin 33-44 fibronectin 1 Homo sapiens 69-80 3927903-3 1985 We show that native, undenatured calcitonin is an active substrate for oligosaccharyltransferase and that glycosylation of calcitonin by the transferase is inhibited by tunicamycin. Tunicamycin 169-180 calcitonin related polypeptide alpha Homo sapiens 33-43 3927903-3 1985 We show that native, undenatured calcitonin is an active substrate for oligosaccharyltransferase and that glycosylation of calcitonin by the transferase is inhibited by tunicamycin. Tunicamycin 169-180 calcitonin related polypeptide alpha Homo sapiens 123-133 2412675-8 1985 When prostatic tissue slices were incubated with tunicamycin, the unglycosylated arginine esterase obtained had a lower molecular weight than the in vitro translation product, suggesting that a signal peptide had been removed in the living cells. Tunicamycin 49-60 arginine esterase Canis lupus familiaris 81-98 3886013-4 1985 Intact fibroblasts cultured in the presence of tunicamycin synthesized an Mr 20 000 form of tissue inhibitor of metalloproteinases, detectable intracellularly and extracellularly. Tunicamycin 47-58 TIMP metallopeptidase inhibitor 1 Homo sapiens 92-130 2989336-9 1985 Tunicamycin-treated Hep G2 cells secreted five discrete forms of angiotensinogen, a predominant form of mol wt 46,200, with other forms (mol wt 46,800, 48,100, 49,200, and 49,600) representing 10% of secreted angiotensinogen. Tunicamycin 0-11 angiotensinogen Homo sapiens 65-80 2989336-9 1985 Tunicamycin-treated Hep G2 cells secreted five discrete forms of angiotensinogen, a predominant form of mol wt 46,200, with other forms (mol wt 46,800, 48,100, 49,200, and 49,600) representing 10% of secreted angiotensinogen. Tunicamycin 0-11 angiotensinogen Homo sapiens 209-224 2989336-12 1985 The other higher molecular weight forms of angiotensinogen secreted by tunicamycin-treated Hep G2 cells were shown to represent O-glycosylated angiotensinogen in that they were reduced to 46,200 mol wt by treatment with trifluoromethane sulfonic acid. Tunicamycin 71-82 angiotensinogen Homo sapiens 43-58 2989336-12 1985 The other higher molecular weight forms of angiotensinogen secreted by tunicamycin-treated Hep G2 cells were shown to represent O-glycosylated angiotensinogen in that they were reduced to 46,200 mol wt by treatment with trifluoromethane sulfonic acid. Tunicamycin 71-82 angiotensinogen Homo sapiens 143-158 3875019-11 1985 We have shown, however, that the peptide backbone of p43, as studied by both tunicamycin treatment of cells and endoglycosidase F digestion of immunoprecipitates, was identical in size to that of murine Qa-1. Tunicamycin 77-88 aminoacyl tRNA synthetase complex-interacting multifunctional protein 1 Mus musculus 53-56 3871610-2 1985 Unglycosylated alpha 1-proteinase inhibitor was synthesized by hepatocytes in the presence of tunicamycin. Tunicamycin 94-105 serpin family A member 1 Rattus norvegicus 15-43 2580532-4 1985 For example, three glycoproteins are exported with rapid kinetics and secretion of only one, alpha 1-protease inhibitor, is inhibited by tunicamycin treatment. Tunicamycin 137-148 serpin family A member 1 Homo sapiens 93-119 2580532-5 1985 In addition, three glycoproteins are secreted with intermediate kinetics and tunicamycin-treatment inhibits the secretion of two of these proteins, alpha 2-macroglobulin and ceruloplasmin but not the third, plasminogen. Tunicamycin 77-88 alpha-2-macroglobulin Homo sapiens 148-169 2580532-5 1985 In addition, three glycoproteins are secreted with intermediate kinetics and tunicamycin-treatment inhibits the secretion of two of these proteins, alpha 2-macroglobulin and ceruloplasmin but not the third, plasminogen. Tunicamycin 77-88 ceruloplasmin Homo sapiens 174-187 3893560-0 1985 The effect of tunicamycin on transferrin synthesis and secretion in hormonally stimulated explants of rabbit mammary gland. Tunicamycin 14-25 serotransferrin Oryctolagus cuniculus 29-40 2983087-7 1985 Polypeptide p73 was immunodetected in the presence of tunicamycin and designated as a nascent recipient of N-linked sugars, whereas gp88 was considered to contain O-linked oligosaccharides because its synthesis was not affected by tunicamycin. Tunicamycin 54-65 tumor protein p73 Homo sapiens 12-15 3967652-5 1985 Tunicamycin treatment of cultures significantly delayed the secretion of hemopexin but not that of transferrin. Tunicamycin 0-11 hemopexin Rattus norvegicus 73-82 3902570-10 1985 Production of mature mouse IL-2 was inhibited by tunicamycin (TM), with precursor molecules accumulating in the cell extract. Tunicamycin 49-60 interleukin 2 Mus musculus 27-31 3888262-6 1985 In the presence of tunicamycin, both mnn9 and wild-type X2180 cells made a mannoprotein fraction with an average molecular weight of 140 000, whereas in the absence of the glycosylation inhibitor, the mnn9 mutant made material with a molecular weight of 180 000 and the mannoprotein made by wild-type cells was too large to penetrate the polyacrylamide gel. Tunicamycin 19-30 mannosyltransferase complex subunit MNN9 Saccharomyces cerevisiae S288C 37-41 3965045-2 1985 Tissue factor activity was inducible by endotoxin, and its induction was inhibited by 1 microgram/mL of actinomycin D, 10 micrograms/mL of cycloheximide, and 0.2 micrograms/mL of tunicamycin. Tunicamycin 179-190 coagulation factor III Mus musculus 0-13 4092492-3 1985 Thus, treatment of 3T3-L1 adipocytes with tunicamycin causes the depletion of cellular insulin binding activity and the accumulation of an inactive aglyco proreceptor. Tunicamycin 42-53 insulin Homo sapiens 87-94 6092384-0 1984 Effect of tunicamycin and monensin on secretion of thyroxine-binding globulin by cultured human hepatoma (Hep G2) cells. Tunicamycin 10-21 serpin family A member 7 Homo sapiens 51-77 2991546-3 1985 These decreased cellular responses are probably due to an underglycosylation of the NGF receptor, since the effects of tunicamycin are correlated with a decrease in 3H-fucose incorporation rather than a general decline in cellular metabolism as measured by viability and protein synthesis. Tunicamycin 119-130 nerve growth factor receptor Rattus norvegicus 84-96 2858069-10 1985 (3) Acetylcholinesterase release was also decreased by an inhibitor of protein glycosylation, tunicamycin. Tunicamycin 94-105 acetylcholinesterase Rattus norvegicus 4-24 2858069-14 1985 (3) Tunicamycin acts by decreasing the intracellular activity of acetylcholinesterase, possibly via enhanced proteolytic breakdown. Tunicamycin 4-15 acetylcholinesterase Rattus norvegicus 65-85 3931095-7 1985 Nearly all of the IRBP secreted by bovine retinas incubated with (3H)-leucine in the presence of tunicamycin was nonglycosylated and did not bind to concanavalin A. Tunicamycin 97-108 retinol binding protein 3 Bos taurus 18-22 6092384-10 1984 Tunicamycin, 5 micrograms/ml, completely blocked glycosylation and markedly affected TBG secretion, almost doubling the time required for the secretion of 50% of the protein. Tunicamycin 0-11 serpin family A member 7 Homo sapiens 85-88 6237101-5 1984 The precursor of the IL 2 receptor isolated from tunicamycin-treated HUT102B2 or 12-O-tetradecanoyl phorbol 13-acetate-induced CCRF-CEM cells had the same Mr and isoelectric point. Tunicamycin 49-60 interleukin 2 Homo sapiens 21-25 6096695-7 1984 We identified a gene, ALG7, that is probably the structural gene for UDP-N-acetylglucosamine-1-P transferase, the enzyme inhibited by tunicamycin. Tunicamycin 134-145 UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase Saccharomyces cerevisiae S288C 22-26 16593518-8 1984 Furthermore, the appearance of the mature polypeptide associated with carbonic anhydrase activity in the periplasmic space of C. reinhardtii is inhibited by tunicamycin, an antibiotic that prevents core glycosylation of polypeptides on the endoplasmic reticulum. Tunicamycin 157-168 uncharacterized protein Chlamydomonas reinhardtii 70-88 6432920-11 1984 These results suggest that maturation of tyrosinase may occur via T1" and T1"" as precursors of T3, or possibly T1 through the addition of N-glycosydically linked oligosaccharide moieties which can be interrupted by glucosamine and tunicamycin. Tunicamycin 232-243 tyrosinase Mus musculus 41-51 6205259-0 1984 Identification and partial characterization of the unglycosylated peptide of carcinoembryonic antigen synthesized by human tumor cell lines in the presence of tunicamycin. Tunicamycin 159-170 CEA cell adhesion molecule 3 Homo sapiens 77-101 6088499-6 1984 In the presence of tunicamycin newly synthesized ASGP-R is a 34,000-Da nonglycosylated species which appears on the Hep G2 cell surface where it specifically binds 125I-ASOR. Tunicamycin 19-30 asialoglycoprotein receptor 1 Homo sapiens 49-55 6088499-7 1984 There is no major effect on subsequent uptake and degradation of 125I-ASOR in cells whose ASGP-R was synthesized in the presence of tunicamycin. Tunicamycin 132-143 asialoglycoprotein receptor 1 Homo sapiens 90-96 6088499-8 1984 The turnover of ASGP-R synthesized in the presence of either swainsonine or tunicamycin is not significantly altered from that found for the normal 46,000-Da species. Tunicamycin 76-87 asialoglycoprotein receptor 1 Homo sapiens 16-22 6205259-1 1984 Unglycosylated peptide backbones of carcinoembryonic antigen (CEA) synthesized by human tumor cell lines in the presence of tunicamycin were identified and analyzed by SDS-polyacrylamide gel electrophoresis. Tunicamycin 124-135 CEA cell adhesion molecule 3 Homo sapiens 36-60 6205259-1 1984 Unglycosylated peptide backbones of carcinoembryonic antigen (CEA) synthesized by human tumor cell lines in the presence of tunicamycin were identified and analyzed by SDS-polyacrylamide gel electrophoresis. Tunicamycin 124-135 CEA cell adhesion molecule 3 Homo sapiens 62-65 6205259-4 1984 In contrast, in the presence of tunicamycin, the native CEA molecules disappeared, and a new component that was precipitated with anti-CEA antibodies and labeled only with [3H]leucine but not with [14C]glucosamine was identified in each cell line. Tunicamycin 32-43 CEA cell adhesion molecule 3 Homo sapiens 56-59 6327813-5 1984 A study of surface iodination revealed that the former component was membrane-associated mature IL2R , and a pulse-chase study showed that the latter component was a precursor for IL2R that already possessed tunicamycin-sensitive N-linked sugar side chain(s). Tunicamycin 208-219 interleukin 2 receptor subunit alpha Homo sapiens 180-184 6375731-8 1984 Tunicamycin present during perfusion also induced a drop in lipoprotein lipase and tissue neutral lipase activity, indicating that glycosylation is necessary for secretion of lipoprotein lipase. Tunicamycin 0-11 lipoprotein lipase Rattus norvegicus 60-78 6375731-8 1984 Tunicamycin present during perfusion also induced a drop in lipoprotein lipase and tissue neutral lipase activity, indicating that glycosylation is necessary for secretion of lipoprotein lipase. Tunicamycin 0-11 lipase G, endothelial type Rattus norvegicus 72-78 6375731-8 1984 Tunicamycin present during perfusion also induced a drop in lipoprotein lipase and tissue neutral lipase activity, indicating that glycosylation is necessary for secretion of lipoprotein lipase. Tunicamycin 0-11 lipoprotein lipase Rattus norvegicus 175-193 6427217-15 1984 Neural retinas incubated with 3H-labeled leucine in the presence of tunicamycin secreted a form of IRBP that did not bind concanavalin A and had an Mr reduced by approximately 5,000. Tunicamycin 68-79 retinol binding protein 3 Bos taurus 99-103 6697962-2 1984 Inhibition of glycosylation with tunicamycin permitted identification of the nonglycosylated form of secreted angiotensinogen. Tunicamycin 33-44 angiotensinogen Rattus norvegicus 110-125 6725264-7 1984 Addition of tunicamycin (5 micrograms/ml) inhibited glycosylation of the initial form of haptoglobin detected, but subsequent proteolytic processing into alpha and beta chains still occurred. Tunicamycin 12-23 haptoglobin Oryctolagus cuniculus 89-100 6323131-4 1984 To determine whether this loss of LH/hCG receptors was due to accelerated receptor degradation, turnover measurements were made using tunicamycin to inhibit LH/hCG receptor synthesis. Tunicamycin 134-145 hypertrichosis 2 (generalised, congenital) Homo sapiens 160-163 6706977-5 1984 Purified liver parenchymal cells cultured in the presence of tunicamycin secrete fibrinogen polypeptides which lack carbohydrate moieties. Tunicamycin 61-72 fibrinogen alpha chain S homeolog Xenopus laevis 81-91 6425062-10 1984 Exposure of the cells to tunicamycin, on the other hand, caused a prominent cytoplasmic accumulation of VIIIR:Ag and, within 96 h, led to the disappearance of most of the VIIIR:Ag-positive granules but did not affect the intracellular distribution of fibronectin. Tunicamycin 25-36 fibronectin 1 Homo sapiens 251-262 6363129-2 1984 The effect of tunicamycin on synthesis and intracellular transport of pig small intestinal aminopeptidase N (EC 3.4.11.2), sucrase-isomaltase (EC 3.2.1.48-10) and maltase-glucoamylase (EC 3.2.1.20) was studied by labelling of mucosal explants with [35S]methionine. Tunicamycin 14-25 alanyl aminopeptidase, membrane Sus scrofa 91-107 6363129-5 1984 Treatment of aminopeptidase N and sucrase-isomaltase with endo F reduced the size of the high mannose forms approximately to those seen in the presence of tunicamycin. Tunicamycin 155-166 alanyl aminopeptidase, membrane Sus scrofa 13-29 6363129-5 1984 Treatment of aminopeptidase N and sucrase-isomaltase with endo F reduced the size of the high mannose forms approximately to those seen in the presence of tunicamycin. Tunicamycin 155-166 sucrase-isomaltase Sus scrofa 34-52 6319010-5 1984 TGF-beta has little effect on the rate of overall protein synthesis, but the increase it induces in EGF binding can be completely inhibited by cycloheximide and tunicamycin. Tunicamycin 161-172 epidermal growth factor like 1 Rattus norvegicus 100-103 6100257-7 1984 The protein glycosylation inhibitor tunicamycin was found to inhibit the ACTH produced increase in steroidogenesis and also to inhibit the synthesis of protein i under conditions which did not inhibit overall protein synthesis. Tunicamycin 36-47 proopiomelanocortin Homo sapiens 73-77 6373801-9 1984 Inhibition of N-linked glycosylation of apolipoprotein B with tunicamycin affects neither the assembly of glycerolipids into VLDL nor the secretion of the VLDL particle, indicating that aglyco -apolipoprotein B can serve as a functional component for VLDL assembly and secretion. Tunicamycin 62-73 apolipoprotein B Gallus gallus 40-56 6630229-1 1983 Tunicamycin, an inhibitor of asparagine-linked glycosylation of glycoprotein, has been used here to examine the role of N-linked oligosaccharides in secretion of ZP2 and ZP3, two of the three glycoproteins that constitute the mouse egg"s extracellular coat (zona pellucida). Tunicamycin 0-11 zona pellucida glycoprotein 2 Mus musculus 162-165 6630229-1 1983 Tunicamycin, an inhibitor of asparagine-linked glycosylation of glycoprotein, has been used here to examine the role of N-linked oligosaccharides in secretion of ZP2 and ZP3, two of the three glycoproteins that constitute the mouse egg"s extracellular coat (zona pellucida). Tunicamycin 0-11 zona pellucida glycoprotein 3 Mus musculus 170-173 6630229-11 1983 The apparent rates of synthesis of core-glycosylated ZP2 and ZP3 precursors synthesized in the absence of tunicamycin and of precursors synthesized in the presence of the drug are virtually identical. Tunicamycin 106-117 zona pellucida glycoprotein 2 Mus musculus 53-56 6630229-11 1983 The apparent rates of synthesis of core-glycosylated ZP2 and ZP3 precursors synthesized in the absence of tunicamycin and of precursors synthesized in the presence of the drug are virtually identical. Tunicamycin 106-117 zona pellucida glycoprotein 3 Mus musculus 61-64 6630229-12 1983 On the other hand, in the presence of tunicamycin, nascent ZP3 is incorporated into the zona pellucida as an extremely heterogeneous species (approximately equal to 51,000 Mr) at about three times the rate observed for mature ZP3 in the absence of tunicamycin. Tunicamycin 38-49 zona pellucida glycoprotein 3 Mus musculus 59-62 6630229-12 1983 On the other hand, in the presence of tunicamycin, nascent ZP3 is incorporated into the zona pellucida as an extremely heterogeneous species (approximately equal to 51,000 Mr) at about three times the rate observed for mature ZP3 in the absence of tunicamycin. Tunicamycin 38-49 zona pellucida glycoprotein 3 Mus musculus 226-229 6630229-12 1983 On the other hand, in the presence of tunicamycin, nascent ZP3 is incorporated into the zona pellucida as an extremely heterogeneous species (approximately equal to 51,000 Mr) at about three times the rate observed for mature ZP3 in the absence of tunicamycin. Tunicamycin 248-259 zona pellucida glycoprotein 3 Mus musculus 59-62 6630229-13 1983 In the presence of tunicamycin, ZP2 is incorporated into the zona pellucida as 81,000 and 76,000 Mr species at about one-sixth the rate observed for mature ZP2 in the absence of the drug. Tunicamycin 19-30 zona pellucida glycoprotein 2 Mus musculus 32-35 6630229-13 1983 In the presence of tunicamycin, ZP2 is incorporated into the zona pellucida as 81,000 and 76,000 Mr species at about one-sixth the rate observed for mature ZP2 in the absence of the drug. Tunicamycin 19-30 zona pellucida glycoprotein 2 Mus musculus 156-159 6630229-15 1983 ZP2 synthesized in the presence of tunicamycin is relatively stable and accumulates intracellularly. Tunicamycin 35-46 zona pellucida glycoprotein 2 Mus musculus 0-3 6874686-9 1983 Second, incubation of C-6 cells with N-acetylglucosamine simultaneously with tunicamycin was accompanied by prevention of the drug"s effect on both HMG-CoA reductase and glycoprotein synthesis. Tunicamycin 77-88 complement C6 Homo sapiens 22-25 6200362-4 1984 In the presence of tunicamycin an unglycosylated form of M alpha 1-antitrypsin appears in the incubation medium but no corresponding unglycosylated version of the Z protein is secreted. Tunicamycin 19-30 serpin family A member 1 Homo sapiens 59-78 6323296-3 1984 alpha 1-AT export to medium was delayed by tunicamycin, inhibited by cycloheximide but unaffected by colchicine. Tunicamycin 43-54 serpin family A member 1 Homo sapiens 0-10 6202280-1 1984 Synthesis of murine gamma interferon (MuIFN gamma) by phytohemagglutinin (PHA)-stimulated spleen cells was inhibited in a dose-dependent manner by graded concentrations of tunicamycin or 2-deoxy-glucose, both of which inhibit glycosylation. Tunicamycin 172-183 interferon gamma Mus musculus 20-49 6605248-3 1983 Treatment of hepatocytes with tunicamycin led to the secretion of an unglycosylated alpha 1-proteinase inhibitor (Mr 41 000) which also formed a complex with elastase (Mr 66 000). Tunicamycin 30-41 serpin family A member 1 Rattus norvegicus 84-112 6675524-6 1983 Glycosylation-deficient CEA obtained from cells harvested from media supplemented with non-toxic levels of tunicamycin showed lower molecular weight and delayed filtration through Sephadex-G200. Tunicamycin 107-118 CEA cell adhesion molecule 3 Homo sapiens 24-27 6628320-1 1983 Tunicamycin, an inhibitor of glycosylation, was incubated with ovine thyroid cells in culture to determine the role of glycosylation in the subsequent processing of thyroglobulin to form thyroid hormone. Tunicamycin 0-11 thyroglobulin Homo sapiens 165-178 6628320-5 1983 A low mol wt fragment of thyroglobulin was found after tunicamycin treatment, indicating increased susceptibility to or contact with proteases. Tunicamycin 55-66 thyroglobulin Homo sapiens 25-38 6316327-5 1983 Inhibition of protein glycosylation by tunicamycin generates smaller 125I-NGF-receptor complexes. Tunicamycin 39-50 nerve growth factor Rattus norvegicus 74-77 6226284-10 1983 The transport of the precursors of cathepsin D into lysosomes is inhibited by tunicamycin. Tunicamycin 78-89 cathepsin D Homo sapiens 35-46 6351631-1 1983 We have examined the effect of insulin and tunicamycin, which cause decreases in cell surface insulin receptor numbers in peripheral tissues, on insulin receptors in neuron-enriched brain cell cultures. Tunicamycin 43-54 insulin receptor Rattus norvegicus 94-110 6874686-0 1983 Effect of tunicamycin on 3-hydroxy-3-methylglutaryl coenzyme A reductase in C-6 glial cells. Tunicamycin 10-21 complement C6 Homo sapiens 76-79 6697962-3 1984 Whereas angiotensinogen secreted by hepatoma cells and hepatocytes showed electrophoretic heterogeneity (mol wt, 52-62 X 10(3], tunicamycin-treated cells secreted only a single angiotensinogen species [mol wt, 48.3 +/- 0.7 X 10(3) (mean +/- SD)], which could be cleaved by renin. Tunicamycin 128-139 angiotensinogen Rattus norvegicus 177-192 6697962-3 1984 Whereas angiotensinogen secreted by hepatoma cells and hepatocytes showed electrophoretic heterogeneity (mol wt, 52-62 X 10(3], tunicamycin-treated cells secreted only a single angiotensinogen species [mol wt, 48.3 +/- 0.7 X 10(3) (mean +/- SD)], which could be cleaved by renin. Tunicamycin 128-139 renin Rattus norvegicus 273-278 6697962-9 1984 4) The des-angiotensin I-angiotensinogen generated by renin treatment of the lysate had an electrophoretic mobility identical to that of des-AI-angiotensinogen produced by renin treatment of nonglycosylated angiotensinogen secreted by tunicamycin-treated hepatoma cells and hepatocytes. Tunicamycin 235-246 angiotensinogen Rattus norvegicus 25-40 6697962-9 1984 4) The des-angiotensin I-angiotensinogen generated by renin treatment of the lysate had an electrophoretic mobility identical to that of des-AI-angiotensinogen produced by renin treatment of nonglycosylated angiotensinogen secreted by tunicamycin-treated hepatoma cells and hepatocytes. Tunicamycin 235-246 renin Rattus norvegicus 54-59 6697962-9 1984 4) The des-angiotensin I-angiotensinogen generated by renin treatment of the lysate had an electrophoretic mobility identical to that of des-AI-angiotensinogen produced by renin treatment of nonglycosylated angiotensinogen secreted by tunicamycin-treated hepatoma cells and hepatocytes. Tunicamycin 235-246 renin Rattus norvegicus 172-177 6605298-0 1983 Expression of H-2 and viral antigens and resistance to the antitumor lysis of tunicamycin-treated MBL-2 lymphoma cells. Tunicamycin 78-89 histocompatibility-2, MHC Mus musculus 14-17 6190759-0 1983 Tunicamycin treatment inhibits the antiviral activity of interferon in mice. Tunicamycin 0-11 interferon alpha 1 Homo sapiens 57-67 6605298-0 1983 Expression of H-2 and viral antigens and resistance to the antitumor lysis of tunicamycin-treated MBL-2 lymphoma cells. Tunicamycin 78-89 mannose-binding lectin (protein C) 2 Mus musculus 98-103 6605298-2 1983 Treatment of the Moloney-virus-induced H-2b lymphoma target cells, MBL-2, with tunicamycin (TM), an inhibitor of the protein-N-linked glycosilation, was found to cause a loss of susceptibility to lysis by MSV-immune syngeneic effectors cells, while the same target cells remained fully sensitive to the lytic action of anti-H-2b-immune lymphocytes. Tunicamycin 79-90 mannose-binding lectin (protein C) 2 Mus musculus 67-72 6602705-10 1983 Tunicamycin led to a marked reduction of the secretion of alpha 2-macroglobulin, alpha 1-acid glycoprotein and alpha 1-proteinase inhibitor, whereas the secretion of transferrin was less affected. Tunicamycin 0-11 alpha-2-macroglobulin Rattus norvegicus 58-79 6602705-10 1983 Tunicamycin led to a marked reduction of the secretion of alpha 2-macroglobulin, alpha 1-acid glycoprotein and alpha 1-proteinase inhibitor, whereas the secretion of transferrin was less affected. Tunicamycin 0-11 serpin family A member 1 Rattus norvegicus 111-139 6190759-1 1983 Earlier we reported that tunicamycin (TM) treatment of L cells in vitro significantly enhances the antiviral activity of interferon (IFN) against viruses (such as vesicular stomatitis, Sindbis, and herpes simplex) which bud from membranes. Tunicamycin 25-36 interferon alpha 1 Homo sapiens 121-131 6190759-1 1983 Earlier we reported that tunicamycin (TM) treatment of L cells in vitro significantly enhances the antiviral activity of interferon (IFN) against viruses (such as vesicular stomatitis, Sindbis, and herpes simplex) which bud from membranes. Tunicamycin 25-36 interferon alpha 1 Homo sapiens 133-136 6190759-1 1983 Earlier we reported that tunicamycin (TM) treatment of L cells in vitro significantly enhances the antiviral activity of interferon (IFN) against viruses (such as vesicular stomatitis, Sindbis, and herpes simplex) which bud from membranes. Tunicamycin 38-40 interferon alpha 1 Homo sapiens 121-131 6190759-1 1983 Earlier we reported that tunicamycin (TM) treatment of L cells in vitro significantly enhances the antiviral activity of interferon (IFN) against viruses (such as vesicular stomatitis, Sindbis, and herpes simplex) which bud from membranes. Tunicamycin 38-40 interferon alpha 1 Homo sapiens 133-136 6304240-2 1983 In the presence of tunicamycin, they produced non-glycosylated, biologically active, IFN-beta with a molecular weight of 17000. Tunicamycin 19-30 interferon beta 1 Homo sapiens 85-93 6864547-4 1983 Furthermore, 27,000 POMC comigrated with a previously characterized unglycosylated form of this prohormone produced by treatment of cells with tunicamycin. Tunicamycin 143-154 pro-opiomelanocortin-alpha Mus musculus 20-24 6852052-6 1983 Acinar cells cultured in the presence of increasing concentrations of the N-glycosylation inhibitor tunicamycin synthesize 5-6 distinct precursor GP-2 species with apparent molecular weights decreasing from 73000-61000. Tunicamycin 100-111 glycoprotein 2 Rattus norvegicus 146-150 6854740-8 1983 Analysis by immunoprecipitation and sodium dodecyl sulfate-gel electrophoresis of intracellular [35S]methionine-labeled structural proteins synthesized in the presence and absence of tunicamycin supported the conclusion that E1 and E2 are glycoproteins. Tunicamycin 183-194 small nucleolar RNA, H/ACA box 73A Homo sapiens 225-234 6192804-6 1983 Tunicamycin reduced the incorporation of glucosamine into AFP with a concomitant decrease in molecular weight and microheterogeneity. Tunicamycin 0-11 alpha fetoprotein Mus musculus 58-61 6349621-2 1983 Tunicamycin (1 microgram/ml) induced a steady decrease of insulin binding, which was decreased by 50% after 13 h. As the total number of binding sites per hepatocyte was 20000, the rate of the receptor degradation could not exceed 13 sites/min per hepatocyte. Tunicamycin 0-11 insulin Homo sapiens 58-65 6349621-7 1983 First, the rate of release of degraded insulin into the medium was 600 molecules/min per hepatocyte with 1 nM labelled hormone, and increased (preincubation with cycloheximide) or decreased (tunicamycin) as a function of the amount of cell-bound insulin. Tunicamycin 191-202 insulin Homo sapiens 39-46 6189826-7 1983 The in vitro synthesized polypeptides migrate on NaDodSO4-polyacrylamide gel electrophoresis slower than the respective unglycosylated laminin and entactin chains isolated from cells treated with tunicamycin. Tunicamycin 196-207 nidogen 1 Mus musculus 147-155 6344077-5 1983 Immunoprecipitation of N-CAM from 9-day brain cells treated with tunicamycin yielded corresponding components of Mr 130,000 and 160,000, suggesting that the differences between these two components of N-CAM are in the polypeptide rather than the carbohydrate portions of the molecules. Tunicamycin 65-76 neural cell adhesion molecule 1 Homo sapiens 23-28 6344077-5 1983 Immunoprecipitation of N-CAM from 9-day brain cells treated with tunicamycin yielded corresponding components of Mr 130,000 and 160,000, suggesting that the differences between these two components of N-CAM are in the polypeptide rather than the carbohydrate portions of the molecules. Tunicamycin 65-76 neural cell adhesion molecule 1 Homo sapiens 201-206 7228853-1 1981 Tunicamycin, which inhibits N-linked oligosaccharide chain addition to nascent polypeptides, interrupts glycosylation of the insulin receptor in 3T3-L1 adipocytes giving rise to inactive receptors. Tunicamycin 0-11 insulin Homo sapiens 125-132 6822533-0 1983 Effect of tunicamycin, an inhibitor of protein glycosylation, on the biological properties of acetylcholine receptor in cultured muscle cells. Tunicamycin 10-21 cholinergic receptor nicotinic delta subunit Gallus gallus 94-116 6822533-1 1983 We have studied the effect of tunicamycin (TM), an antibiotic which inhibits the glycosylation of nascent proteins, on the properties of the acetylcholine receptor (AChR) at the surface of embryonic chick skeletal muscle cells. Tunicamycin 30-41 cholinergic receptor nicotinic delta subunit Gallus gallus 141-163 6822533-1 1983 We have studied the effect of tunicamycin (TM), an antibiotic which inhibits the glycosylation of nascent proteins, on the properties of the acetylcholine receptor (AChR) at the surface of embryonic chick skeletal muscle cells. Tunicamycin 30-41 cholinergic receptor nicotinic delta subunit Gallus gallus 165-169 6822533-1 1983 We have studied the effect of tunicamycin (TM), an antibiotic which inhibits the glycosylation of nascent proteins, on the properties of the acetylcholine receptor (AChR) at the surface of embryonic chick skeletal muscle cells. Tunicamycin 43-45 cholinergic receptor nicotinic delta subunit Gallus gallus 141-163 6822533-1 1983 We have studied the effect of tunicamycin (TM), an antibiotic which inhibits the glycosylation of nascent proteins, on the properties of the acetylcholine receptor (AChR) at the surface of embryonic chick skeletal muscle cells. Tunicamycin 43-45 cholinergic receptor nicotinic delta subunit Gallus gallus 165-169 6829167-5 1983 The unglycosylated form of the altered PE2 synthesized in the presence of tunicamycin migrated at the same position as the unglycosylated PE2 obtained from tunicamycin-treated, parent strain-infected cells. Tunicamycin 74-85 ETS2 repressor factor Homo sapiens 39-42 6829167-5 1983 The unglycosylated form of the altered PE2 synthesized in the presence of tunicamycin migrated at the same position as the unglycosylated PE2 obtained from tunicamycin-treated, parent strain-infected cells. Tunicamycin 156-167 ETS2 repressor factor Homo sapiens 39-42 6829167-5 1983 The unglycosylated form of the altered PE2 synthesized in the presence of tunicamycin migrated at the same position as the unglycosylated PE2 obtained from tunicamycin-treated, parent strain-infected cells. Tunicamycin 156-167 ETS2 repressor factor Homo sapiens 138-141 6292303-8 1983 Release of the IgE isotype-specific helper factor was inhibited by cycloheximide and tunicamycin, and its activity was destroyed by treatment with trypsin and neuraminidase. Tunicamycin 85-96 immunoglobulin heavy constant epsilon Homo sapiens 15-18 6820801-0 1982 Effect of tunicamycin on exo-1,3-beta-D-glucanase synthesis and secretion by cells and protoplasts of Saccharomyces cerevisiae. Tunicamycin 10-21 Rad2 family nuclease EXO1 Saccharomyces cerevisiae S288C 25-30 6820801-1 1982 Addition of tunicamycin to the culture medium of growing Saccharomyces cerevisiae protoplasts or cells resulted in the formation of a modified exo-1,3-beta-D-glucanase which was detectable in both extracellular and intracellular fractions. Tunicamycin 12-23 Rad2 family nuclease EXO1 Saccharomyces cerevisiae S288C 143-148 6820801-4 1982 Antibodies raised against the native protein readily precipitated the exo-1,3-beta-D-glucanase produced after tunicamycin treatment. Tunicamycin 110-121 Rad2 family nuclease EXO1 Saccharomyces cerevisiae S288C 70-75 6286640-0 1982 Effect of tunicamycin on the synthesis, processing, and secretion of pro-opiomelanocortin peptides in mouse pituitary cells. Tunicamycin 10-21 pro-opiomelanocortin-alpha Mus musculus 69-89 6286640-2 1982 When glycosylation of POMC is inhibited in AtT-20 cells with the drug tunicamycin, a 26,000-dalton protein appears in place of the glycosylated 29,000- and 32,000-dalton forms of POMC. Tunicamycin 70-81 pro-opiomelanocortin-alpha Mus musculus 22-26 6286640-2 1982 When glycosylation of POMC is inhibited in AtT-20 cells with the drug tunicamycin, a 26,000-dalton protein appears in place of the glycosylated 29,000- and 32,000-dalton forms of POMC. Tunicamycin 70-81 pro-opiomelanocortin-alpha Mus musculus 179-183 6286640-3 1982 The 26,000-dalton form found in tunicamycin-treated cells has the same [35S]methionine tryptic peptides as 29,000- and 32,000-dalton POMC, indicating that the decrease in apparent mass is most likely due to loss of carbohydrate and not to changes in the peptide backbone. Tunicamycin 32-43 pro-opiomelanocortin-alpha Mus musculus 133-137 6286640-6 1982 Pulse-chase studies demonstrate that the 26,000-dalton unglycosylated POMC is the precursor of the smaller ACTH and endorphin molecules in tunicamycin-treated cells. Tunicamycin 139-150 pro-opiomelanocortin-alpha Mus musculus 70-74 6286640-6 1982 Pulse-chase studies demonstrate that the 26,000-dalton unglycosylated POMC is the precursor of the smaller ACTH and endorphin molecules in tunicamycin-treated cells. Tunicamycin 139-150 pro-opiomelanocortin-alpha Mus musculus 107-111 6286640-7 1982 Furthermore, all of the forms of ACTH and endorphin found in tunicamycin-treated cells are secreted. Tunicamycin 61-72 pro-opiomelanocortin-alpha Mus musculus 33-37 7117256-0 1982 Effect of tunicamycin on thyroglobulin secretion. Tunicamycin 10-21 thyroglobulin Rattus norvegicus 25-38 7117256-2 1982 When followed over periods of 4 h, the secretion of [14C]leucine-labeled thyroglobulin into the medium was reduced by 60-95% in the presence of 1 microgram/ml and 5 micrograms/ml of tunicamycin. Tunicamycin 182-193 thyroglobulin Rattus norvegicus 73-86 7117256-6 1982 It is concluded that tunicamycin suppresses thyroglobulin secretion and that this is not due to inhibited protein synthesis. Tunicamycin 21-32 thyroglobulin Rattus norvegicus 44-57 6802485-4 1982 Assay of tyrosinase of glucosamine- or tunicamycin-induced unpigmented melanoma cells has revealed a selective and marked decrease in the melanosome-rich large-granule fraction, but no substantial decrease in the total activity of remaining subcellular fractions. Tunicamycin 39-50 tyrosinase Homo sapiens 9-19 7053388-6 1982 The antibiotic tunicamycin was shown to inhibit [3H] glucosamine incorporation into microsomal vitellogenin by 70%, without any significant effect on the synthesis of the protein backbone. Tunicamycin 15-26 a1-a Xenopus laevis 95-107 7336169-4 1981 On the other hand, treatment of melanoma cells with tunicamycin (final concentration, 1.0 microgram/ml) reduced the expression of MAA but did not affect susceptibility to ADCC. Tunicamycin 52-63 MAA Homo sapiens 130-133 7028131-8 1981 These data indicate that the number of insulin binding sites in the cultured Chinese hamster kidney epithelial cells increased with high glucose concentrations in the culture medium, whereas tunicamycin, an inhibitor of protein glycosylation, lowered the number of insulin binding sites. Tunicamycin 191-202 insulin Cricetulus griseus 39-46 7028131-8 1981 These data indicate that the number of insulin binding sites in the cultured Chinese hamster kidney epithelial cells increased with high glucose concentrations in the culture medium, whereas tunicamycin, an inhibitor of protein glycosylation, lowered the number of insulin binding sites. Tunicamycin 191-202 insulin Cricetulus griseus 265-272 7341241-6 1981 A, B1, B2 and C polypeptides are all glycosylated by an intracellular process involving the addition of tunicamycin and endo-beta-N-acetylglucosaminidase-H-sensitive N-linked oligosaccharide side chains. Tunicamycin 104-115 B.burgdorferi-associated arthritis 2 Mus musculus 3-15 6975776-4 1981 Addition of tunicamycin (2 microgram/ml) or 2-deoxy-D-glucose (10 mM) to the culture neither decreased the yield of CSF relative to the cell number grown nor induced heterogeneity of the produced CSF. Tunicamycin 12-23 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 116-119 6975776-4 1981 Addition of tunicamycin (2 microgram/ml) or 2-deoxy-D-glucose (10 mM) to the culture neither decreased the yield of CSF relative to the cell number grown nor induced heterogeneity of the produced CSF. Tunicamycin 12-23 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 196-199 6975776-5 1981 However, CSF produced in the presence of tunicamycin (CSF-tm) was about 23 percent smaller in its molecular weight than normally produced CSF (CSF-normal). Tunicamycin 41-52 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 9-12 6975776-5 1981 However, CSF produced in the presence of tunicamycin (CSF-tm) was about 23 percent smaller in its molecular weight than normally produced CSF (CSF-normal). Tunicamycin 41-52 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 54-57 6975776-5 1981 However, CSF produced in the presence of tunicamycin (CSF-tm) was about 23 percent smaller in its molecular weight than normally produced CSF (CSF-normal). Tunicamycin 41-52 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 54-57 6975776-5 1981 However, CSF produced in the presence of tunicamycin (CSF-tm) was about 23 percent smaller in its molecular weight than normally produced CSF (CSF-normal). Tunicamycin 41-52 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 54-57 6170312-2 1981 In RAJI cells the HLA-A, -B, and -C antigen heavy chains become core-glycosylated in the endoplasmic reticulum as evidenced by their sensitivity to endo-H digestion and tunicamycin treatment. Tunicamycin 169-180 major histocompatibility complex, class I, A Homo sapiens 18-35 6171878-3 1981 Immunoprecipitation of HLA-A,B,C antigens from tunicamycin-treated cells with four monoclonal antibodies specific for the heavy chain and one specific for beta 2-microglobulin showed that the heavy-chain determinant detected by the antibody Q6/64 is absent from the non-glycosylated molecule. Tunicamycin 47-58 major histocompatibility complex, class I, A Homo sapiens 23-30 6171878-3 1981 Immunoprecipitation of HLA-A,B,C antigens from tunicamycin-treated cells with four monoclonal antibodies specific for the heavy chain and one specific for beta 2-microglobulin showed that the heavy-chain determinant detected by the antibody Q6/64 is absent from the non-glycosylated molecule. Tunicamycin 47-58 beta-2-microglobulin Homo sapiens 155-175 6269546-0 1981 Glycosylation of cell surface receptors: tunicamycin treatment decreases insulin and growth hormone binding to different levels in cultured lymphocytes. Tunicamycin 41-52 growth hormone 1 Homo sapiens 85-99 6972252-6 1981 The activity of the D-factor was slightly decreased by treating the L-cells with tunicamycin (0.5 microgram/ml) in the presence of 2% fetal calf serum, without any decrease in CSF activity. Tunicamycin 81-92 leukemia inhibitory factor Mus musculus 20-28 6972252-9 1981 D-factor produced in the presence of tunicamycin had an apparent molecular weight of 25,000. Tunicamycin 37-48 leukemia inhibitory factor Mus musculus 0-8 6972252-10 1981 On the other hand, most of the CSF was eluted in the void volume, even when it was produced in the presence of tunicamycin. Tunicamycin 111-122 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 31-34 6972252-11 1981 The D-factor produced in the presence of tunicamycin was more sensitive than normal D-factor was to trypsin or heat treatment at 70 degrees. Tunicamycin 41-52 leukemia inhibitory factor Mus musculus 4-12 6972252-12 1981 The CSF produced in the presence of tunicamycin was resistant to these treatments. Tunicamycin 36-47 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 4-7 7228853-7 1981 This strongly suggests that inactive aglycoinsulin receptor accumulated post-translationally during chronic treatment with tunicamycin and then re-entered the glycosylation pathway when the inhibitor was removed giving rise to a functional insulin receptor. Tunicamycin 123-134 insulin receptor Homo sapiens 43-59 11892795-3 1983 We have now used rabbit antisera that recognize ZP3 to immunoprecipitate [35S]methionine-labeled, intracellular precursors of this glycoprotein from growing oocytes cultured in vitro in the presence or absence of tunicamycin, a drug that prevents addition of N-linked oligosaccharides to nascent polypeptide chains. Tunicamycin 213-224 zona pellucida glycoprotein 3 Mus musculus 48-51 6816905-1 1982 Tunicamycin alters the biological properties of human interferon-alpha (HuIFN-alpha) produced in its presence by changing the mixture of IFN-alpha subtypes produced. Tunicamycin 0-11 interferon alpha 1 Homo sapiens 74-83 6749836-3 1982 In the presence of tunicamycin, an inhibitor of the synthesis of protein-asparagine linked carbohydrate moieties, two smaller molecular forms each of precursor and mature proteinase A were synthesized, indicating that proteinase A contains N-linked carbohydrate which is apparently not required for processing. Tunicamycin 19-30 proteinase A Saccharomyces cerevisiae S288C 171-183 6749836-3 1982 In the presence of tunicamycin, an inhibitor of the synthesis of protein-asparagine linked carbohydrate moieties, two smaller molecular forms each of precursor and mature proteinase A were synthesized, indicating that proteinase A contains N-linked carbohydrate which is apparently not required for processing. Tunicamycin 19-30 proteinase A Saccharomyces cerevisiae S288C 218-230 6749836-4 1982 Tunicamycin interferes also with the glycosylation of the proteinase B precursor, whereas no unglycosylated mature proteinase B could be detected. Tunicamycin 0-11 proteinase B Saccharomyces cerevisiae S288C 58-70 7045125-2 1982 Nonglycosylated fibronectin, from tunicamycin-treated chicken embryo fibroblasts, was degraded more rapidly to acid-soluble products than glycosylated fibronectin by pronase, thermolysin, trypsin, and chymotrypsin. Tunicamycin 34-45 fibronectin 1 Gallus gallus 16-27 6922701-3 1982 Tunicamycin blocked glycosylation of pro-C4, C2 and factor B and inhibited secretion of the corresponding native complement proteins synthesized by guinea-pig peritoneal macrophages in tissue culture. Tunicamycin 0-11 complement C2 Cavia porcellus 45-60 6802828-3 1982 We have found that secreted type heavy chains (mus) are rapidly degraded in these cells, with a half-life of 1.3 h. Some of the membrane type heavy chains (mum) are also rapidly catabolized but some are expressed in a stable form with a half-life of 13 h. Inhibiting the initial glycosylation of heavy chains with tunicamycin has differential effects on the catabolic rates of mus and mum chains. Tunicamycin 314-325 latexin Homo sapiens 156-159 6802828-4 1982 The turnover of mus chains is not affected by this inhibitor, but the degradation of mum chains is much more rapid after tunicamycin treatment. Tunicamycin 121-132 latexin Homo sapiens 85-88 6802828-6 1982 Tunicamycin treatment of Daudi cells thus seems to inhibit formation of stable mum protein, possibly by altering mu chain conformation and inhibiting its interaction with light chains. Tunicamycin 0-11 latexin Homo sapiens 79-82 6951191-2 1982 Loss of 40--60% of DNA polymerase alpha 2 activity was observed in tunicamycin-treated cells. Tunicamycin 67-78 DNA polymerase alpha 1, catalytic subunit Homo sapiens 19-39 6951191-4 1982 However, DNA polymerase alpha 2 isolated from tunicamycin-treated cells was insensitive to ricin 1B. Tunicamycin 46-57 DNA polymerase alpha 1, catalytic subunit Homo sapiens 9-29 6951191-5 1982 Heat treatment studies at 50 degrees C showed two completely different inactivation profiles for the DNA polymerase alpha 2 enzymes isolated from the tunicamycin-treated and untreated cells. Tunicamycin 150-161 DNA polymerase alpha 1, catalytic subunit Homo sapiens 101-121 6281457-2 1982 In vivo synthesis of this env precursor in the presence of the core glycosylation inhibitor tunicamycin yielded a precursor of approximately 61,000 daltons (P61env). Tunicamycin 92-103 endogenous retrovirus group W member 1, envelope Homo sapiens 26-29 6116713-15 1981 The oligosaccharide moieties of procathepsin D and of the single chain and heavy chain forms of cathepsin D are cleaved by endoglycosidase H. Treatment of cells with tunicamycin arrests the biosynthetic pathway of cathepsin D at procathepsin D. The nonglycosylated procathepsin D is not proteolytically processed and its secretion is greatly inhibited. Tunicamycin 166-177 cathepsin D Canis lupus familiaris 35-46 6116713-15 1981 The oligosaccharide moieties of procathepsin D and of the single chain and heavy chain forms of cathepsin D are cleaved by endoglycosidase H. Treatment of cells with tunicamycin arrests the biosynthetic pathway of cathepsin D at procathepsin D. The nonglycosylated procathepsin D is not proteolytically processed and its secretion is greatly inhibited. Tunicamycin 166-177 cathepsin D Canis lupus familiaris 96-107 7228853-2 1981 Chronic exposure of cells to low levels (100 ng/ml) of high performance liquid chromatography-purified tunicamycin causes a greater than or equal to 90% depletion of insulin binding to cell surface and Triton X-100-extractable receptors and a 93% inhibition of [3H]glucosamine incorporation into protein in alkali-stable form. Tunicamycin 103-114 insulin Homo sapiens 166-173 6783700-4 1981 In the presence of 5 microgram/ml tunicamycin (Tm), glycosylation of both membrane and secreted IgM is at least 90% inhibited, but total protein synthesis is equivalent in control and Tm-treated cells. Tunicamycin 34-45 immunoglobulin heavy constant mu Mus musculus 96-99 6457668-0 1981 [Tunicamycin inhibition of carbohydrate incorporation into thyroglobulin]. Tunicamycin 1-12 thyroglobulin Rattus norvegicus 59-72 6457668-2 1981 Tg biosynthesis has been investigated by in vitro experiments, incubating rat thyroid glands with labeled amino-acid and carbohydrate in the presence of tunicamycin, a specific inhibitor of protein glycosylation. Tunicamycin 153-164 thyroglobulin Rattus norvegicus 0-2 6457668-3 1981 Tunicamycin inhibit Tg biosynthesis which is impaired in carbohydrate chains addition but slightly in the polypeptide synthesis, as shown by inhibition of 3H-glucosamine incorporation. Tunicamycin 0-11 thyroglobulin Rattus norvegicus 20-22 6457668-4 1981 Thus tunicamycin inhibits carbohydrate incorporation into Tg without affecting the polypeptide chain growth and decreases its secretion into the follicles. Tunicamycin 5-16 thyroglobulin Rattus norvegicus 58-60 6162638-4 1981 However, ovalbumin, which is transferred across the endoplasmic reticulum in the presence of tunicamycin and which is indistinguishable by immunoprecipitation, by two-dimensional gel electrophoresis and by concanavalin-A--Sepharose binding from the cytosolic form, is still secreted. Tunicamycin 93-104 ovalbumin (SERPINB14) Gallus gallus 9-18 7328676-4 1981 Tunicamycin-treated B16-F1 and B16-F10 cells lost their lung colonization abilities when injected intravenously into C57BL/6 mice, concomitant with lowered rates of adhesion to endothelial cell monolayers, endothelial extracellular matrix (basal lamina), and polyvinyl-immobilized fibronectin in vitro, suggesting that this drug inhibits experimental metastasis by modifying the surface glycoproteins involved in determining the adhesive properties of malignant cells. Tunicamycin 0-11 fibronectin 1 Mus musculus 281-292 7005335-1 1981 The effects of the inhibitor of N-linked glycosylation, tunicamycin, on the synthesis of HLA-A and -B antigens in the human lymphoblastoid cell line JY are described. Tunicamycin 56-67 major histocompatibility complex, class I, A Homo sapiens 89-101 6173591-0 1981 Use of tunicamycin to prepare carbohydrate-deficient human immune interferon. Tunicamycin 7-18 interferon gamma Homo sapiens 59-76 6992777-0 1980 Tunicamycin inhibits the differentiation of ST 13 fibroblasts to adipocytes with suppression of the insulin binding activity. Tunicamycin 0-11 insulin Homo sapiens 100-107 486403-0 1979 N-Acetylglucosamine- 1 -phosphate transferase from hen oviduct: solubilization, characterization, and inhibition by tunicamycin. Tunicamycin 116-127 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 0-45 7396520-0 1980 Effect of tunicamycin on the glycosylation of rhodopsin. Tunicamycin 10-21 rhodopsin Homo sapiens 46-55 7354085-0 1980 Effect of tunicamycin on the biosynthesis of the major human red cell sialoglycoprotein, glycophorin A, in the leukemia cell line K562. Tunicamycin 10-21 glycophorin A (MNS blood group) Homo sapiens 89-102 7354085-4 1980 The synthesis of the N-glycosidic oligosaccharide of glycophorin A is inhibited by the antibiotic tunicamycin, while the O-glycosidic oligosaccharides are not affected. Tunicamycin 98-109 glycophorin A (MNS blood group) Homo sapiens 53-66 20487725-4 1980 The participation of the dolichol pathway in the glycosylation of rhodopsin was demonstrated by the inhibition of core-region glycosylation of this glycoprotein by the antibiotic, tunicamycin. Tunicamycin 180-191 rhodopsin Homo sapiens 66-75 118450-10 1979 Gel filtration in Nonidet P-40 of the cell lysates of tunicamycin-treated lymphocytes showed that the nonsecretory 8S IgM contains this second type of mu chains, whereas the IgM molecules of the secretory type contain plasma cell-like mu chains. Tunicamycin 54-65 immunoglobulin heavy constant mu Mus musculus 118-121 118450-10 1979 Gel filtration in Nonidet P-40 of the cell lysates of tunicamycin-treated lymphocytes showed that the nonsecretory 8S IgM contains this second type of mu chains, whereas the IgM molecules of the secretory type contain plasma cell-like mu chains. Tunicamycin 54-65 immunoglobulin heavy constant mu Mus musculus 174-177 291008-1 1979 We have investigated the role of the carbohydrate moiety in the biological activity of fibronectin in vitro by using tunicamycin to inhibit the glycosylation of this glycoprotein. Tunicamycin 117-128 fibronectin 1 Gallus gallus 87-98 448154-2 1979 Tunicamycin greatly inhibited the secretion of nonglycosylated MOPC 315 IgA in trypsin-treated cells. Tunicamycin 0-11 immunoglobulin heavy constant alpha Mus musculus 72-75 448154-5 1979 Sodium dodecyl sulfate polyacrylamide gel electrophoresis of 125I-labeled cell surface IgA re-expressed in the presence of tunicamycin revealed a protein with an apparent m.w. Tunicamycin 123-134 immunoglobulin heavy constant alpha Mus musculus 87-90 291008-3 1979 Fibronectin synthesized in the presence of 0.5 microgram of tunicamycin per ml was not glycosylated, as determined by amino sugar analysis, lack of incorporation of [14C]glucosamine and [3H]mannose, and concanavalin A binding studies. Tunicamycin 60-71 fibronectin 1 Gallus gallus 0-11 457783-0 1979 Tunicamycin-mediated depletion of insulin receptors in 3T3-L1 adipocytes. Tunicamycin 0-11 insulin Homo sapiens 34-41 315316-4 1979 Furthermore, populations of cytolytic cells which had been pretreated with doses of tunicamycin sufficient to block the incorporation of mannose (or 2-DG) into glycoproteins were still fully susceptible to inhibition by 2-DG. Tunicamycin 84-95 olfactory receptor family 7 subfamily E member 55 pseudogene Homo sapiens 146-153 457783-1 1979 Tunicamycin, an antibiotic that inhibits protein glycosylation, elicited a rapid depletion of insulin binding activity at the surface of 3T3-L1 adipocytes. Tunicamycin 0-11 insulin Homo sapiens 94-101 457783-2 1979 Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anti-insulin receptor antibody on hexose uptake and metabolism. Tunicamycin 76-87 insulin Homo sapiens 17-24 457783-2 1979 Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anti-insulin receptor antibody on hexose uptake and metabolism. Tunicamycin 76-87 insulin Homo sapiens 240-247 457783-2 1979 Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anti-insulin receptor antibody on hexose uptake and metabolism. Tunicamycin 76-87 insulin Homo sapiens 240-247 479287-6 1979 We have also examined the fate of PE2 and E1 in cells treated with tunicamycin, an inhibitor of glycosylation. Tunicamycin 67-78 ETS2 repressor factor Homo sapiens 34-37 791099-7 1976 Tunicamycin also inhibits the apparent formation of proteinase A, whereas it does not affect the increase in the activities of a number of other enzymes. Tunicamycin 0-11 proteinase A Saccharomyces cerevisiae S288C 52-64 209036-3 1978 Tunicamycin inhibited glucosamine incorporation into rat liver transferrin and the apoprotein B chain of chick liver very low density lipoprotein (VLDL) by 75 to 90%. Tunicamycin 0-11 transferrin Rattus norvegicus 63-74 209036-3 1978 Tunicamycin inhibited glucosamine incorporation into rat liver transferrin and the apoprotein B chain of chick liver very low density lipoprotein (VLDL) by 75 to 90%. Tunicamycin 0-11 very low density lipoprotein receptor Gallus gallus 117-145 209036-3 1978 Tunicamycin inhibited glucosamine incorporation into rat liver transferrin and the apoprotein B chain of chick liver very low density lipoprotein (VLDL) by 75 to 90%. Tunicamycin 0-11 very low density lipoprotein receptor Gallus gallus 147-151 386885-4 1978 Loss of cell surface fibronectin as a result of viral transformation, or due to treatment of normal cells with tunicamycin, an inhibitor of protein glycosylation, may contribute to the reduced adhesion and altered morphology observed in these circumstances. Tunicamycin 111-122 fibronectin 1 Homo sapiens 21-32 198786-6 1977 Analysis of biosynthetically labeled proteins showed that a high-molecular-weight protein, presumed to be related to fibronectin, is markedly reduced in the medium of cells cultured in the presence of tunicamycin. Tunicamycin 201-212 fibronectin 1 Mus musculus 117-128 33907834-0 2021 Attenuation of the upregulation of NF-kappaB and AP-1 DNA-binding activities induced by tunicamycin or hypoxia/reoxygenation in neonatal rat cardiomyocytes by SERCA2a overexpression. Tunicamycin 88-99 Jun proto-oncogene, AP-1 transcription factor subunit Rattus norvegicus 49-53 33964350-6 2021 We showed that tunicamycin (Tm)-activated sXBP1 bound to the TGTCAT domain and suppressed XRCC2 expression. Tunicamycin 15-26 X-ray repair cross complementing 2 Homo sapiens 90-95 33964350-6 2021 We showed that tunicamycin (Tm)-activated sXBP1 bound to the TGTCAT domain and suppressed XRCC2 expression. Tunicamycin 28-30 X-ray repair cross complementing 2 Homo sapiens 90-95 32740777-5 2021 Here, we found that elevated sestrin2 is a protective process in neurons against chemical ER stress induced by tunicamycin (TM) or traumatic invasion, while treatment with PERK inhibitor or knockdown of ATF4 reduces sestrin2 expression upon ER stress. Tunicamycin 111-122 sestrin 2 Homo sapiens 29-37 32740777-5 2021 Here, we found that elevated sestrin2 is a protective process in neurons against chemical ER stress induced by tunicamycin (TM) or traumatic invasion, while treatment with PERK inhibitor or knockdown of ATF4 reduces sestrin2 expression upon ER stress. Tunicamycin 124-126 sestrin 2 Homo sapiens 29-37 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 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 X-box binding protein 1 Homo sapiens 112-116 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 X-box binding protein 1 Homo sapiens 198-202 33666503-3 2021 Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by chemical and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia/reperfusion (sI/R), respectively. Tunicamycin 160-171 fatty acyl CoA reductase 1 Rattus norvegicus 53-79 34015469-6 2021 Treatment with ER stressors thapsigargin, tunicamycin, and dithiolthreitol significantly increased PORCN gene expression, while treatment with thapsigargin and dithiolthreitol increased WLS gene expression. Tunicamycin 42-53 porcupine O-acyltransferase Homo sapiens 99-104 33979382-10 2021 Furthermore, UPR upregulation by glucose-regulated protein 78 (GRP78) suppression or low dose tunicamycin alleviated IFNalpha mediated liver injury. Tunicamycin 94-105 interferon alpha Mus musculus 117-125 33939297-8 2021 Furthermore, nesfatin-1-mediated protection against H/R injury also vanished in the presence of tunicamycin (TM), an ER stress inducer. Tunicamycin 96-107 nucleobindin 2 Rattus norvegicus 13-23 33939297-8 2021 Furthermore, nesfatin-1-mediated protection against H/R injury also vanished in the presence of tunicamycin (TM), an ER stress inducer. Tunicamycin 109-111 nucleobindin 2 Rattus norvegicus 13-23 33738958-6 2021 Tunicamycin-(TM)-loaded transcytosis-targeting-peptide-(TTP)-decorated NPs (TM@TTP) are used to boost BBB transcytosis via inhibiting Mfsd2a. Tunicamycin 0-11 major facilitator superfamily domain containing 2A Homo sapiens 134-140 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 caspase 3 Rattus norvegicus 108-117 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 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 annexin A3 Rattus norvegicus 136-139 33931075-16 2021 Importantly, both attenuation of glycosylation using tunicamycin and inhibition of TGFBR2 using LY2109761 differentially abrogated the stimulatory effect of ALG3 overexpression on cancer stemness and radioresistance. Tunicamycin 53-64 ALG3 alpha-1,3- mannosyltransferase Homo sapiens 157-161 33846370-5 2021 We modulated PERK expression using a plasmid, tunicamycin and siRNA against PERK, and then confirmed the target gene expression with real-time PCR and Northern blotting. Tunicamycin 46-57 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 13-17 33392644-6 2021 Inhibition of the N-glycosylation with tunicamycin caused a significant increase of NaV1.5 channel current (INa) when applied for 24 h. Tunicamycin shifted the steady-state inactivation curve to the hyperpolarization direction, whereas the activation curve was unaffected. Tunicamycin 39-50 sodium voltage-gated channel alpha subunit 5 Homo sapiens 84-90 33392644-6 2021 Inhibition of the N-glycosylation with tunicamycin caused a significant increase of NaV1.5 channel current (INa) when applied for 24 h. Tunicamycin shifted the steady-state inactivation curve to the hyperpolarization direction, whereas the activation curve was unaffected. Tunicamycin 136-147 sodium voltage-gated channel alpha subunit 5 Homo sapiens 84-90 33916165-7 2021 Treatment with tunicamycin or thapsigargin, which induces ER stress, increases HTRA1 expression. Tunicamycin 15-26 HtrA serine peptidase 1 Homo sapiens 79-84 33840662-11 2021 At the same time, lipid accumulation was observed in the Sepp1 high expression cells induced by endoplasmic reticulum (ER) activator tunicamycin (Tm). Tunicamycin 133-144 selenoprotein P Homo sapiens 57-62 33840662-11 2021 At the same time, lipid accumulation was observed in the Sepp1 high expression cells induced by endoplasmic reticulum (ER) activator tunicamycin (Tm). Tunicamycin 146-148 selenoprotein P Homo sapiens 57-62 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 solute carrier family 5 member 5 Rattus norvegicus 147-170 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 solute carrier family 5 member 5 Rattus norvegicus 172-175 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 thyroid peroxidase Rattus norvegicus 198-201 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 thyroglobulin Rattus norvegicus 207-220 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 thyroid stimulating hormone receptor Rattus norvegicus 256-276 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 thyroid stimulating hormone receptor Rattus norvegicus 278-282 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 transcription termination factor 1 Rattus norvegicus 317-322 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 transcription termination factor 2 Rattus norvegicus 357-362 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 paired box 8 Rattus norvegicus 368-385 33922129-1 2021 Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes. Tunicamycin 31-42 paired box 8 Rattus norvegicus 387-392 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 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 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 solute carrier family 5 member 5 Rattus norvegicus 223-226 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 thyroid peroxidase Rattus norvegicus 228-231 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 thyroid stimulating hormone receptor Rattus norvegicus 237-241 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 transcription termination factor 1 Rattus norvegicus 243-248 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 transcription termination factor 2 Rattus norvegicus 250-255 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 paired box 8 Rattus norvegicus 260-265 33717236-6 2021 It was subsequently demonstrated that IL-1beta induced A549 cell autophagy, while tunicamycin-induced autophagy increased the IL-1beta expression level and weakened paclitaxel sensitivity. Tunicamycin 82-93 interleukin 1 alpha Homo sapiens 126-134 33666503-3 2021 Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by chemical and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia/reperfusion (sI/R), respectively. Tunicamycin 160-171 fatty acyl CoA reductase 1 Rattus norvegicus 81-85 33666503-3 2021 Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by chemical and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia/reperfusion (sI/R), respectively. Tunicamycin 173-175 fatty acyl CoA reductase 1 Rattus norvegicus 53-79 33666503-3 2021 Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by chemical and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia/reperfusion (sI/R), respectively. Tunicamycin 173-175 fatty acyl CoA reductase 1 Rattus norvegicus 81-85 33655503-6 2021 Treatment with PNGase F and tunicamycin resulted in a reduction in both two-protein species, ~43 kDa and~85 kDa in size, by 2-4 kDa. Tunicamycin 28-39 N-glycanase 1 Homo sapiens 15-21 33714955-6 2021 Furthermore, we found that ATF4 inhibition reduced tunicamycin-induced caspase-3 activation, ROS production, ELAM-1 expression, and HTMCs phagocytosis impairment. Tunicamycin 51-62 activating transcription factor 4 Homo sapiens 27-31 33714955-6 2021 Furthermore, we found that ATF4 inhibition reduced tunicamycin-induced caspase-3 activation, ROS production, ELAM-1 expression, and HTMCs phagocytosis impairment. Tunicamycin 51-62 caspase 3 Homo sapiens 71-80 33714955-6 2021 Furthermore, we found that ATF4 inhibition reduced tunicamycin-induced caspase-3 activation, ROS production, ELAM-1 expression, and HTMCs phagocytosis impairment. Tunicamycin 51-62 selectin E Homo sapiens 109-115 33507306-5 2021 We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs). Tunicamycin 14-25 nuclear factor kappa B subunit 1 Homo sapiens 54-63 33609179-7 2021 Two common ERS stimulators, tunicamycin (Tm) and dithiothreitol (DTT) blocked the ameliorative effect of apelin on AHF. Tunicamycin 28-39 APLN Oryctolagus cuniculus 105-111 33609179-7 2021 Two common ERS stimulators, tunicamycin (Tm) and dithiothreitol (DTT) blocked the ameliorative effect of apelin on AHF. Tunicamycin 41-43 APLN Oryctolagus cuniculus 105-111 33603856-8 2021 TM injection significantly increased BiP expression and modified the topographic expression patterns of the UPR signaling proteins. Tunicamycin 0-2 heat shock protein 5 Mus musculus 37-40 33603856-9 2021 In addition, immunohistochemical analysis of Beclin1 revealed an increased pericentral staining intensity following TM pretreatment. Tunicamycin 116-118 beclin 1, autophagy related Mus musculus 45-52 33279504-8 2021 ERS stimulator (tunicamycin or DTT) blocked the beneficial effect of apelin. Tunicamycin 16-27 apelin Rattus norvegicus 69-75 33422538-3 2021 In the present study, tunicamycin-induced ER stress resulted in reactive astrogliosis-like events showing astroglial hypertrophy with the elevated extracellular signal-activated protein kinase 1/2 (ERK1/2) and cyclin-dependent kinase 5 (CDK5) phosphorylations in the CA1 region of the rat hippocampus. Tunicamycin 22-33 mitogen activated protein kinase 3 Rattus norvegicus 198-204 33422538-3 2021 In the present study, tunicamycin-induced ER stress resulted in reactive astrogliosis-like events showing astroglial hypertrophy with the elevated extracellular signal-activated protein kinase 1/2 (ERK1/2) and cyclin-dependent kinase 5 (CDK5) phosphorylations in the CA1 region of the rat hippocampus. Tunicamycin 22-33 cyclin-dependent kinase 5 Rattus norvegicus 210-235 33422538-3 2021 In the present study, tunicamycin-induced ER stress resulted in reactive astrogliosis-like events showing astroglial hypertrophy with the elevated extracellular signal-activated protein kinase 1/2 (ERK1/2) and cyclin-dependent kinase 5 (CDK5) phosphorylations in the CA1 region of the rat hippocampus. Tunicamycin 22-33 cyclin-dependent kinase 5 Rattus norvegicus 237-241 33422538-3 2021 In the present study, tunicamycin-induced ER stress resulted in reactive astrogliosis-like events showing astroglial hypertrophy with the elevated extracellular signal-activated protein kinase 1/2 (ERK1/2) and cyclin-dependent kinase 5 (CDK5) phosphorylations in the CA1 region of the rat hippocampus. Tunicamycin 22-33 carbonic anhydrase 1 Rattus norvegicus 267-270 33422538-4 2021 However, tunicamycin increased CDK5, but not ERK1/2, phosphorylation in the molecular layer of the dentate gyrus. Tunicamycin 9-20 cyclin-dependent kinase 5 Rattus norvegicus 31-35 33422538-5 2021 Roscovitine (a CDK5 inhibitor) suppressed the effect of tunicamycin in the molecular layer of the dentate gyrus and the CA1 region, while U0126 (an ERK1/2 inhibitor) reversed it in the CA1 region. Tunicamycin 56-67 cyclin-dependent kinase 5 Rattus norvegicus 15-19 33507306-5 2021 We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs). Tunicamycin 14-25 interleukin 6 Homo sapiens 106-110 33507306-5 2021 We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs). Tunicamycin 14-25 mitochondrially encoded cytochrome c oxidase II Homo sapiens 115-119 33507306-5 2021 We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs). Tunicamycin 14-25 tumor necrosis factor Homo sapiens 135-144 33507306-5 2021 We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs). Tunicamycin 14-25 interleukin 1 alpha Homo sapiens 149-157 33507306-6 2021 Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta. Tunicamycin 0-11 immunoglobulin kappa variable 1-27 Homo sapiens 40-43 33507306-6 2021 Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta. Tunicamycin 0-11 CCAAT enhancer binding protein alpha Homo sapiens 48-57 33507306-6 2021 Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta. Tunicamycin 0-11 nuclear factor kappa B subunit 1 Homo sapiens 92-101 33507306-6 2021 Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta. Tunicamycin 0-11 nuclear factor kappa B subunit 1 Homo sapiens 131-140 33507306-6 2021 Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta. Tunicamycin 0-11 tumor necrosis factor Homo sapiens 174-183 33507306-6 2021 Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta. Tunicamycin 0-11 interleukin 1 alpha Homo sapiens 188-196 33507306-9 2021 In contrast, upregulation of ER stress by tunicamycin significantly reduced IL-6 and COX2 production by inhibiting NF-kappaB activity in ECSCs. Tunicamycin 42-53 interleukin 6 Homo sapiens 76-80 33507306-9 2021 In contrast, upregulation of ER stress by tunicamycin significantly reduced IL-6 and COX2 production by inhibiting NF-kappaB activity in ECSCs. Tunicamycin 42-53 mitochondrially encoded cytochrome c oxidase II Homo sapiens 85-89 33507306-9 2021 In contrast, upregulation of ER stress by tunicamycin significantly reduced IL-6 and COX2 production by inhibiting NF-kappaB activity in ECSCs. Tunicamycin 42-53 nuclear factor kappa B subunit 1 Homo sapiens 115-124 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 181-185 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 eukaryotic translation initiation factor 2A Homo sapiens 186-195 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 activating transcription factor 4 Homo sapiens 196-200 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 33127435-12 2021 In conclusion, TGF-beta1 partially protects CF apoptosis induced by sI/R or Tn, through a mechanism that would involve ER stress. Tunicamycin 76-78 transforming growth factor, beta 1 Rattus norvegicus 15-24 33300079-13 2021 In addition, miR-6324 mimic partially reversed the effects of Dancr overexpression on Tm-induced apoptosis, ERS and autophagy. Tunicamycin 86-88 microRNA 6324 Rattus norvegicus 13-21 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 reticulon 4 Mus musculus 65-71 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 DNA-damage inducible transcript 3 Mus musculus 152-156 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 interleukin 6 Mus musculus 158-162 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 tumor necrosis factor Mus musculus 167-176 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 reticulon 4 Mus musculus 65-69 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 DNA-damage inducible transcript 3 Mus musculus 249-253 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 interleukin 6 Mus musculus 255-259 33572505-10 2021 In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha. Tunicamycin 88-99 tumor necrosis factor Mus musculus 264-273 33430288-5 2021 Tunicamycin-administered mice developed hyperinsulinemia, augmented lipolysis and increased circulating leptin and adiponectin. Tunicamycin 0-11 leptin Mus musculus 104-110 33413231-8 2021 Moreover, the data indicated that both the ER-resident and the secreted AGR2 enhance the survival capacity of PANC-1 cells after tunicamycin-induced ER stress and gemcitabine treatment. Tunicamycin 129-140 epiregulin Homo sapiens 43-45 33413231-8 2021 Moreover, the data indicated that both the ER-resident and the secreted AGR2 enhance the survival capacity of PANC-1 cells after tunicamycin-induced ER stress and gemcitabine treatment. Tunicamycin 129-140 anterior gradient 2, protein disulphide isomerase family member Homo sapiens 72-76 33413231-8 2021 Moreover, the data indicated that both the ER-resident and the secreted AGR2 enhance the survival capacity of PANC-1 cells after tunicamycin-induced ER stress and gemcitabine treatment. Tunicamycin 129-140 epiregulin Homo sapiens 149-151 33430288-5 2021 Tunicamycin-administered mice developed hyperinsulinemia, augmented lipolysis and increased circulating leptin and adiponectin. Tunicamycin 0-11 adiponectin, C1Q and collagen domain containing Mus musculus 115-126 33430288-6 2021 Renal unfolded protein response (UPR) gene expression markers, the lipogenic transcription factor SREBP1 and the phosphorylation of eIF2alpha increased 8 h after tunicamycin administration. Tunicamycin 162-173 sterol regulatory element binding transcription factor 1 Mus musculus 98-104 33430288-6 2021 Renal unfolded protein response (UPR) gene expression markers, the lipogenic transcription factor SREBP1 and the phosphorylation of eIF2alpha increased 8 h after tunicamycin administration. Tunicamycin 162-173 eukaryotic translation initiation factor 2A Mus musculus 132-141 33430442-7 2021 We also studied the replication of gt1 HEV in the ORF4-expressing tunicamycin-treated cell line. Tunicamycin 66-77 cortactin binding protein 2 Homo sapiens 50-54 33272572-3 2021 The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Tunicamycin 188-199 X-box binding protein 1 Mus musculus 65-69 33272572-3 2021 The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Tunicamycin 188-199 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 74-78 33300079-13 2021 In addition, miR-6324 mimic partially reversed the effects of Dancr overexpression on Tm-induced apoptosis, ERS and autophagy. Tunicamycin 86-88 differentiation antagonizing non-protein coding RNA Rattus norvegicus 62-67 33272572-3 2021 The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Tunicamycin 188-199 activating transcription factor 4 Mus musculus 79-83 33272572-3 2021 The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Tunicamycin 243-254 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 60-64 33272572-3 2021 The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Tunicamycin 243-254 X-box binding protein 1 Mus musculus 65-69 33272572-3 2021 The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Tunicamycin 243-254 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 74-78 33272572-3 2021 The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Tunicamycin 243-254 activating transcription factor 4 Mus musculus 79-83 33296727-8 2021 Moreover, using an animal model of ER-stress-induced neurodegeneration, we demonstrated that MANF deficiency potentiated tunicamycin (TM)-induced ER stress and neurodegeneration. Tunicamycin 121-132 mesencephalic astrocyte-derived neurotrophic factor Mus musculus 93-97 33111200-9 2021 As a negative control, we have also analyzed the DEGs following treatment with an endoplasmic reticulum (ER) stress-inducing agent, tunicamycin, which was affected by BMAL1 deletion minimally. Tunicamycin 132-143 aryl hydrocarbon receptor nuclear translocator like Homo sapiens 167-172 33249722-10 2021 Further in vitro assays revealed that ATF4-OA-Exo promoted chondrocyte autophagy and inhibited chondrocyte apoptosis in the TNF-alpha- or tunicamycin-treated chondrocytes. Tunicamycin 138-149 activating transcription factor 4 Mus musculus 38-42 33249722-10 2021 Further in vitro assays revealed that ATF4-OA-Exo promoted chondrocyte autophagy and inhibited chondrocyte apoptosis in the TNF-alpha- or tunicamycin-treated chondrocytes. Tunicamycin 138-149 5'-3' exoribonuclease 1 Mus musculus 46-49 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 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 X-box binding protein 1 Homo sapiens 94-99 33296727-8 2021 Moreover, using an animal model of ER-stress-induced neurodegeneration, we demonstrated that MANF deficiency potentiated tunicamycin (TM)-induced ER stress and neurodegeneration. Tunicamycin 134-136 mesencephalic astrocyte-derived neurotrophic factor Mus musculus 93-97 32878739-11 2020 In CHO HcD6 cells treated with tunicamycin, the expression level of pdia4 was significantly increased. Tunicamycin 31-42 protein disulfide-isomerase A4 Cricetulus griseus 68-73 33354279-9 2020 Notably, activating ER stress with tunicamycin (TM) reduced therapeutic effects of FGF10-PLGA microspheres in wound healing, whereas inhibition of ER stress with 4-phenyl butyric acid (4-PBA) improved the function of FGF10-PLGA microspheres. Tunicamycin 35-46 fibroblast growth factor 10 Homo sapiens 83-88 33354279-9 2020 Notably, activating ER stress with tunicamycin (TM) reduced therapeutic effects of FGF10-PLGA microspheres in wound healing, whereas inhibition of ER stress with 4-phenyl butyric acid (4-PBA) improved the function of FGF10-PLGA microspheres. Tunicamycin 48-50 fibroblast growth factor 10 Homo sapiens 83-88 32888957-15 2020 Tunicamycin promoted OGD/R-induced decrease in cell viability and reversed NOD1 silencing-induced increase in cell viability. Tunicamycin 0-11 nucleotide-binding oligomerization domain containing 1 Rattus norvegicus 75-79 32888957-16 2020 Tunicamycin also enhanced OGD/R-induced autophagy and reversed NOD1 silencing-induced inhibition in autophagy. Tunicamycin 0-11 nucleotide-binding oligomerization domain containing 1 Rattus norvegicus 63-67 33045248-4 2020 We showed that deletion of MED2 leads to sensitivity to the ER stress inducer tunicamycin (TM) as well as a shortened replicative lifespan (RLS), accompanied by increased intracellular ROS levels and hyperpolarization of mitochondria. Tunicamycin 78-89 Med2p Saccharomyces cerevisiae S288C 27-31 33272572-2 2021 In comparison to their normal counterparts, Optn-deficient mouse embryonic fibroblasts showed significantly higher cell death and caspase-3 activation upon treatment with tunicamycin and thapsigargin, inducers of ER stress. Tunicamycin 171-182 caspase 3 Mus musculus 130-139 33272572-3 2021 The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice. Tunicamycin 188-199 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 60-64 33298866-10 2020 In GECs incubated with tunicamycin, deletion of IRE1alpha attenuated upregulation of ER chaperones, LC3 lipidation, and LC3 transcription, compared with control GECs. Tunicamycin 23-34 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 48-57 33164499-4 2020 The antibiotic compound tunicamycin is a natural product inhibitor of MraY that is also toxic to eukaryotes through its binding to GPT. Tunicamycin 24-35 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 131-134 33097029-2 2020 Our previous studies found that bleomycin and tunicamycin could induce ER stress and consequently trigger EMT accompanying with IL-32 overexpression. Tunicamycin 46-57 interleukin 32 Homo sapiens 128-133 32607937-6 2020 We find that exposure of neural and endocrine cells to the cell stressors tunicamycin and thapsigargin increases cellular proSAAS mRNA and protein in Neuro2A cells. Tunicamycin 74-85 proprotein convertase subtilisin/kexin type 1 inhibitor Mus musculus 122-129 32996649-10 2020 Deglycosylation of CREBH induced by Tm could inhibit the proteolysis of CREBH induced by PA. Tunicamycin 36-38 cAMP responsive element binding protein 3-like 3 Mus musculus 19-24 32996649-10 2020 Deglycosylation of CREBH induced by Tm could inhibit the proteolysis of CREBH induced by PA. Tunicamycin 36-38 cAMP responsive element binding protein 3-like 3 Mus musculus 72-77 32996245-8 2020 Salubrinal restored the tunicamycin-induced decrease in the viability of primary calvarial osteoblasts and increased the expression of Runx2 and ALP, and decreased p-eIF2alpha/eIF2alpha in a dose-dependent manner. Tunicamycin 24-35 RUNX family transcription factor 2 Rattus norvegicus 135-140 32996245-8 2020 Salubrinal restored the tunicamycin-induced decrease in the viability of primary calvarial osteoblasts and increased the expression of Runx2 and ALP, and decreased p-eIF2alpha/eIF2alpha in a dose-dependent manner. Tunicamycin 24-35 eukaryotic translation initiation factor 2A Rattus norvegicus 166-175 32996245-8 2020 Salubrinal restored the tunicamycin-induced decrease in the viability of primary calvarial osteoblasts and increased the expression of Runx2 and ALP, and decreased p-eIF2alpha/eIF2alpha in a dose-dependent manner. Tunicamycin 24-35 eukaryotic translation initiation factor 2A Rattus norvegicus 176-185 33014334-0 2020 Tunicamycin promotes metastasis through upregulating endoplasmic reticulum stress induced GRP78 expression in thyroid carcinoma. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 90-95 33149811-6 2020 Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM). Tunicamycin 157-168 mitofusin 2 Homo sapiens 13-17 33149811-6 2020 Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM). Tunicamycin 157-168 epiregulin Homo sapiens 65-67 33149811-6 2020 Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM). Tunicamycin 157-168 epiregulin Homo sapiens 90-92 33149811-6 2020 Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM). Tunicamycin 157-168 epiregulin Homo sapiens 90-92 33149811-6 2020 Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM). Tunicamycin 170-172 mitofusin 2 Homo sapiens 13-17 33149811-6 2020 Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM). Tunicamycin 170-172 epiregulin Homo sapiens 65-67 33149811-6 2020 Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM). Tunicamycin 170-172 epiregulin Homo sapiens 90-92 33149811-6 2020 Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM). Tunicamycin 170-172 epiregulin Homo sapiens 90-92 33149811-8 2020 Mfn2 silencing attenuated mitochondrial oxidative stress and Ca2+ overload, increased mitochondrial membrane potential and mitochondrial oxygen consumption, and protected cells from TM-induced apoptosis. Tunicamycin 182-184 mitofusin 2 Homo sapiens 0-4 32981418-3 2021 We demonstrate that downregulation of RNF-5 decreased sensitivity to tunicamycin both in wild type and in an ire-1 mutant. Tunicamycin 69-80 E3 ubiquitin ligase rnf-5;RING finger protein 5;RING-type domain-containing protein Caenorhabditis elegans 38-43 32981418-3 2021 We demonstrate that downregulation of RNF-5 decreased sensitivity to tunicamycin both in wild type and in an ire-1 mutant. Tunicamycin 69-80 Endoribonuclease;Serine/threonine-protein kinase Caenorhabditis elegans 109-114 33050595-4 2020 Therefore, in this study, we aimed to explore the relationship between ER stress induced by tunicamycin and LXRalpha in hepatocytes and macrophages and clarify their possible mechanisms and roles in AS. Tunicamycin 92-103 nuclear receptor subfamily 1 group H member 3 Homo sapiens 108-116 33050595-6 2020 Tunicamycin-induced ER stress caused liver injury; promoted the accumulation of cholesterol and triglycerides; inhibited the expression of LXRalpha, ABCA1 and ABCG1 in the livers of mice, thus reducing serum high-density lipoprotein (HDL)-C, low-density lipoprotein (LDL)-C, total cholesterol and triglyceride levels; however, LXR-623 could attenuate ER stress and reverse these changes. Tunicamycin 0-11 nuclear receptor subfamily 1, group H, member 3 Mus musculus 139-147 33050595-6 2020 Tunicamycin-induced ER stress caused liver injury; promoted the accumulation of cholesterol and triglycerides; inhibited the expression of LXRalpha, ABCA1 and ABCG1 in the livers of mice, thus reducing serum high-density lipoprotein (HDL)-C, low-density lipoprotein (LDL)-C, total cholesterol and triglyceride levels; however, LXR-623 could attenuate ER stress and reverse these changes. Tunicamycin 0-11 ATP-binding cassette, sub-family A (ABC1), member 1 Mus musculus 149-154 33050595-6 2020 Tunicamycin-induced ER stress caused liver injury; promoted the accumulation of cholesterol and triglycerides; inhibited the expression of LXRalpha, ABCA1 and ABCG1 in the livers of mice, thus reducing serum high-density lipoprotein (HDL)-C, low-density lipoprotein (LDL)-C, total cholesterol and triglyceride levels; however, LXR-623 could attenuate ER stress and reverse these changes. Tunicamycin 0-11 ATP binding cassette subfamily G member 1 Mus musculus 159-164 33050595-8 2020 ER stress induced by tunicamycin could clearly be reversed by activating LXRalpha because it promoted cholesterol efflux by enhancing the expression of ABCA1 and ABCG1 in hepatocytes and macrophages, contributing to attenuation of the development of AS. Tunicamycin 21-32 nuclear receptor subfamily 1 group H member 3 Homo sapiens 73-81 33050595-8 2020 ER stress induced by tunicamycin could clearly be reversed by activating LXRalpha because it promoted cholesterol efflux by enhancing the expression of ABCA1 and ABCG1 in hepatocytes and macrophages, contributing to attenuation of the development of AS. Tunicamycin 21-32 ATP binding cassette subfamily A member 1 Homo sapiens 152-157 33050595-8 2020 ER stress induced by tunicamycin could clearly be reversed by activating LXRalpha because it promoted cholesterol efflux by enhancing the expression of ABCA1 and ABCG1 in hepatocytes and macrophages, contributing to attenuation of the development of AS. Tunicamycin 21-32 ATP binding cassette subfamily G member 1 Homo sapiens 162-167 33014334-8 2020 In addition, tunicamycin-induced ER stress up-regulated the expression of GRP78, PERK and XBP1 as well as reversed the metastatic ability of GRP78 in ATC cells. Tunicamycin 13-24 heat shock protein family A (Hsp70) member 5 Homo sapiens 74-79 33014334-8 2020 In addition, tunicamycin-induced ER stress up-regulated the expression of GRP78, PERK and XBP1 as well as reversed the metastatic ability of GRP78 in ATC cells. Tunicamycin 13-24 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 81-85 33014334-8 2020 In addition, tunicamycin-induced ER stress up-regulated the expression of GRP78, PERK and XBP1 as well as reversed the metastatic ability of GRP78 in ATC cells. Tunicamycin 13-24 X-box binding protein 1 Homo sapiens 90-94 33014334-8 2020 In addition, tunicamycin-induced ER stress up-regulated the expression of GRP78, PERK and XBP1 as well as reversed the metastatic ability of GRP78 in ATC cells. Tunicamycin 13-24 heat shock protein family A (Hsp70) member 5 Homo sapiens 141-146 32673694-11 2020 Knockdown or chemical inhibition of CSNK2B and ACSL1 in Caco-2 cells reduced activity of the ATF6-dependent ERSE reporter gene, diminished transcription of the ATF6 target genes HSP90B1 and HSPA5 and reduced NF-kappaB reporter gene activation upon tunicamycin stimulation. Tunicamycin 248-259 casein kinase 2 beta Homo sapiens 36-42 32780887-3 2020 Here, we present data showing the b-ZIP transcription factor E4BP4 in both the hepatocytes and the mouse liver is potently induced by the chemical ER stress inducer tunicamycin or by high-fat, low-methionine, and choline-deficient (HFLMCD) diet. Tunicamycin 165-176 nuclear factor, interleukin 3, regulated Mus musculus 61-66 32780887-5 2020 Tunicamycin promotes the lipid droplet formation and alters lipid metabolic gene expression in primary mouse hepatocytes from E4bp4flox/flox but not E4bp4 liver-specific KO (E4bp4-LKO) mice. Tunicamycin 0-11 nuclear factor, interleukin 3, regulated Mus musculus 126-131 32673694-11 2020 Knockdown or chemical inhibition of CSNK2B and ACSL1 in Caco-2 cells reduced activity of the ATF6-dependent ERSE reporter gene, diminished transcription of the ATF6 target genes HSP90B1 and HSPA5 and reduced NF-kappaB reporter gene activation upon tunicamycin stimulation. Tunicamycin 248-259 acyl-CoA synthetase long chain family member 1 Homo sapiens 47-52 32673694-11 2020 Knockdown or chemical inhibition of CSNK2B and ACSL1 in Caco-2 cells reduced activity of the ATF6-dependent ERSE reporter gene, diminished transcription of the ATF6 target genes HSP90B1 and HSPA5 and reduced NF-kappaB reporter gene activation upon tunicamycin stimulation. Tunicamycin 248-259 activating transcription factor 6 Homo sapiens 93-97 32673694-13 2020 Inhibitors of ACSL1 or CSNK2B prevented activation of ATF6 and reduced CXCL1 and TNF expression in these organoids upon induction of ER stress with tunicamycin. Tunicamycin 148-159 acyl-CoA synthetase long chain family member 1 Homo sapiens 14-19 32673694-13 2020 Inhibitors of ACSL1 or CSNK2B prevented activation of ATF6 and reduced CXCL1 and TNF expression in these organoids upon induction of ER stress with tunicamycin. Tunicamycin 148-159 casein kinase 2 beta Homo sapiens 23-29 32673694-13 2020 Inhibitors of ACSL1 or CSNK2B prevented activation of ATF6 and reduced CXCL1 and TNF expression in these organoids upon induction of ER stress with tunicamycin. Tunicamycin 148-159 activating transcription factor 6 Homo sapiens 54-58 32673694-14 2020 Injection of mice with inhibitors of ACSL1 or CSNK2B significantly reduced tunicamycin-mediated intestinal inflammation and IEC death and expression of CXCL1 and TNF in Atg16l1DeltaIEC mice. Tunicamycin 75-86 acyl-CoA synthetase long-chain family member 1 Mus musculus 37-42 32673694-14 2020 Injection of mice with inhibitors of ACSL1 or CSNK2B significantly reduced tunicamycin-mediated intestinal inflammation and IEC death and expression of CXCL1 and TNF in Atg16l1DeltaIEC mice. Tunicamycin 75-86 casein kinase 2, beta polypeptide Mus musculus 46-52 32039481-8 2020 The UPR activators dithiothreitol (DTT) and tunicamycin (TN) activated the UPR and reduced MYOCD along with SMC markers in vitro. Tunicamycin 44-55 myocardin Homo sapiens 91-96 32039481-8 2020 The UPR activators dithiothreitol (DTT) and tunicamycin (TN) activated the UPR and reduced MYOCD along with SMC markers in vitro. Tunicamycin 57-59 myocardin Homo sapiens 91-96 32592208-9 2020 Our study revealed that the tunicamycin-induced persistent UPR expression led to apoptosis of chondrocytes and activation of autophagy incorporation with GRP78. Tunicamycin 28-39 heat shock protein family A (Hsp70) member 5 Homo sapiens 154-159 32039481-9 2020 The IRE1alpha inhibitor 4mu8C counteracted the effect of DTT and TN on SMC markers and MYOCD expression. Tunicamycin 65-67 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 4-29 32039481-9 2020 The IRE1alpha inhibitor 4mu8C counteracted the effect of DTT and TN on SMC markers and MYOCD expression. Tunicamycin 65-67 myocardin Homo sapiens 87-92 32039481-11 2020 MRTFs also antagonized the UPR as indicated by reduced TN and DTT-mediated induction of CRELD2, MANF, PDIA4, and SDF2L1 following overexpression of MRTFs. Tunicamycin 55-57 protein disulfide isomerase family A member 4 Homo sapiens 102-107 32039481-11 2020 MRTFs also antagonized the UPR as indicated by reduced TN and DTT-mediated induction of CRELD2, MANF, PDIA4, and SDF2L1 following overexpression of MRTFs. Tunicamycin 55-57 stromal cell derived factor 2 like 1 Homo sapiens 113-119 32962446-7 2021 Our findings suggest that short term TN treatment did not affect leukocyte movement to lymphoid compartments of the small intestine, but it altered villus architecture due to decreased PECAM-1 expression. Tunicamycin 37-39 platelet and endothelial cell adhesion molecule 1 Homo sapiens 185-192 32910713-6 2021 When compared to wild-type CH12 cells, tfg KO CH12 cells were more sensitive towards ER stress induced by tunicamycin, monensin and proteasome inhibition or by expression of an ER-bound immunoglobulin (Ig) mu heavy (microH) chain. Tunicamycin 106-117 Trk-fused gene Mus musculus 39-42 32836022-7 2020 This stress up-regulated the expression of five glutamate decarboxylase (GAD) genes except GAD2 and GABA content of A. thaliana plants increased with an increasing concentration of tunicamycin (0.1 mug ml-1 and 0.25 mug ml-1). Tunicamycin 181-192 glutamate decarboxylase Arabidopsis thaliana 48-71 32836022-7 2020 This stress up-regulated the expression of five glutamate decarboxylase (GAD) genes except GAD2 and GABA content of A. thaliana plants increased with an increasing concentration of tunicamycin (0.1 mug ml-1 and 0.25 mug ml-1). Tunicamycin 181-192 glutamate decarboxylase Arabidopsis thaliana 73-76 32836022-7 2020 This stress up-regulated the expression of five glutamate decarboxylase (GAD) genes except GAD2 and GABA content of A. thaliana plants increased with an increasing concentration of tunicamycin (0.1 mug ml-1 and 0.25 mug ml-1). Tunicamycin 181-192 glutamate decarboxylase 2 Arabidopsis thaliana 91-95 32945983-13 2021 More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group. Tunicamycin 54-65 family with sequence similarity 172 member A Homo sapiens 33-40 32945983-13 2021 More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group. Tunicamycin 54-65 eukaryotic translation initiation factor 2 subunit alpha Homo sapiens 45-50 32973403-8 2020 Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha. Tunicamycin 118-129 centromere protein F Homo sapiens 9-14 32973403-8 2020 Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha. Tunicamycin 118-129 centromere protein F Homo sapiens 162-167 32973403-8 2020 Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha. Tunicamycin 131-133 centromere protein F Homo sapiens 9-14 32973403-8 2020 Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha. Tunicamycin 131-133 centromere protein F Homo sapiens 162-167 32973403-8 2020 Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha. Tunicamycin 131-133 X-box binding protein 1 Homo sapiens 196-200 32973403-8 2020 Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha. Tunicamycin 131-133 activating transcription factor 6 Homo sapiens 205-214 32910713-9 2021 The GFP:RFP ratio of tandem-fluorescent-LC3 was higher in tunicamycin-treated CH12 tfg KO B cells, suggesting less autophagy flux during induced ER stress. Tunicamycin 58-69 tripartite motif-containing 27 Mus musculus 8-11 32910713-9 2021 The GFP:RFP ratio of tandem-fluorescent-LC3 was higher in tunicamycin-treated CH12 tfg KO B cells, suggesting less autophagy flux during induced ER stress. Tunicamycin 58-69 Trk-fused gene Mus musculus 83-86 33209200-4 2020 The results showed that tunicamycin (TM) induced downregulation of miR-637 in gastric cancer cells (AGS) and increase of apoptosis and ER stress. Tunicamycin 24-35 microRNA 637 Homo sapiens 67-74 33209200-4 2020 The results showed that tunicamycin (TM) induced downregulation of miR-637 in gastric cancer cells (AGS) and increase of apoptosis and ER stress. Tunicamycin 37-39 microRNA 637 Homo sapiens 67-74 33209200-7 2020 The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells. Tunicamycin 138-140 microRNA 637 Homo sapiens 23-30 33209200-7 2020 The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells. Tunicamycin 138-140 calreticulin Homo sapiens 35-39 33209200-7 2020 The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells. Tunicamycin 138-140 calreticulin Homo sapiens 64-68 33209200-7 2020 The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells. Tunicamycin 138-140 microRNA 637 Homo sapiens 127-134 32810137-8 2020 In contrast, tunicamycin induced (ER stress associated) apoptosis is further increased by ATM knockdown or inhibition, but not by P53 knockdown. Tunicamycin 13-24 ATM serine/threonine kinase Rattus norvegicus 90-93 32402213-6 2020 In contrast, structure-function experiments demonstrated that IL-13 binding to IL-13Ralpha2 was dependent on each of the four sites of N-glycosylation in IL-13Ralpha2, and experiments with tunicamycin and PNGase F demonstrated that IL-13-IL-13Ralpha2 binding was decreased when IL-13Ralpha2 N-glycosylation was diminished. Tunicamycin 189-200 interleukin 13 Homo sapiens 62-67 32402213-6 2020 In contrast, structure-function experiments demonstrated that IL-13 binding to IL-13Ralpha2 was dependent on each of the four sites of N-glycosylation in IL-13Ralpha2, and experiments with tunicamycin and PNGase F demonstrated that IL-13-IL-13Ralpha2 binding was decreased when IL-13Ralpha2 N-glycosylation was diminished. Tunicamycin 189-200 interleukin 13 receptor subunit alpha 2 Homo sapiens 79-91 32402213-6 2020 In contrast, structure-function experiments demonstrated that IL-13 binding to IL-13Ralpha2 was dependent on each of the four sites of N-glycosylation in IL-13Ralpha2, and experiments with tunicamycin and PNGase F demonstrated that IL-13-IL-13Ralpha2 binding was decreased when IL-13Ralpha2 N-glycosylation was diminished. Tunicamycin 189-200 interleukin 13 Homo sapiens 79-84 32965004-5 2020 Different concentration of glucose was used to culture CHs for both 24 h and 72 h. Furthermore, Tunicamycin (TM) and 4-Phenylbutyric acid (4-PBA) were used to mediate ER stress of CHs, and human recombinant Skp2 protein was used to promote Skp2 expression. Tunicamycin 109-111 S-phase kinase associated protein 2 Homo sapiens 207-211 32965004-5 2020 Different concentration of glucose was used to culture CHs for both 24 h and 72 h. Furthermore, Tunicamycin (TM) and 4-Phenylbutyric acid (4-PBA) were used to mediate ER stress of CHs, and human recombinant Skp2 protein was used to promote Skp2 expression. Tunicamycin 109-111 S-phase kinase associated protein 2 Homo sapiens 240-244 32748834-5 2020 GRP78 and GRP94 expression was increased in cells treated with 3 nM thapsigargin or 0.1 mug/mL tunicamycin for 24 h, referred to as mild ER stress condition. Tunicamycin 95-106 heat shock protein 5 Mus musculus 0-5 32748834-5 2020 GRP78 and GRP94 expression was increased in cells treated with 3 nM thapsigargin or 0.1 mug/mL tunicamycin for 24 h, referred to as mild ER stress condition. Tunicamycin 95-106 heat shock protein 90, beta (Grp94), member 1 Mus musculus 10-15 32237184-8 2020 Also, induction of autophagy by tunicamycin resulted in apoptosis in diabetic PBMCs as observed by caspase 3 cleavage and reduced expression of Bcl2. Tunicamycin 32-43 caspase 3 Homo sapiens 99-108 32237184-8 2020 Also, induction of autophagy by tunicamycin resulted in apoptosis in diabetic PBMCs as observed by caspase 3 cleavage and reduced expression of Bcl2. Tunicamycin 32-43 BCL2 apoptosis regulator Homo sapiens 144-148 32724824-4 2020 In the present study, we induced ER stress by tunicamycin (TM) treatment and showed that infection of MIN6 cells with Ad-DHCR24-myc rendered these cells resistant to caspase-3-mediated apoptosis induced by TM, while cells transfected with siRNAs targeting DHCR24 were more sensitive to TM. Tunicamycin 59-61 24-dehydrocholesterol reductase Mus musculus 121-127 32724824-4 2020 In the present study, we induced ER stress by tunicamycin (TM) treatment and showed that infection of MIN6 cells with Ad-DHCR24-myc rendered these cells resistant to caspase-3-mediated apoptosis induced by TM, while cells transfected with siRNAs targeting DHCR24 were more sensitive to TM. Tunicamycin 59-61 myelocytomatosis oncogene Mus musculus 52-55 32724824-6 2020 Cells infected with Ad-LacZ exhibited a rapid and strong activation of ATF6 and p38, peaking at 3 h after TM exposure. Tunicamycin 106-108 activating transcription factor 6 Mus musculus 71-75 32724824-6 2020 Cells infected with Ad-LacZ exhibited a rapid and strong activation of ATF6 and p38, peaking at 3 h after TM exposure. Tunicamycin 106-108 mitogen-activated protein kinase 14 Mus musculus 80-83 32826849-9 2020 Furthermore, C57BL/6 mice was used to induce ER stress with TM intraperitoneal injection, PPARalpha and autophagy was upregulated in the mild-ER stress while downregulated in the serious ER stress, measured by qRT-PCR and immunoblotting, further confirmed the finding in vitro. Tunicamycin 60-62 peroxisome proliferator activated receptor alpha Mus musculus 90-99 32626998-7 2020 The ERS activator tunicamycin (TM) was used to counteract the ERO1alpha-induced reduction in ERS; however, the percentage of apoptotic cells and the level of mitochondrial damage did not change. Tunicamycin 18-29 endoplasmic reticulum oxidoreductase 1 alpha Homo sapiens 62-71 32626998-7 2020 The ERS activator tunicamycin (TM) was used to counteract the ERO1alpha-induced reduction in ERS; however, the percentage of apoptotic cells and the level of mitochondrial damage did not change. Tunicamycin 31-33 endoplasmic reticulum oxidoreductase 1 alpha Homo sapiens 62-71 32718038-8 2020 In a previous report we demonstrated that the pharmacological agent tunicamycin (TM) induced ER stress through altered protein glycosylation and induced high amounts of C/EBP-homologous protein (CHOP), resulting in hepatocyte apoptosis. Tunicamycin 68-79 DNA-damage inducible transcript 3 Mus musculus 169-193 32718038-8 2020 In a previous report we demonstrated that the pharmacological agent tunicamycin (TM) induced ER stress through altered protein glycosylation and induced high amounts of C/EBP-homologous protein (CHOP), resulting in hepatocyte apoptosis. Tunicamycin 68-79 DNA-damage inducible transcript 3 Mus musculus 195-199 32718038-8 2020 In a previous report we demonstrated that the pharmacological agent tunicamycin (TM) induced ER stress through altered protein glycosylation and induced high amounts of C/EBP-homologous protein (CHOP), resulting in hepatocyte apoptosis. Tunicamycin 81-83 DNA-damage inducible transcript 3 Mus musculus 169-193 32718038-8 2020 In a previous report we demonstrated that the pharmacological agent tunicamycin (TM) induced ER stress through altered protein glycosylation and induced high amounts of C/EBP-homologous protein (CHOP), resulting in hepatocyte apoptosis. Tunicamycin 81-83 DNA-damage inducible transcript 3 Mus musculus 195-199 32718038-9 2020 We compared TM-induced ER stress in wild type, Lcn2-/-, and Chop null (Chop-/-) primary hepatocytes and found Chop-/- hepatocytes to attenuate ER stress responses and resist ER stress-induced hepatocyte apoptosis through canonical eIF2alpha/GADD34 signaling, inhibiting protein synthesis. Tunicamycin 12-14 lipocalin 2 Mus musculus 47-51 32718038-9 2020 We compared TM-induced ER stress in wild type, Lcn2-/-, and Chop null (Chop-/-) primary hepatocytes and found Chop-/- hepatocytes to attenuate ER stress responses and resist ER stress-induced hepatocyte apoptosis through canonical eIF2alpha/GADD34 signaling, inhibiting protein synthesis. Tunicamycin 12-14 eukaryotic translation initiation factor 2A Mus musculus 231-240 32718038-9 2020 We compared TM-induced ER stress in wild type, Lcn2-/-, and Chop null (Chop-/-) primary hepatocytes and found Chop-/- hepatocytes to attenuate ER stress responses and resist ER stress-induced hepatocyte apoptosis through canonical eIF2alpha/GADD34 signaling, inhibiting protein synthesis. Tunicamycin 12-14 protein phosphatase 1, regulatory subunit 15A Mus musculus 241-247 32407927-0 2020 Luteolin prevents liver from tunicamycin-induced endoplasmic reticulum stress via nuclear factor erythroid 2-related factor 2-dependent sestrin 2 induction. Tunicamycin 29-40 NFE2 like bZIP transcription factor 2 Homo sapiens 82-125 32407927-0 2020 Luteolin prevents liver from tunicamycin-induced endoplasmic reticulum stress via nuclear factor erythroid 2-related factor 2-dependent sestrin 2 induction. Tunicamycin 29-40 sestrin 2 Homo sapiens 136-145 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 32714930-7 2020 At the same time, staurosporine, nifedipine, and tunicamycin elicited an intermediate activation of caspase-3. Tunicamycin 49-60 caspase 3 Homo sapiens 100-109 32724824-4 2020 In the present study, we induced ER stress by tunicamycin (TM) treatment and showed that infection of MIN6 cells with Ad-DHCR24-myc rendered these cells resistant to caspase-3-mediated apoptosis induced by TM, while cells transfected with siRNAs targeting DHCR24 were more sensitive to TM. Tunicamycin 46-57 24-dehydrocholesterol reductase Mus musculus 121-127 32660483-4 2020 The purpose of this study is to investigate the effects of CaMKIV on ER stress, autophagic function and insulin signaling in tunicamycin-treated adipocytes. Tunicamycin 125-136 calcium/calmodulin dependent protein kinase IV Homo sapiens 59-65 32660483-4 2020 The purpose of this study is to investigate the effects of CaMKIV on ER stress, autophagic function and insulin signaling in tunicamycin-treated adipocytes. Tunicamycin 125-136 insulin Homo sapiens 104-111 32660483-6 2020 Tunicamycin-treated 3 T3-L1 adipocytes were treated with recombinant CaMKIV in the presence or absence of targeted-siRNA mediated down-regulation of CREB and mTOR. Tunicamycin 0-11 calcium/calmodulin dependent protein kinase IV Homo sapiens 69-75 32660483-6 2020 Tunicamycin-treated 3 T3-L1 adipocytes were treated with recombinant CaMKIV in the presence or absence of targeted-siRNA mediated down-regulation of CREB and mTOR. Tunicamycin 0-11 cAMP responsive element binding protein 1 Homo sapiens 149-153 32660483-6 2020 Tunicamycin-treated 3 T3-L1 adipocytes were treated with recombinant CaMKIV in the presence or absence of targeted-siRNA mediated down-regulation of CREB and mTOR. Tunicamycin 0-11 mechanistic target of rapamycin kinase Homo sapiens 158-162 32660483-8 2020 RESULTS: Treatment with CaMKIV significantly reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II. Tunicamycin 54-65 calcium/calmodulin dependent protein kinase IV Homo sapiens 24-30 32660483-8 2020 RESULTS: Treatment with CaMKIV significantly reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II. Tunicamycin 54-65 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 90-94 32660483-8 2020 RESULTS: Treatment with CaMKIV significantly reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II. Tunicamycin 54-65 activating transcription factor 6 Homo sapiens 104-108 32660483-8 2020 RESULTS: Treatment with CaMKIV significantly reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II. Tunicamycin 54-65 autophagy related 7 Homo sapiens 110-114 32660483-12 2020 However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes. Tunicamycin 147-158 calcium/calmodulin dependent protein kinase IV Homo sapiens 35-41 32660483-12 2020 However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes. Tunicamycin 147-158 insulin Homo sapiens 56-63 32660483-12 2020 However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes. Tunicamycin 147-158 mechanistic target of rapamycin kinase Homo sapiens 131-135 32660483-12 2020 However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes. Tunicamycin 147-158 cAMP responsive element binding protein 1 Homo sapiens 139-143 32660483-13 2020 CONCLUSION: This study proves recombinant CaMKIV inhibits tunicamycin-induced ER stress and insulin resistance by regulating autophagy. Tunicamycin 58-69 calcium/calmodulin dependent protein kinase IV Homo sapiens 42-48 32664460-5 2020 Treatment with tunicamycin (Tm), the inhibitor of N-glycosylation of secreted glycoproteins, increased the transcript levels of SlBiP. Tunicamycin 15-26 BEL1-like homeodomain protein 2 Solanum lycopersicum 128-133 32664460-5 2020 Treatment with tunicamycin (Tm), the inhibitor of N-glycosylation of secreted glycoproteins, increased the transcript levels of SlBiP. Tunicamycin 28-30 BEL1-like homeodomain protein 2 Solanum lycopersicum 128-133 32203149-6 2020 Urinary ERdj3 and MANF increased in rats injected with tunicamycin (in the absence of proteinuria). Tunicamycin 55-66 DnaJ heat shock protein family (Hsp40) member B11 Rattus norvegicus 8-13 32378324-8 2020 Notably, chronic treatment of PCK rats with 4-PBA decreased liver weight, as well as both liver and cystic volumes, of animals under baseline conditions or after TM administration compared to controls. Tunicamycin 162-164 phosphoenolpyruvate carboxykinase 1 Rattus norvegicus 30-33 32332156-5 2020 We show that lactogens protect INS1 cells, primary rodent and human beta-cells in vitro against two distinct ER stressors, tunicamycin and thapsigargin, through activation of the JAK2/STAT5 pathway. Tunicamycin 123-134 Janus kinase 2 Homo sapiens 179-183 32203149-6 2020 Urinary ERdj3 and MANF increased in rats injected with tunicamycin (in the absence of proteinuria). Tunicamycin 55-66 mesencephalic astrocyte-derived neurotrophic factor Rattus norvegicus 18-22 32579556-3 2020 Overexpression of ISR1 is lethal and, at lower levels, causes sensitivity to tunicamycin and resistance to calcofluor white, implying impaired protein glycosylation and reduced chitin deposition. Tunicamycin 77-88 putative protein kinase ISR1 Saccharomyces cerevisiae S288C 18-22 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 60-65 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 32586376-8 2020 Further study indicated that ER stress agonist (tunicamycin) treatment in MSLC results in the translocation of XBP1, an ER stress sensor, into the nucleus to induce MCL-1 expression through direct binding to the - 313- to - 308-bp region of MCL-1 promoter. Tunicamycin 48-59 X-box binding protein 1 Homo sapiens 111-115 32586376-8 2020 Further study indicated that ER stress agonist (tunicamycin) treatment in MSLC results in the translocation of XBP1, an ER stress sensor, into the nucleus to induce MCL-1 expression through direct binding to the - 313- to - 308-bp region of MCL-1 promoter. Tunicamycin 48-59 myeloid cell leukemia sequence 1 Mus musculus 165-170 32586376-8 2020 Further study indicated that ER stress agonist (tunicamycin) treatment in MSLC results in the translocation of XBP1, an ER stress sensor, into the nucleus to induce MCL-1 expression through direct binding to the - 313- to - 308-bp region of MCL-1 promoter. Tunicamycin 48-59 myeloid cell leukemia sequence 1 Mus musculus 241-246 32522979-8 2020 Experiments with HCC xenograft models revealed that restoring SHQ1 levels enhanced the anti-tumor activity of the endoplasmic reticulum (ER) stress inducer tunicamycin (TM) and common chemotherapy drug paclitaxel (PTX). Tunicamycin 156-167 SHQ1, H/ACA ribonucleoprotein assembly factor Homo sapiens 62-66 32522979-8 2020 Experiments with HCC xenograft models revealed that restoring SHQ1 levels enhanced the anti-tumor activity of the endoplasmic reticulum (ER) stress inducer tunicamycin (TM) and common chemotherapy drug paclitaxel (PTX). Tunicamycin 169-171 SHQ1, H/ACA ribonucleoprotein assembly factor Homo sapiens 62-66 32031621-8 2020 Tunicamycin elicited time-dependent increase in GRP78 protein levels, direct interaction with latent TGF-beta1, and activated TGF-beta1 signaling. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 48-53 31975462-3 2020 ch1 plants in low light exhibited a moderate activation of UPR genes, in particular bZIP60, and low concentrations of the UPR-inducer tunicamycin enhanced tolerance to photooxidative stress, together suggesting a role for UPR in plant acclimation to low 1 O2 levels. Tunicamycin 134-145 Pheophorbide a oxygenase family protein with Rieske 2Fe-2S domain-containing protein Arabidopsis thaliana 0-3 32504039-6 2020 FliI-KD cells treated with ER stress inducers, thapsigargin (TG), and tunicamycin exhibited activation of the unfolded protein response (UPR) and induction of UPR-related gene expression, which eventually triggered apoptosis. Tunicamycin 70-81 flightless I actin binding protein Mus musculus 0-4 32031621-8 2020 Tunicamycin elicited time-dependent increase in GRP78 protein levels, direct interaction with latent TGF-beta1, and activated TGF-beta1 signaling. Tunicamycin 0-11 transforming growth factor beta 1 Homo sapiens 101-110 32031621-8 2020 Tunicamycin elicited time-dependent increase in GRP78 protein levels, direct interaction with latent TGF-beta1, and activated TGF-beta1 signaling. Tunicamycin 0-11 transforming growth factor beta 1 Homo sapiens 126-135 32266019-5 2020 In the present study, RIPK1 was significantly downregulated in tunicamycin (TM)-induced ER stressed-human melanocytes. Tunicamycin 63-74 receptor interacting serine/threonine kinase 1 Homo sapiens 22-27 32266019-5 2020 In the present study, RIPK1 was significantly downregulated in tunicamycin (TM)-induced ER stressed-human melanocytes. Tunicamycin 76-78 receptor interacting serine/threonine kinase 1 Homo sapiens 22-27 32266019-9 2020 Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes. Tunicamycin 141-143 BCL2 associated X, apoptosis regulator Homo sapiens 58-61 32266019-9 2020 Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes. Tunicamycin 141-143 caspase 3 Homo sapiens 66-75 32266019-9 2020 Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes. Tunicamycin 141-143 BCL2 apoptosis regulator Homo sapiens 114-119 32295457-11 2020 Subsequently, B7-33 (100 nmol/L) reduced tunicamycin (2.5 mug/mL) induced upregulation of GRP78 in an extracellular signal-regulated kinase 1/2-dependent manner. Tunicamycin 41-52 heat shock protein 5 Mus musculus 90-95 32332695-3 2020 Here, we found that a pseudogene-derived lncRNA, Golgin A2 pseudogene 10 (GOLGA2P10), was frequently upregulated in HCC tissues and significantly elevated in hepatoma cells treated with ER stress inducers, such as tunicamycin and thapsigargin. Tunicamycin 214-225 GOLGA2 pseudogene 10 Homo sapiens 49-72 32332695-3 2020 Here, we found that a pseudogene-derived lncRNA, Golgin A2 pseudogene 10 (GOLGA2P10), was frequently upregulated in HCC tissues and significantly elevated in hepatoma cells treated with ER stress inducers, such as tunicamycin and thapsigargin. Tunicamycin 214-225 GOLGA2 pseudogene 10 Homo sapiens 74-83 32295457-11 2020 Subsequently, B7-33 (100 nmol/L) reduced tunicamycin (2.5 mug/mL) induced upregulation of GRP78 in an extracellular signal-regulated kinase 1/2-dependent manner. Tunicamycin 41-52 mitogen-activated protein kinase 3 Mus musculus 102-143 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 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 heat shock protein family A (Hsp70) member 4 Homo sapiens 135-140 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 171-228 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 unc-51 like autophagy activating kinase 1 Homo sapiens 372-376 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 autophagy related 13 Homo sapiens 381-386 32035621-6 2020 Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin. Tunicamycin 160-171 insulin Homo sapiens 0-7 32035621-6 2020 Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin. Tunicamycin 160-171 ribosomal protein S6 kinase B1 Homo sapiens 53-83 32035621-6 2020 Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin. Tunicamycin 160-171 ribosomal protein S6 kinase B1 Homo sapiens 85-92 32035621-6 2020 Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin. Tunicamycin 160-171 AKT serine/threonine kinase 1 Homo sapiens 98-127 32035621-6 2020 Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin. Tunicamycin 160-171 AKT serine/threonine kinase 1 Homo sapiens 129-133 32035621-7 2020 Notably, ATG13 and ULK1 deficiency ameliorated tunicamycin-induced insulin resistance, with enhanced RPS6KB1 and AKT1 phosphorylation in KO cells compared to WT cells. Tunicamycin 47-58 autophagy related 13 Homo sapiens 9-14 32035621-7 2020 Notably, ATG13 and ULK1 deficiency ameliorated tunicamycin-induced insulin resistance, with enhanced RPS6KB1 and AKT1 phosphorylation in KO cells compared to WT cells. Tunicamycin 47-58 unc-51 like autophagy activating kinase 1 Homo sapiens 19-23 32035621-7 2020 Notably, ATG13 and ULK1 deficiency ameliorated tunicamycin-induced insulin resistance, with enhanced RPS6KB1 and AKT1 phosphorylation in KO cells compared to WT cells. Tunicamycin 47-58 insulin Homo sapiens 67-74 32035621-8 2020 Although ULK1 and ATG13 are necessary for autophagy induction after tunicamycin-induced ER stress, autophagy does not seem to directly affect tunicamycin-induced cell death, ER stress, or insulin resistance. Tunicamycin 68-79 unc-51 like autophagy activating kinase 1 Homo sapiens 9-13 32035621-8 2020 Although ULK1 and ATG13 are necessary for autophagy induction after tunicamycin-induced ER stress, autophagy does not seem to directly affect tunicamycin-induced cell death, ER stress, or insulin resistance. Tunicamycin 68-79 autophagy related 13 Homo sapiens 18-23 32268491-3 2020 Here, we elucidated the mechanism of tunicamycin resistance in P-gp-positive cells. Tunicamycin 37-48 phosphoglycolate phosphatase Mus musculus 63-67 32268491-4 2020 We found that tunicamycin at a sublethal concentration of 0.1 microM induced retention of the cells in the G1 phase of the cell cycle only in the P-gp negative variant of L1210 cells. Tunicamycin 14-25 phosphoglycolate phosphatase Mus musculus 146-150 32205450-8 2020 SVB showed time-dependent induction after tunicamycin-induced ER stress, which depended on IRE1 and bZIP60 but not bZIP17 and bZIP28 in the unfolded protein response (UPR). Tunicamycin 42-53 basic region/leucine zipper motif 60 Arabidopsis thaliana 100-106 32268491-5 2020 P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein). Tunicamycin 143-154 phosphoglycolate phosphatase Mus musculus 0-4 32268491-5 2020 P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein). Tunicamycin 143-154 heat shock protein 5 Mus musculus 83-88 32268491-5 2020 P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein). Tunicamycin 143-154 heat shock protein 5 Mus musculus 89-92 32268491-5 2020 P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein). Tunicamycin 143-154 phosphoglycolate phosphatase Mus musculus 113-117 32268491-5 2020 P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein). Tunicamycin 143-154 DNA-damage inducible transcript 3 Mus musculus 186-190 32268491-5 2020 P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein). Tunicamycin 143-154 DNA-damage inducible transcript 3 Mus musculus 192-216 32268491-6 2020 Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle. Tunicamycin 97-108 phosphoglycolate phosphatase Mus musculus 30-34 32268491-6 2020 Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle. Tunicamycin 97-108 heat shock protein 5 Mus musculus 75-80 32268491-6 2020 Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle. Tunicamycin 97-108 heat shock protein 5 Mus musculus 81-84 32268491-6 2020 Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle. Tunicamycin 97-108 DNA-damage inducible transcript 3 Mus musculus 117-121 32268491-6 2020 Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle. Tunicamycin 145-156 phosphoglycolate phosphatase Mus musculus 30-34 32268491-6 2020 Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle. Tunicamycin 145-156 heat shock protein 5 Mus musculus 75-80 32268491-6 2020 Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle. Tunicamycin 145-156 heat shock protein 5 Mus musculus 81-84 32268491-7 2020 Taken together, these data suggest that the resistance of P-gp-positive cells to tunicamycin is due to increased levels of GRP78/BiP, which is overexpressed in both resistant variants of L1210 cells. Tunicamycin 81-92 phosphoglycolate phosphatase Mus musculus 58-62 32268491-7 2020 Taken together, these data suggest that the resistance of P-gp-positive cells to tunicamycin is due to increased levels of GRP78/BiP, which is overexpressed in both resistant variants of L1210 cells. Tunicamycin 81-92 heat shock protein 5 Mus musculus 123-128 32268491-7 2020 Taken together, these data suggest that the resistance of P-gp-positive cells to tunicamycin is due to increased levels of GRP78/BiP, which is overexpressed in both resistant variants of L1210 cells. Tunicamycin 81-92 heat shock protein 5 Mus musculus 129-132 32256145-6 2020 Our results demonstrate that PKR inhibition suppresses tunicamycin-mediated ER stress without altering the insulin production capacity of the cells. Tunicamycin 55-66 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 29-32 31904542-9 2020 The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P < 0.05). Tunicamycin 29-40 LOW QUALITY PROTEIN: X-box-binding protein 1 Larimichthys crocea 101-105 32057287-9 2020 The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner. Tunicamycin 27-38 heat shock protein 5 Mus musculus 53-58 32057287-9 2020 The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner. Tunicamycin 27-38 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 63-67 32057287-9 2020 The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner. Tunicamycin 40-42 heat shock protein 5 Mus musculus 53-58 32057287-9 2020 The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner. Tunicamycin 40-42 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 63-67 32057287-10 2020 Low dosage of TM abated LC3I expression, increased LC3II and Beclin1 expression, triggered ER stress and AM autophagy, and alleviated pathological changes of AMs in ALI mice. Tunicamycin 14-16 beclin 1, autophagy related Mus musculus 61-68 32057287-11 2020 Also, in ALI mice, low dosage of TM attenuated goblet cell proliferation of tracheal wall, and declined LW/BW ratio, ELGV, total cells and neutrophils, protein concentrations in BALF, and IL-6 and TNF-alpha expression in lung tissues and BALF. Tunicamycin 33-35 interleukin 6 Mus musculus 188-192 32057287-11 2020 Also, in ALI mice, low dosage of TM attenuated goblet cell proliferation of tracheal wall, and declined LW/BW ratio, ELGV, total cells and neutrophils, protein concentrations in BALF, and IL-6 and TNF-alpha expression in lung tissues and BALF. Tunicamycin 33-35 tumor necrosis factor Mus musculus 197-206 32268491-0 2020 Overexpression of GRP78/BiP in P-Glycoprotein-Positive L1210 Cells is Responsible for Altered Response of Cells to Tunicamycin as a Stressor of the Endoplasmic Reticulum. Tunicamycin 115-126 heat shock protein 5 Mus musculus 18-23 32268491-0 2020 Overexpression of GRP78/BiP in P-Glycoprotein-Positive L1210 Cells is Responsible for Altered Response of Cells to Tunicamycin as a Stressor of the Endoplasmic Reticulum. Tunicamycin 115-126 heat shock protein 5 Mus musculus 24-27 32268491-2 2020 However, we found previously that P-gp-positive sublines of L1210 murine leukemia cells (R and T) but not parental P-gp-negative parental cells (S) are resistant to the endoplasmic reticulum (ER) stressor tunicamycin (an N-glycosylation inhibitor). Tunicamycin 205-216 phosphoglycolate phosphatase Mus musculus 34-38 31940218-6 2020 Exposure of hASM to tunicamycin was used as a positive control. Tunicamycin 20-31 H19 imprinted maternally expressed transcript Homo sapiens 12-16 31940218-9 2020 We found that exposure of hASM cells to tunicamycin activated all three ER stress pathways. Tunicamycin 40-51 H19 imprinted maternally expressed transcript Homo sapiens 26-30 31904504-9 2020 Moreover, more than one-third of the cobalt-sensitive mutants were also sensitive to tunicamycin, and cobalt stress might induce the unfolded protein response (UPR) through serine/threonine kinase and endoribonuclease Ire1. Tunicamycin 85-96 bifunctional endoribonuclease/protein kinase IRE1 Saccharomyces cerevisiae S288C 218-222 31904542-9 2020 The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P < 0.05). Tunicamycin 29-40 tumor necrosis factor b (TNF superfamily, member 2) Larimichthys crocea 187-214 31904542-9 2020 The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P < 0.05). Tunicamycin 29-40 tumor necrosis factor b (TNF superfamily, member 2) Larimichthys crocea 216-224 31904542-9 2020 The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P < 0.05). Tunicamycin 29-40 interleukin-1 beta Larimichthys crocea 252-269 31904542-9 2020 The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P < 0.05). Tunicamycin 42-44 LOW QUALITY PROTEIN: X-box-binding protein 1 Larimichthys crocea 101-105 31904542-9 2020 The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P < 0.05). Tunicamycin 42-44 tumor necrosis factor b (TNF superfamily, member 2) Larimichthys crocea 187-214 31904542-9 2020 The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P < 0.05). Tunicamycin 42-44 tumor necrosis factor b (TNF superfamily, member 2) Larimichthys crocea 216-224 31904542-9 2020 The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P < 0.05). Tunicamycin 42-44 interleukin-1 beta Larimichthys crocea 252-269 31904542-10 2020 When KIRA6, the IRE1alpha kinase inhibitor, was used to block the IRE1alpha-XBP1s signaling pathway, the Tm and PA-induced pro-inflammatory genes expression was significantly suppressed (P < 0.05). Tunicamycin 105-107 LOW QUALITY PROTEIN: X-box-binding protein 1 Larimichthys crocea 76-80 32059483-6 2020 In response to TN- or isoproterenol-induced ER stress, mice deficient for SIRT1 exhibited suppressed autophagy along with exacerbated cardiac dysfunction. Tunicamycin 15-17 sirtuin 1 Mus musculus 74-79 31965068-11 2020 UCP1 mRNA expression in differentiated human white adipocytes was significantly reduced after incubation with thapsigargin, tunicamycin, homocysteine, TNF-alpha, or IL-beta, and significantly increased after incubation with exendin 4, dapagliflozin, and telmisartan. Tunicamycin 124-135 uncoupling protein 1 Homo sapiens 0-4 32086320-9 2020 GRP78 autoantigen expression was upregulated among human aortic endothelial cells (HAECs) stressed by incubation with tunicamycin (an unfolded protein response inducer) or exposure to culture media flow disturbances. Tunicamycin 118-129 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 169-202 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 204-208 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 heat shock protein family A (Hsp70) member 4 Homo sapiens 240-245 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 257-262 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 activating transcription factor 4 Homo sapiens 298-302 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 activating transcription factor 6 Homo sapiens 305-309 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 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 71-82 X-box binding protein 1 Homo sapiens 365-388 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 vitamin D receptor Homo sapiens 453-471 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 vitamin D receptor Homo sapiens 473-476 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 169-202 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 204-208 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 heat shock protein family A (Hsp70) member 4 Homo sapiens 240-245 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 257-262 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 activating transcription factor 4 Homo sapiens 298-302 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 activating transcription factor 6 Homo sapiens 305-309 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 32040528-4 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 X-box binding protein 1 Homo sapiens 365-388 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 vitamin D receptor Homo sapiens 453-471 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 vitamin D receptor Homo sapiens 473-476 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 activating transcription factor 4 Homo sapiens 109-113 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 activating transcription factor 6 Homo sapiens 115-119 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 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 131-136 32040528-6 2020 In addition, 1,25D3 (100 nM) antagonized the effect of TG (10 nM) and TM (1 mug/mL) on mRNA and protein levels of VDR and mRNA levels of genes involved in production and degradation of 1,25D3 in MCF-7 cells (P < 0.05). Tunicamycin 70-72 vitamin D receptor Homo sapiens 114-117 31926341-4 2020 PLK4 expression was dramatically reduced under ER stress induced by brefeldin A (BFA), tunicamycin (TM), or thapsigargin (TG) and down regulation of PLK4 expression was dependent on activating transcription factor 6 (ATF6) and CCAAT/enhancer-binding proteinbeta (C/EBPbeta). Tunicamycin 87-98 polo like kinase 4 Homo sapiens 0-4 31926341-4 2020 PLK4 expression was dramatically reduced under ER stress induced by brefeldin A (BFA), tunicamycin (TM), or thapsigargin (TG) and down regulation of PLK4 expression was dependent on activating transcription factor 6 (ATF6) and CCAAT/enhancer-binding proteinbeta (C/EBPbeta). Tunicamycin 100-102 polo like kinase 4 Homo sapiens 0-4 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 121-173 31563460-5 2020 Furthermore, CCL5 attenuated tunicamycin-induced endoplasmic reticulum (ER) stress signaling, and lipopolysaccharides-triggered inflammatory responses in pLE and pTr cells. Tunicamycin 29-40 C-C motif chemokine 5 Sus scrofa 13-17 31894252-7 2020 Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94). Tunicamycin 89-100 activating transcription factor 6 Homo sapiens 173-206 31894252-7 2020 Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94). Tunicamycin 89-100 X-box binding protein 1 Homo sapiens 252-275 31894252-7 2020 Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94). Tunicamycin 89-100 gastrin releasing peptide Homo sapiens 350-353 31894252-7 2020 Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94). Tunicamycin 89-100 eukaryotic translation initiation factor 2A Homo sapiens 380-423 31894252-7 2020 Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94). Tunicamycin 89-100 heat shock protein 90 beta family member 1 Homo sapiens 453-458 31837328-3 2020 The present study focuses on exploring the effects of CTCF on tunicamycin (TM)-induced endoplasmic reticulum (ER) stress, and investigating the underlying mechanisms. Tunicamycin 62-73 CCCTC-binding factor Homo sapiens 54-58 31837328-3 2020 The present study focuses on exploring the effects of CTCF on tunicamycin (TM)-induced endoplasmic reticulum (ER) stress, and investigating the underlying mechanisms. Tunicamycin 75-77 CCCTC-binding factor Homo sapiens 54-58 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 175-179 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 eukaryotic translation initiation factor 2A Homo sapiens 243-252 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 121-173 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 175-179 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 eukaryotic translation initiation factor 2A Homo sapiens 243-252 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 31974624-7 2020 Reverse transcription-quantitative PCR analysis demonstrated that TM promoted miR-421 expression in human melanocytes. Tunicamycin 66-68 microRNA 421 Homo sapiens 78-85 31974624-9 2020 RIPK1 expression was significantly downregulated in TM-induced human melanocytes. Tunicamycin 52-54 receptor interacting serine/threonine kinase 1 Homo sapiens 0-5 31974624-12 2020 In addition, the miR-421 inhibitor increased viability and reduced apoptosis in TM-treated melanocytes. Tunicamycin 80-82 microRNA 421 Homo sapiens 17-24 31974624-13 2020 Furthermore, all these effects of the miR-421 inhibitor on TM-induced human melanocytes were reversed by RIPK1-shRNA. Tunicamycin 59-61 microRNA 421 Homo sapiens 38-45 31974624-13 2020 Furthermore, all these effects of the miR-421 inhibitor on TM-induced human melanocytes were reversed by RIPK1-shRNA. Tunicamycin 59-61 receptor interacting serine/threonine kinase 1 Homo sapiens 105-110 31974624-14 2020 Further analyses revealed that the miR-421 inhibitor activated the phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin signaling pathway in TM-induced human melanocytes. Tunicamycin 161-163 microRNA 421 Homo sapiens 35-42 32259048-5 2020 Pharmacologic induction of UPR with tunicamycin (Tm)-stimulated RANKL expression in cultures of primary osteoblastic cells and in osteoblast and osteocyte cell lines. Tunicamycin 36-47 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 64-69 31834612-4 2020 IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays. Tunicamycin 122-133 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 0-9 31834612-4 2020 IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays. Tunicamycin 122-133 X-box binding protein 1 Mus musculus 50-54 31834612-4 2020 IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays. Tunicamycin 122-133 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 0-4 31834612-4 2020 IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays. Tunicamycin 135-137 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 0-9 31834612-4 2020 IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays. Tunicamycin 135-137 X-box binding protein 1 Mus musculus 50-54 31834612-4 2020 IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays. Tunicamycin 135-137 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 0-4 31834612-5 2020 However, cell viability and protein expression of other ER stress-responsive factors in the IRE1alpha-deficient cells were comparable to those in the parental wild-type cells with or without Tm treatment. Tunicamycin 191-193 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 92-101 31834612-10 2020 Co-treatment with KIRA6 and Tm induced LC3 II, cleaved caspase-9, and cleaved caspase-3; however, IRE1alpha-deficiency did not abolish the expression of these two cleaved caspases. Tunicamycin 28-30 caspase 9 Mus musculus 55-64 31834612-10 2020 Co-treatment with KIRA6 and Tm induced LC3 II, cleaved caspase-9, and cleaved caspase-3; however, IRE1alpha-deficiency did not abolish the expression of these two cleaved caspases. Tunicamycin 28-30 caspase 9 Mus musculus 171-179 31834612-11 2020 On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells. Tunicamycin 36-38 activating transcription factor 4 Mus musculus 47-51 31834612-11 2020 On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells. Tunicamycin 36-38 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 68-72 31834612-11 2020 On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells. Tunicamycin 36-38 activating transcription factor 4 Mus musculus 185-189 31834612-11 2020 On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells. Tunicamycin 130-132 caspase 9 Mus musculus 169-177 31834612-11 2020 On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells. Tunicamycin 130-132 activating transcription factor 4 Mus musculus 185-189 31978676-7 2020 RESULTS: Induction of ER stress in TM treated groups were confirmed by significantly increased mRNA and protein levels of GRP78. Tunicamycin 35-37 heat shock protein family A (Hsp70) member 5 Homo sapiens 122-127 31978676-10 2020 A significant increase was observed in C22-C24 CERs, C1P, caspase-3, caspase-12, NFkappaB1 mRNA and NF-kappaB p65 protein levels in cells treated with TM compared to controls. Tunicamycin 151-153 caspase 3 Homo sapiens 58-67 31978676-10 2020 A significant increase was observed in C22-C24 CERs, C1P, caspase-3, caspase-12, NFkappaB1 mRNA and NF-kappaB p65 protein levels in cells treated with TM compared to controls. Tunicamycin 151-153 nuclear factor kappa B subunit 1 Homo sapiens 81-90 31978676-10 2020 A significant increase was observed in C22-C24 CERs, C1P, caspase-3, caspase-12, NFkappaB1 mRNA and NF-kappaB p65 protein levels in cells treated with TM compared to controls. Tunicamycin 151-153 RELA proto-oncogene, NF-kB subunit Homo sapiens 100-113 31940720-9 2020 p-AMPK and FTO induced mild ER stress; however, tunicamycin-induced severe ER stress suppressed FTO expression and AMPK activation. Tunicamycin 48-59 fat mass and obesity associated Mus musculus 96-99 32259048-5 2020 Pharmacologic induction of UPR with tunicamycin (Tm)-stimulated RANKL expression in cultures of primary osteoblastic cells and in osteoblast and osteocyte cell lines. Tunicamycin 49-51 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 64-69 32259048-6 2020 Pharmacologic inhibition of the UPR blunted Tm-induced RANKL production. Tunicamycin 44-46 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 55-60 31548168-7 2020 RESULTS: Tunicamycin or d-galactosamine significantly induced ER stress and necroptosis, as well as eIF2alpha phosphorylation, in mice and LO2 cells (p<0.05). Tunicamycin 9-20 eukaryotic translation initiation factor 2A Mus musculus 100-109 31548168-11 2020 TNFR1 expression was reduced in d-galactosamine-treated mice (p<0.05) and cells incubated with tunicamycin for 12 and 24h (p<0.05). Tunicamycin 98-109 tumor necrosis factor receptor superfamily, member 1a Mus musculus 0-5 31919559-8 2020 The concomitant inflammation/metabolism TRN occurred similarly after acute LPS and tunicamycin challenges, in chronic mouse models and also in human liver diseases. Tunicamycin 83-94 transportin 1 Mus musculus 40-43 31630283-8 2020 In addition, FFAs induced phosphorylation of the p65 subunit of NF-kappaB was largely inhibited by pretreatment with tunicamycin in 3T3-L1 adipocytes. Tunicamycin 117-128 RELA proto-oncogene, NF-kB subunit Homo sapiens 49-73 31746423-10 2020 Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin. Tunicamycin 15-17 activating transcription factor 6 Homo sapiens 189-194 31746423-10 2020 Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin. Tunicamycin 15-17 activating transcription factor 4 Homo sapiens 196-200 31746423-10 2020 Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin. Tunicamycin 15-17 fibronectin 1 Homo sapiens 259-270 31746423-10 2020 Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin. Tunicamycin 15-17 vimentin Homo sapiens 272-280 31746423-10 2020 Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin. Tunicamycin 15-17 cadherin 2 Homo sapiens 312-327 32046379-10 2020 Overexpression of IRS1 significantly ameliorated palmitate- or tunicamycin-induced impairment of aromatase expression and estradiol generation. Tunicamycin 63-74 insulin receptor substrate 1 Mus musculus 18-22 31689235-8 2020 We further demonstrated that tunicamycin-induced ER stress in HepG2 cells led to increased p66Shc protein abundance, suggesting that ER stress may underlie the programmed effects observed in vivo. Tunicamycin 29-40 SHC adaptor protein 1 Rattus norvegicus 91-97 31566068-1 2020 Tunicamycins, which are nucleoside natural products, inhibit both bacterial phospho-N-acetylmuraminic acid (MurNAc)-pentapeptide translocase (MraY) and human UDP-N-acetylglucosamine (GlcNAc): polyprenol phosphate translocase (GPT). Tunicamycin 0-12 glutamic--pyruvic transaminase Homo sapiens 226-229 31834935-3 2019 Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor. Tunicamycin 119-130 lysine methyltransferase 2A Homo sapiens 283-286 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 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 caspase 12 Rattus norvegicus 141-151 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 erythropoietin Rattus norvegicus 261-264 31834935-3 2019 Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor. Tunicamycin 119-130 fms related receptor tyrosine kinase 3 Homo sapiens 336-340 31834935-3 2019 Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor. Tunicamycin 132-134 lysine methyltransferase 2A Homo sapiens 283-286 31834935-3 2019 Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor. Tunicamycin 132-134 fms related receptor tyrosine kinase 3 Homo sapiens 336-340 31861550-0 2019 Unification of Opposites between Two Antioxidant Transcription Factors Nrf1 and Nrf2 in Mediating Distinct Cellular Responses to the Endoplasmic Reticulum Stressor Tunicamycin. Tunicamycin 164-175 nuclear respiratory factor 1 Homo sapiens 71-75 31888113-6 2019 Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells. Tunicamycin 44-55 prostaglandin-endoperoxide synthase 2 Homo sapiens 95-111 31888113-6 2019 Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells. Tunicamycin 44-55 prostaglandin-endoperoxide synthase 2 Homo sapiens 113-118 31888113-6 2019 Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells. Tunicamycin 44-55 heat shock protein family A (Hsp70) member 5 Homo sapiens 151-156 31888113-6 2019 Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells. Tunicamycin 44-55 mitogen-activated protein kinase 14 Homo sapiens 193-196 31888113-6 2019 Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells. Tunicamycin 44-55 AKT serine/threonine kinase 1 Homo sapiens 207-210 31888113-8 2019 Consistent with the inhibition of COX-2 or p38 MAPK, copretreatment with TM and MLPE drastically recovered cytotoxicity and caspase-3 activation in the presence of DOX. Tunicamycin 73-75 prostaglandin-endoperoxide synthase 2 Homo sapiens 34-39 31888113-8 2019 Consistent with the inhibition of COX-2 or p38 MAPK, copretreatment with TM and MLPE drastically recovered cytotoxicity and caspase-3 activation in the presence of DOX. Tunicamycin 73-75 mitogen-activated protein kinase 14 Homo sapiens 43-46 31888113-8 2019 Consistent with the inhibition of COX-2 or p38 MAPK, copretreatment with TM and MLPE drastically recovered cytotoxicity and caspase-3 activation in the presence of DOX. Tunicamycin 73-75 caspase 3 Homo sapiens 124-133 31713417-6 2019 Additionally, using ERNB we evaluated CES2 regulation in DL-dithiothreitol (DTT) and tunicamycin-induced ER stress. Tunicamycin 85-96 carboxylesterase 2 Homo sapiens 38-42 31861550-0 2019 Unification of Opposites between Two Antioxidant Transcription Factors Nrf1 and Nrf2 in Mediating Distinct Cellular Responses to the Endoplasmic Reticulum Stressor Tunicamycin. Tunicamycin 164-175 NFE2 like bZIP transcription factor 2 Homo sapiens 80-84 31861550-3 2019 Herein, we report a unity of opposites between these two antioxidant transcription factors, Nrf1 and Nrf2, in coordinating distinct cellular responses to the ER stressor tunicamycin (TU). Tunicamycin 170-181 nuclear respiratory factor 1 Homo sapiens 92-96 31861550-3 2019 Herein, we report a unity of opposites between these two antioxidant transcription factors, Nrf1 and Nrf2, in coordinating distinct cellular responses to the ER stressor tunicamycin (TU). Tunicamycin 170-181 NFE2 like bZIP transcription factor 2 Homo sapiens 101-105 31861550-3 2019 Herein, we report a unity of opposites between these two antioxidant transcription factors, Nrf1 and Nrf2, in coordinating distinct cellular responses to the ER stressor tunicamycin (TU). Tunicamycin 183-185 nuclear respiratory factor 1 Homo sapiens 92-96 31861550-3 2019 Herein, we report a unity of opposites between these two antioxidant transcription factors, Nrf1 and Nrf2, in coordinating distinct cellular responses to the ER stressor tunicamycin (TU). Tunicamycin 183-185 NFE2 like bZIP transcription factor 2 Homo sapiens 101-105 31861550-4 2019 The TU-inducible transcription of Nrf1 and Nrf2, as well as GCLM (glutamate cysteine ligase modifier subunit) and HO-1 (heme oxygenase 1), was accompanied by activation of ER stress signaling networks. Tunicamycin 4-6 nuclear respiratory factor 1 Homo sapiens 34-38 31861550-4 2019 The TU-inducible transcription of Nrf1 and Nrf2, as well as GCLM (glutamate cysteine ligase modifier subunit) and HO-1 (heme oxygenase 1), was accompanied by activation of ER stress signaling networks. Tunicamycin 4-6 NFE2 like bZIP transcription factor 2 Homo sapiens 43-47 31861550-4 2019 The TU-inducible transcription of Nrf1 and Nrf2, as well as GCLM (glutamate cysteine ligase modifier subunit) and HO-1 (heme oxygenase 1), was accompanied by activation of ER stress signaling networks. Tunicamycin 4-6 glutamate-cysteine ligase modifier subunit Homo sapiens 60-64 31861550-4 2019 The TU-inducible transcription of Nrf1 and Nrf2, as well as GCLM (glutamate cysteine ligase modifier subunit) and HO-1 (heme oxygenase 1), was accompanied by activation of ER stress signaling networks. Tunicamycin 4-6 heme oxygenase 1 Homo sapiens 66-136 31861550-7 2019 Interestingly, Nrf1 glycosylation and its trans-activity to mediate the transcriptional expression of the 26S proteasomal subunits, were repressed by TU. Tunicamycin 150-152 nuclear respiratory factor 1 Homo sapiens 15-19 31861550-9 2019 Furthermore,&nbsp;caNrf2DeltaN also enhanced induction of PERK and IRE1 by TU, but reduced expression of ATF4 and HO-1. Tunicamycin 79-81 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 62-66 31861550-9 2019 Furthermore,&nbsp;caNrf2DeltaN also enhanced induction of PERK and IRE1 by TU, but reduced expression of ATF4 and HO-1. Tunicamycin 79-81 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 71-75 31861550-9 2019 Furthermore,&nbsp;caNrf2DeltaN also enhanced induction of PERK and IRE1 by TU, but reduced expression of ATF4 and HO-1. Tunicamycin 79-81 heme oxygenase 1 Homo sapiens 118-122 31861550-10 2019 Thus, it is inferred that such distinct roles of Nrf1 and Nrf2 are unified to maintain cell homeostasis by a series of coordinated ER-to-nuclear signaling responses to TU. Tunicamycin 168-170 nuclear respiratory factor 1 Homo sapiens 49-53 31861550-10 2019 Thus, it is inferred that such distinct roles of Nrf1 and Nrf2 are unified to maintain cell homeostasis by a series of coordinated ER-to-nuclear signaling responses to TU. Tunicamycin 168-170 NFE2 like bZIP transcription factor 2 Homo sapiens 58-62 31861550-13 2019 Interestingly, Nrf1 is more potent than Nrf2 at mediating the cytoprotective responses against the cytotoxicity of TU alone plus tBHQ (tert-butylhydroquinone). Tunicamycin 115-117 nuclear respiratory factor 1 Homo sapiens 15-19 31861550-13 2019 Interestingly, Nrf1 is more potent than Nrf2 at mediating the cytoprotective responses against the cytotoxicity of TU alone plus tBHQ (tert-butylhydroquinone). Tunicamycin 115-117 NFE2 like bZIP transcription factor 2 Homo sapiens 40-44 31138438-0 2019 MANF deletion abrogates early larval Caenorhabditis elegans stress response to tunicamycin and Pseudomonas aeruginosa. Tunicamycin 79-90 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 0-4 31787756-5 2019 The inhibition of PRMT1 augments tunicamycin (TN)-triggered ER stress response in cardiomyocytes while PRMT1 overexpression attenuates it. Tunicamycin 33-44 protein arginine methyltransferase 1 Homo sapiens 18-23 31787756-5 2019 The inhibition of PRMT1 augments tunicamycin (TN)-triggered ER stress response in cardiomyocytes while PRMT1 overexpression attenuates it. Tunicamycin 46-48 protein arginine methyltransferase 1 Homo sapiens 18-23 31138438-6 2019 Surprisingly, larval growth arrest observed in wild-type nematodes reared on tunicamycin is completely prevented in the manf-1 (tm3603) mutant. Tunicamycin 77-88 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 120-124 31138438-7 2019 Transcriptional microarray analysis revealed that manf-1 mutant L1 larvae exhibit a novel modulation of innate immunity genes in response to tunicamycin. Tunicamycin 141-152 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 50-54 31721015-5 2019 Notably, UFL1 expression in BMECs was increased by endoplasmic reticulum (ER) stress induced by treatment with tunicamycin (TM). Tunicamycin 111-122 UFM1 specific ligase 1 Bos taurus 9-13 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Tunicamycin 149-160 fms related receptor tyrosine kinase 3 Homo sapiens 23-27 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Tunicamycin 149-160 fms related receptor tyrosine kinase 3 Homo sapiens 124-128 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Tunicamycin 149-160 fms related receptor tyrosine kinase 3 Homo sapiens 124-128 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Tunicamycin 149-160 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 226-231 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Tunicamycin 149-160 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 281-286 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Tunicamycin 149-160 fms related receptor tyrosine kinase 3 Homo sapiens 124-128 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Tunicamycin 149-160 heat shock protein 90 alpha family class A member 1 Homo sapiens 311-316 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Tunicamycin 149-160 fms related receptor tyrosine kinase 3 Homo sapiens 124-128 31604108-9 2019 KEY FINDING: TG or TM induced H9c2 cell injury and ER-phagy and upregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation, and expression of ATF4, Beclin 1, and LC3B-II compared with control cells. Tunicamycin 19-21 calreticulin Rattus norvegicus 76-79 31604108-9 2019 KEY FINDING: TG or TM induced H9c2 cell injury and ER-phagy and upregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation, and expression of ATF4, Beclin 1, and LC3B-II compared with control cells. Tunicamycin 19-21 NFE2 like bZIP transcription factor 2 Rattus norvegicus 114-118 31604108-9 2019 KEY FINDING: TG or TM induced H9c2 cell injury and ER-phagy and upregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation, and expression of ATF4, Beclin 1, and LC3B-II compared with control cells. Tunicamycin 19-21 activating transcription factor 4 Rattus norvegicus 160-164 31604108-9 2019 KEY FINDING: TG or TM induced H9c2 cell injury and ER-phagy and upregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation, and expression of ATF4, Beclin 1, and LC3B-II compared with control cells. Tunicamycin 19-21 beclin 1 Rattus norvegicus 166-174 31604108-10 2019 Treatment with ERS inhibitors decreased TG- or TM-induced ER-phagy, downregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation and the expression of ATF4, Beclin 1 and LC3B-II. Tunicamycin 47-49 activating transcription factor 4 Rattus norvegicus 169-173 31604108-10 2019 Treatment with ERS inhibitors decreased TG- or TM-induced ER-phagy, downregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation and the expression of ATF4, Beclin 1 and LC3B-II. Tunicamycin 47-49 beclin 1 Rattus norvegicus 175-183 31604108-11 2019 Moreover, a Nrf2 inhibitor downregulated the expression of ATF4, Beclin 1 and LC3B-II and alleviated TG- or TM-induced ER-phagy and H9c2 cell injury. Tunicamycin 108-110 NFE2 like bZIP transcription factor 2 Rattus norvegicus 12-16 31604108-11 2019 Moreover, a Nrf2 inhibitor downregulated the expression of ATF4, Beclin 1 and LC3B-II and alleviated TG- or TM-induced ER-phagy and H9c2 cell injury. Tunicamycin 108-110 activating transcription factor 4 Rattus norvegicus 59-63 31619316-5 2019 NOD2 deficiency increased ER stress-induced cell death and expression levels of apoptosis mediators (cleaved caspase-3, Bax, and Bak) in VSMCs in the presence of tunicamycin (TM), an ER stress inducer. Tunicamycin 162-173 nucleotide-binding oligomerization domain containing 2 Mus musculus 0-4 31619316-5 2019 NOD2 deficiency increased ER stress-induced cell death and expression levels of apoptosis mediators (cleaved caspase-3, Bax, and Bak) in VSMCs in the presence of tunicamycin (TM), an ER stress inducer. Tunicamycin 175-177 nucleotide-binding oligomerization domain containing 2 Mus musculus 0-4 31619316-5 2019 NOD2 deficiency increased ER stress-induced cell death and expression levels of apoptosis mediators (cleaved caspase-3, Bax, and Bak) in VSMCs in the presence of tunicamycin (TM), an ER stress inducer. Tunicamycin 175-177 BCL2-antagonist/killer 1 Mus musculus 129-132 31619316-9 2019 Taken together, these data suggest that the induction of ER stress through NOD2 expression can protect against TM-induced cell death in VSMCs. Tunicamycin 111-113 nucleotide-binding oligomerization domain containing 2 Mus musculus 75-79 31721015-5 2019 Notably, UFL1 expression in BMECs was increased by endoplasmic reticulum (ER) stress induced by treatment with tunicamycin (TM). Tunicamycin 124-126 UFM1 specific ligase 1 Bos taurus 9-13 31721015-6 2019 ER stress-related gene expression was further increased in UFL1 knockdown cells upon TM treatment. Tunicamycin 85-87 UFM1 specific ligase 1 Bos taurus 59-63 31315072-11 2019 A further in vivo analysis showed that Suhuang-driven pharmacological inactivation of NLRP3 inflammasome and amelioration of pulmonary dysfunction were reversed by an ER stress inducer tunicamycin, well confirming the beneficial effects of Suhuang on pulmonary function by regulation of ER stress. Tunicamycin 185-196 NLR family pyrin domain containing 3 Homo sapiens 86-91 31504391-5 2019 Enhanced susceptibility to tunicamycin-induced ER stress was observed in AtT-20/PC2 cell clones in which murine PC1/3 was replaced by human N221D PC1/3, as compared to wild-type human PC1/3. Tunicamycin 27-38 proprotein convertase subtilisin/kexin type 2 Mus musculus 80-83 31504391-5 2019 Enhanced susceptibility to tunicamycin-induced ER stress was observed in AtT-20/PC2 cell clones in which murine PC1/3 was replaced by human N221D PC1/3, as compared to wild-type human PC1/3. Tunicamycin 27-38 proprotein convertase subtilisin/kexin type 1 Mus musculus 112-117 31504391-5 2019 Enhanced susceptibility to tunicamycin-induced ER stress was observed in AtT-20/PC2 cell clones in which murine PC1/3 was replaced by human N221D PC1/3, as compared to wild-type human PC1/3. Tunicamycin 27-38 proprotein convertase subtilisin/kexin type 1 Homo sapiens 146-151 31504391-5 2019 Enhanced susceptibility to tunicamycin-induced ER stress was observed in AtT-20/PC2 cell clones in which murine PC1/3 was replaced by human N221D PC1/3, as compared to wild-type human PC1/3. Tunicamycin 27-38 proprotein convertase subtilisin/kexin type 1 Homo sapiens 146-151 31889041-7 2019 Levels of cleaved caspase-12 were significantly decreased in the thapsigargin- or tunicamycin-4-PBA combination treatments. Tunicamycin 82-93 caspase 12 Rattus norvegicus 18-28 31291699-3 2019 Full-length CREB3 detected under resting conditions disappeared following treatment with tunicamycin, brefeldin A and nigericin. Tunicamycin 89-100 cAMP responsive element binding protein 3 Homo sapiens 12-17 31889041-8 2019 Therefore, whether melatonin regulates the amylin expression/oligomerization in thapsigargin- or tunicamycin-combined with Bafilomycin A1 (autophagy inhibitor) or MG132 (proteasome inhibitor) treatments were investigated. Tunicamycin 97-108 islet amyloid polypeptide Rattus norvegicus 43-49 31889041-9 2019 Amylin expression/oligomerization with melatonin treatment was significantly decreased in the thapsigargin- or tunicamycin-combined Bafilomycin A1 or MG132 treatments. Tunicamycin 111-122 islet amyloid polypeptide Rattus norvegicus 0-6 31430074-0 2019 Renal response to tunicamycin-induced endoplasmic reticulum stress in BDNF heterozygous mice. Tunicamycin 18-29 brain derived neurotrophic factor Mus musculus 70-74 31521187-4 2019 RESULTS: We found that hyl1 mutant plants are more sensitive to tunicamycin, an inhibitor of N-linked glycosylation that causes ER stress than wild-type plants. Tunicamycin 64-75 dsRNA-binding domain-like superfamily protein Arabidopsis thaliana 23-27 31430074-2 2019 OBJECTIVES: The aim of this study was to determine whether endogenously produced BDNF protects the kidneys against tunicamycin-induced (Tm) ER stress. Tunicamycin 115-126 brain derived neurotrophic factor Mus musculus 81-85 30861618-7 2019 Based on the docking calculations, top hit compounds were identified to disrupt both Keap1a and Keap1b interaction with Nrf2 which include quercetin 3,4"-diglucoside, flavin adenine dinucleotide disodium salt hydrate, salvianolic acid A, tunicamycin and esculin. Tunicamycin 238-249 kelch-like ECH-associated protein 1a Danio rerio 85-91 30861618-7 2019 Based on the docking calculations, top hit compounds were identified to disrupt both Keap1a and Keap1b interaction with Nrf2 which include quercetin 3,4"-diglucoside, flavin adenine dinucleotide disodium salt hydrate, salvianolic acid A, tunicamycin and esculin. Tunicamycin 238-249 kelch-like ECH-associated protein 1b Danio rerio 96-102 30861618-7 2019 Based on the docking calculations, top hit compounds were identified to disrupt both Keap1a and Keap1b interaction with Nrf2 which include quercetin 3,4"-diglucoside, flavin adenine dinucleotide disodium salt hydrate, salvianolic acid A, tunicamycin and esculin. Tunicamycin 238-249 nfe2 like bZIP transcription factor 2a Danio rerio 120-124 30854665-6 2019 High-throughput sequencing analysis identified miR-23a-3p as one of the most abundant microRNAs in exosomes derived from tunicamycin (TM)-treated HCC cells (Exo-TMs). Tunicamycin 121-132 microRNA 23a Homo sapiens 47-54 30280512-4 2019 The greater growth inhibition in VAMP721/722-deficient plants, induced by tunicamycin, suggests that plants under ER stress maintain physiological homeostasis, at least in part, by regulating VAMP721/722 levels, as VAMP721/722 are known to participate in various biological processes. Tunicamycin 74-85 vesicle-associated membrane protein 721 Arabidopsis thaliana 33-40 30280512-4 2019 The greater growth inhibition in VAMP721/722-deficient plants, induced by tunicamycin, suggests that plants under ER stress maintain physiological homeostasis, at least in part, by regulating VAMP721/722 levels, as VAMP721/722 are known to participate in various biological processes. Tunicamycin 74-85 vesicle-associated membrane protein 721 Arabidopsis thaliana 192-199 30280512-4 2019 The greater growth inhibition in VAMP721/722-deficient plants, induced by tunicamycin, suggests that plants under ER stress maintain physiological homeostasis, at least in part, by regulating VAMP721/722 levels, as VAMP721/722 are known to participate in various biological processes. Tunicamycin 74-85 vesicle-associated membrane protein 721 Arabidopsis thaliana 192-199 31108175-12 2019 It indicated that the rIL-6 can significantly alleviate autophagy induced by Tm. Tunicamycin 77-79 interleukin 6 Rattus norvegicus 22-27 31001857-4 2019 Through systematic screening of FAD mutants, we found that a mutant of FAD2 resulted in a hypersensitive response to tunicamycin, a chemical inducer of ER stress. Tunicamycin 117-128 fatty acid desaturase 2 Arabidopsis thaliana 71-75 31001857-7 2019 Moreover, glycerolipid profiling of both mutants and overexpressors of FAD2 under tunicamycin-induced ER stress conditions, along with phenotypic screening of the mutants of the FAD family, suggested that the ratio of monounsaturated fatty acids to polyunsaturated fatty acids, particularly 18:1 to 18:2 species, may be an important factor in allowing the ER membrane to cope with ER stress. Tunicamycin 82-93 fatty acid desaturase 2 Arabidopsis thaliana 71-75 31167779-6 2019 In this study, we show that the ER stress inducers tunicamycin and thapsigargin lead to the activation of PKD1 in human prostate cancer PC-3 cells and in hepatoma HepG2 cells through a PKCdelta-dependent mechanism. Tunicamycin 51-62 protein kinase D1 Homo sapiens 106-110 30653687-7 2019 mGPDH deletion exacerbated tunicamycin (ER stress inducer)-induced hepatic steatosis, whereas tauroursodeoxycholic acid (ER stress inhibitor) rescued mGPDH depletion-induced steatosis on an HFD. Tunicamycin 27-38 glycerol phosphate dehydrogenase 2, mitochondrial Mus musculus 0-5 30664704-7 2019 Infusion of ER stress inducer (tunicamycin, Tun) in control mice induced ER stress in MRA and reduced phosphorylation of AMPK, eNOS synthase phosphorylation, and EDR in MRA without affecting systolic blood pressure (SBP). Tunicamycin 31-42 nitric oxide synthase 3, endothelial cell Mus musculus 127-131 31534165-7 2019 Tg and Tunicamycin strongly reduced neurosphere forming ability of GSCs that was linked with potent PERK-dependent downregulation of SOX2 protein. Tunicamycin 7-18 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 100-104 31534165-7 2019 Tg and Tunicamycin strongly reduced neurosphere forming ability of GSCs that was linked with potent PERK-dependent downregulation of SOX2 protein. Tunicamycin 7-18 SRY-box transcription factor 2 Homo sapiens 133-137 31336877-0 2019 Tunicamycin Sensitivity-Suppression by High Gene Dosage Reveals New Functions of the Yeast Hog1 MAP Kinase. Tunicamycin 0-11 mitogen-activated protein kinase HOG1 Saccharomyces cerevisiae S288C 91-95 31183612-5 2019 In cells treated with tunicamycin, resveratrol increased the expression of clusterin mRNA and protein and the secreted clusterin protein level in conditioned medium. Tunicamycin 22-33 clusterin Homo sapiens 75-84 31183612-5 2019 In cells treated with tunicamycin, resveratrol increased the expression of clusterin mRNA and protein and the secreted clusterin protein level in conditioned medium. Tunicamycin 22-33 clusterin Homo sapiens 119-128 31183612-6 2019 Resveratrol decreased protein expression of the ER stress markers, p-PERK, p-IRE1alpha, and CHOP, and increased the expression of the ER-associated degradation (ERAD) factors, SEL1L and HRD1, in tunicamycin-treated cells. Tunicamycin 195-206 SEL1L adaptor subunit of ERAD E3 ubiquitin ligase Homo sapiens 176-181 31183612-6 2019 Resveratrol decreased protein expression of the ER stress markers, p-PERK, p-IRE1alpha, and CHOP, and increased the expression of the ER-associated degradation (ERAD) factors, SEL1L and HRD1, in tunicamycin-treated cells. Tunicamycin 195-206 synoviolin 1 Homo sapiens 186-190 30912977-6 2019 SSC-linked NRG1 clusters were severely disrupted in acutely stressed MNs and after tunicamycin-induced ER stress. Tunicamycin 83-94 neuregulin 1 Mus musculus 11-15 30977402-6 2019 Tunicamycin increased the expression of PERK, leading to Nrf2 nuclear import, and tauroursodeoxycholate suppressed Nrf2 activation through PERK during ER stress, indicating that PERK activation is required for Nrf2 nuclear entry. Tunicamycin 0-11 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 40-44 30977402-6 2019 Tunicamycin increased the expression of PERK, leading to Nrf2 nuclear import, and tauroursodeoxycholate suppressed Nrf2 activation through PERK during ER stress, indicating that PERK activation is required for Nrf2 nuclear entry. Tunicamycin 0-11 nuclear factor, erythroid derived 2, like 2 Mus musculus 57-61 31243264-6 2019 We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis. Tunicamycin 101-112 heat shock protein family A (Hsp70) member 5 Homo sapiens 38-43 30417358-4 2019 Thus, in the present study, we aimed to investigate the effects of A2aR activation in MIN6 beta cells undergoing tunicamycin (TM)-mediated ER stress. Tunicamycin 113-124 adenosine A2a receptor Mus musculus 67-71 30417358-4 2019 Thus, in the present study, we aimed to investigate the effects of A2aR activation in MIN6 beta cells undergoing tunicamycin (TM)-mediated ER stress. Tunicamycin 126-128 adenosine A2a receptor Mus musculus 67-71 30417358-13 2019 Altogether, the present study revealed that A2aR signaling through PKA/Akt/CREB mediators alleviated TM cytotoxicity effects in MIN6 beta cells. Tunicamycin 101-103 adenosine A2a receptor Mus musculus 44-48 30417358-13 2019 Altogether, the present study revealed that A2aR signaling through PKA/Akt/CREB mediators alleviated TM cytotoxicity effects in MIN6 beta cells. Tunicamycin 101-103 thymoma viral proto-oncogene 1 Mus musculus 71-74 30417358-13 2019 Altogether, the present study revealed that A2aR signaling through PKA/Akt/CREB mediators alleviated TM cytotoxicity effects in MIN6 beta cells. Tunicamycin 101-103 cAMP responsive element binding protein 1 Mus musculus 75-79 31243264-6 2019 We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis. Tunicamycin 101-112 secreted protein acidic and cysteine rich Homo sapiens 48-53 31243264-6 2019 We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis. Tunicamycin 101-112 heat shock protein family A (Hsp70) member 5 Homo sapiens 145-150 31275960-6 2019 In addition, our findings demonstrated that IRE1 and HAC1 (two upstream modulators of the UPR) are required for the survival of gas1Delta yeast cells under the tunicamycin stress. Tunicamycin 160-171 bifunctional endoribonuclease/protein kinase IRE1 Saccharomyces cerevisiae S288C 44-48 31293572-3 2019 Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered. Tunicamycin 0-11 colony stimulating factor 1 (macrophage) Mus musculus 83-88 31293572-3 2019 Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered. Tunicamycin 0-11 interleukin 12b Mus musculus 216-223 31293572-3 2019 Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered. Tunicamycin 0-11 interleukin 12a Mus musculus 228-235 31293572-3 2019 Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered. Tunicamycin 0-11 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 267-273 31293572-3 2019 Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered. Tunicamycin 13-15 colony stimulating factor 1 (macrophage) Mus musculus 83-88 31293572-3 2019 Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered. Tunicamycin 13-15 interleukin 12b Mus musculus 216-223 31293572-3 2019 Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered. Tunicamycin 13-15 interleukin 12a Mus musculus 228-235 31293572-3 2019 Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered. Tunicamycin 13-15 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 267-273 31281585-6 2019 In vitro, ZYZ-803 ameliorates ERS-related necroptosis induced by tunicamycin, and such effect has been depending on the receptor-interacting protein 3- (RIP3-) Ca2+-calmodulin-dependent protein kinase (CaMKII) signaling pathway. Tunicamycin 65-76 receptor interacting serine/threonine kinase 3 Homo sapiens 120-200 30154447-9 2019 Importantly, these drugs also included ER stress-inducing agents, such as thapsigargin and tunicamycin, a form of cell death for which a critical pro-apoptotic function of caspase-12 has previously been reported. Tunicamycin 91-102 caspase 12 Mus musculus 172-182 31109102-7 2019 Selenate and tunicamycin (Tm) treatment were used to induce SELENOF up-regulation. Tunicamycin 13-24 selenoprotein F Homo sapiens 60-67 31109102-7 2019 Selenate and tunicamycin (Tm) treatment were used to induce SELENOF up-regulation. Tunicamycin 26-28 selenoprotein F Homo sapiens 60-67 30926605-0 2019 The kinase PERK and the transcription factor ATF4 play distinct and essential roles in autophagy resulting from tunicamycin-induced ER stress. Tunicamycin 112-123 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 11-15 30926605-0 2019 The kinase PERK and the transcription factor ATF4 play distinct and essential roles in autophagy resulting from tunicamycin-induced ER stress. Tunicamycin 112-123 activating transcription factor 4 Homo sapiens 45-49 30926605-4 2019 By analyzing the flux of LC3 through the autophagic pathway, as well as the sequestration and degradation of autophagic cargo, we here conclusively show that the classical ER stressor tunicamycin (TM) enhances autophagic activity in mammalian cells. Tunicamycin 184-195 microtubule associated protein 1 light chain 3 alpha Homo sapiens 25-28 30926605-4 2019 By analyzing the flux of LC3 through the autophagic pathway, as well as the sequestration and degradation of autophagic cargo, we here conclusively show that the classical ER stressor tunicamycin (TM) enhances autophagic activity in mammalian cells. Tunicamycin 197-199 microtubule associated protein 1 light chain 3 alpha Homo sapiens 25-28 31275960-6 2019 In addition, our findings demonstrated that IRE1 and HAC1 (two upstream modulators of the UPR) are required for the survival of gas1Delta yeast cells under the tunicamycin stress. Tunicamycin 160-171 transcription factor HAC1 Saccharomyces cerevisiae S288C 53-57 31275960-7 2019 On the other hand, we provided evidence that the GAS1 overexpression caused an obvious sensitivity to the low-tunicamycin-concentration (0.25 mug/mL). Tunicamycin 110-121 1,3-beta-glucanosyltransferase GAS1 Saccharomyces cerevisiae S288C 49-53 30753838-3 2019 Here we report that ZBTB7A functions as an important prosurvival factor in osteosarcoma cells undergoing pharmacological ER stress-induced by tunicamycin (TM) or thapsigargin (TG). Tunicamycin 142-153 zinc finger and BTB domain containing 7A Homo sapiens 20-26 31071981-6 2019 Inducing ER stress with tunicamycin activated the Wnt/beta-catenin pathway, whereas reducing ER stress with 4-phenylbutyric acid inhibited it. Tunicamycin 24-35 catenin beta 1 Homo sapiens 54-66 30336657-3 2019 METHODS: In primary human nasal epithelial cells, the effect of tunicamycin (an ER stress inducer) and 4-phenylbutyric acid (4-PBA, ER stress inhibitor) on the expression of MUC5AC and MUC5B was investigated by reverse transcriptase-polymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassay, and immunoblot analysis. Tunicamycin 64-75 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 174-180 30336657-3 2019 METHODS: In primary human nasal epithelial cells, the effect of tunicamycin (an ER stress inducer) and 4-phenylbutyric acid (4-PBA, ER stress inhibitor) on the expression of MUC5AC and MUC5B was investigated by reverse transcriptase-polymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassay, and immunoblot analysis. Tunicamycin 64-75 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 185-190 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 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 50-56 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 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 61-66 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 X-box binding protein 1 Homo sapiens 152-175 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 X-box binding protein 1 Homo sapiens 177-182 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 30336657-5 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 activating transcription factor 6 Homo sapiens 268-272 30336657-6 2019 In addition, 4-PBA attenuated the tunicamycin-induced expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules. Tunicamycin 34-45 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 69-75 30336657-6 2019 In addition, 4-PBA attenuated the tunicamycin-induced expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules. Tunicamycin 34-45 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 80-85 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 X-box binding protein 1 Homo sapiens 33-38 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 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 activating transcription factor 6 Homo sapiens 50-54 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 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 136-142 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 mucin 5B, oligomeric mucus/gel-forming Homo sapiens 147-152 30824472-6 2019 Our results suggest that sphingolipid/Pkh1/2-TORC1/Sch9 signaling is an important determinant for adaptation to tunicamycin-induced stress. Tunicamycin 112-123 serine/threonine protein kinase SCH9 Saccharomyces cerevisiae S288C 51-55 30894460-3 2019 Treatment with the ER stress inducer tunicamycin resulted in the splicing of a 32-nucleotide fragment of a basic leucine zipper 1 (bZIP1) transcription factor (CrbZIP1) mRNA by CrIRE1 that, in turn, resulted in the loss of the transmembrane domain in CrbZIP1, and the translocation of CrbZIP1 from the ER to the nucleus. Tunicamycin 37-48 uncharacterized protein Chlamydomonas reinhardtii 177-183 30703445-5 2019 The ER stress activators thapsigargin (Tg) and tunicamycin (Tm) markedly reduced Bmal1-Luc oscillation amplitudes and induced phase delay shifts in NIH3T3 cells. Tunicamycin 47-58 aryl hydrocarbon receptor nuclear translocator-like Mus musculus 81-86 30703445-5 2019 The ER stress activators thapsigargin (Tg) and tunicamycin (Tm) markedly reduced Bmal1-Luc oscillation amplitudes and induced phase delay shifts in NIH3T3 cells. Tunicamycin 60-62 aryl hydrocarbon receptor nuclear translocator-like Mus musculus 81-86 30711450-6 2019 Recombinant CCL21 improved pTr and pLE cell proliferation through activation of the PI3K and MAPK pathways and suppression of tunicamycin-induced endoplasmic reticulum (ER) stress or LPS-induced inflammation. Tunicamycin 126-137 C-C motif chemokine ligand 21 Sus scrofa 12-17 30824472-0 2019 Sphingolipid/Pkh1/2-TORC1/Sch9 Signaling Regulates Ribosome Biogenesis in Tunicamycin-Induced Stress Response in Yeast. Tunicamycin 74-85 serine/threonine protein kinase PKH1 Saccharomyces cerevisiae S288C 13-19 30824472-0 2019 Sphingolipid/Pkh1/2-TORC1/Sch9 Signaling Regulates Ribosome Biogenesis in Tunicamycin-Induced Stress Response in Yeast. Tunicamycin 74-85 serine/threonine protein kinase SCH9 Saccharomyces cerevisiae S288C 26-30 30824472-3 2019 Here, we describe a novel regulatory model, in which tunicamycin-mediated stress induces the accumulation of long-chain sphingoid bases and subsequent activation of Pkh1/2 signaling, which leads to decreased expression of ribosomal protein genes via the downstream effectors Pkc1 and Sch9. Tunicamycin 53-64 serine/threonine protein kinase PKH1 Saccharomyces cerevisiae S288C 165-171 30824472-3 2019 Here, we describe a novel regulatory model, in which tunicamycin-mediated stress induces the accumulation of long-chain sphingoid bases and subsequent activation of Pkh1/2 signaling, which leads to decreased expression of ribosomal protein genes via the downstream effectors Pkc1 and Sch9. Tunicamycin 53-64 protein kinase C Saccharomyces cerevisiae S288C 275-279 30824472-3 2019 Here, we describe a novel regulatory model, in which tunicamycin-mediated stress induces the accumulation of long-chain sphingoid bases and subsequent activation of Pkh1/2 signaling, which leads to decreased expression of ribosomal protein genes via the downstream effectors Pkc1 and Sch9. Tunicamycin 53-64 serine/threonine protein kinase SCH9 Saccharomyces cerevisiae S288C 284-288 30824472-6 2019 Our results suggest that sphingolipid/Pkh1/2-TORC1/Sch9 signaling is an important determinant for adaptation to tunicamycin-induced stress. Tunicamycin 112-123 serine/threonine protein kinase PKH1 Saccharomyces cerevisiae S288C 38-44 30753838-3 2019 Here we report that ZBTB7A functions as an important prosurvival factor in osteosarcoma cells undergoing pharmacological ER stress-induced by tunicamycin (TM) or thapsigargin (TG). Tunicamycin 155-157 zinc finger and BTB domain containing 7A Homo sapiens 20-26 30979007-5 2019 Significant changes in gene and protein expression were found upon tunicamycin treatment for CB1 and CB2, as well as for GPR55 receptors, but not for transient receptor potential vanilloid 1 (TRPV1). Tunicamycin 67-78 cannabinoid receptor 2 Homo sapiens 101-104 30979007-6 2019 Deglycosylation experiments with N-glycosidase-F and immunoblot of cell membranes derived from SH-SY5Y cells confirmed the presence of one glycosylated form in CB1 (70 kDa), that was reduced by tunicamycin. Tunicamycin 194-205 cannabinoid receptor 1 Homo sapiens 160-163 30979007-5 2019 Significant changes in gene and protein expression were found upon tunicamycin treatment for CB1 and CB2, as well as for GPR55 receptors, but not for transient receptor potential vanilloid 1 (TRPV1). Tunicamycin 67-78 cannabinoid receptor 1 Homo sapiens 93-96 30979007-7 2019 Morphological studies demonstrated the co-localization of CB1 with GlcNAc residues, and showed that tunicamycin reduced CB1 membrane expression with a marked nuclear localization, as confirmed by immunoblotting. Tunicamycin 100-111 cannabinoid receptor 1 Homo sapiens 120-123 30238980-8 2019 Furthermore, tunicamycin-induced endoplasmic reticulum (ER) stress was inactivated by ephrin A1 treatment of BEND cells. Tunicamycin 13-24 ephrin A1 Bos taurus 86-95 30953513-5 2019 In vitro, tunicamycin treatment and genetic tools were used to produce non-glycosylated and lowly glycosylated CD147. Tunicamycin 10-21 basigin (Ok blood group) Homo sapiens 111-116 31508171-3 2019 In our study, 3T3-L1 adipocytes were pre-treated with ERS inhibitors tauroursodeoxycholic acid (TUDCA), Ex-4 and an ERS inducer tunicamycin (TM) then induced insulin resistance. Tunicamycin 128-139 insulin Homo sapiens 158-165 31508171-3 2019 In our study, 3T3-L1 adipocytes were pre-treated with ERS inhibitors tauroursodeoxycholic acid (TUDCA), Ex-4 and an ERS inducer tunicamycin (TM) then induced insulin resistance. Tunicamycin 141-143 insulin Homo sapiens 158-165 30680482-0 2019 NF-kappaB contributes to Smac mimetic-conferred protection from tunicamycin-induced apoptosis. Tunicamycin 64-75 nuclear factor kappa B subunit 1 Homo sapiens 0-9 30680482-0 2019 NF-kappaB contributes to Smac mimetic-conferred protection from tunicamycin-induced apoptosis. Tunicamycin 64-75 diablo IAP-binding mitochondrial protein Homo sapiens 25-29 30680482-2 2019 Here, we report that Smac mimetic-mediated activation of NF-kappaB contributes to the rescue of cancer cells from tunicamycin (TM)-triggered apoptosis. Tunicamycin 114-125 diablo IAP-binding mitochondrial protein Homo sapiens 21-25 30680482-2 2019 Here, we report that Smac mimetic-mediated activation of NF-kappaB contributes to the rescue of cancer cells from tunicamycin (TM)-triggered apoptosis. Tunicamycin 114-125 nuclear factor kappa B subunit 1 Homo sapiens 57-66 30784934-4 2019 Morin downregulated the expression of GRP78, central regulator of ER stress response, induced by ER stress inducer tunicamycin. Tunicamycin 115-126 heat shock protein family A (Hsp70) member 5 Homo sapiens 38-43 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 143-148 30914711-5 2019 Moreover, PSP/reg expression is induced by the canonical chemical inducers of ER stress, tunicamycin and thapsigargin. Tunicamycin 89-100 regenerating family member 1 alpha Homo sapiens 14-17 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 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 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 161-165 30615971-4 2019 Upon incubation of Lcn2-/- and wild type (wt) primary hepatocytes with tunicamycin (TM) or thapsigargin (TG) we found the Lcn2-/- hepatocytes to react with strong UPR to the ER stress, as evidenced by significantly increased levels of Grp94, Bip and Chop mRNA and protein compared to the wt. Tunicamycin 71-82 lipocalin 2 Mus musculus 19-23 30452882-10 2019 Although the endoplasmic reticulum stressors thapsigargin and tunicamycin induced markedly and sustained expression of ATF4 and XBP-1, they did not induce RAGE shedding to the same level as TNF-alpha, suggesting that ATF4 is necessary but not sufficient alone for TNF-alpha-mediated RAGE shedding. Tunicamycin 62-73 activating transcription factor 4 Homo sapiens 119-123 30452882-10 2019 Although the endoplasmic reticulum stressors thapsigargin and tunicamycin induced markedly and sustained expression of ATF4 and XBP-1, they did not induce RAGE shedding to the same level as TNF-alpha, suggesting that ATF4 is necessary but not sufficient alone for TNF-alpha-mediated RAGE shedding. Tunicamycin 62-73 X-box binding protein 1 Homo sapiens 128-133 30600443-5 2019 N-linked glycosylation synthesis inhibitor tunicamycin causes a reduction of CaV3.1-T-type Ca2+ channel current (CaV3.1-ICa.T) when applied for 12 h or longer. Tunicamycin 43-54 calcium voltage-gated channel subunit alpha1 G Homo sapiens 77-83 30600443-5 2019 N-linked glycosylation synthesis inhibitor tunicamycin causes a reduction of CaV3.1-T-type Ca2+ channel current (CaV3.1-ICa.T) when applied for 12 h or longer. Tunicamycin 43-54 calcium voltage-gated channel subunit alpha1 G Homo sapiens 113-119 30600443-7 2019 Use-dependent inactivation of CaV3.1-ICa.T was accelerated, and recovery from inactivation was prolonged by tunicamycin (24 h). Tunicamycin 108-119 calcium voltage-gated channel subunit alpha1 G Homo sapiens 30-36 30930751-5 2019 In addition, mitochondrial protection of Homer1a was blocked by the ER stress activator Tunicamycin (TM) with a re-escalated ROS level, increasing ATP and MMP loss. Tunicamycin 88-99 homer scaffold protein 1 Homo sapiens 41-48 30930751-5 2019 In addition, mitochondrial protection of Homer1a was blocked by the ER stress activator Tunicamycin (TM) with a re-escalated ROS level, increasing ATP and MMP loss. Tunicamycin 101-103 homer scaffold protein 1 Homo sapiens 41-48 30620686-6 2019 We found that Pak2 cardiac deleted mice (Pak2-CKO) under tunicamycin stress or pressure overload manifested a defective ER response, cardiac dysfunction, and profound cell death. Tunicamycin 57-68 p21 (RAC1) activated kinase 2 Mus musculus 14-18 30620686-6 2019 We found that Pak2 cardiac deleted mice (Pak2-CKO) under tunicamycin stress or pressure overload manifested a defective ER response, cardiac dysfunction, and profound cell death. Tunicamycin 57-68 p21 (RAC1) activated kinase 2 Mus musculus 41-45 30615971-4 2019 Upon incubation of Lcn2-/- and wild type (wt) primary hepatocytes with tunicamycin (TM) or thapsigargin (TG) we found the Lcn2-/- hepatocytes to react with strong UPR to the ER stress, as evidenced by significantly increased levels of Grp94, Bip and Chop mRNA and protein compared to the wt. Tunicamycin 71-82 lipocalin 2 Mus musculus 122-126 30615971-4 2019 Upon incubation of Lcn2-/- and wild type (wt) primary hepatocytes with tunicamycin (TM) or thapsigargin (TG) we found the Lcn2-/- hepatocytes to react with strong UPR to the ER stress, as evidenced by significantly increased levels of Grp94, Bip and Chop mRNA and protein compared to the wt. Tunicamycin 84-86 lipocalin 2 Mus musculus 19-23 30615971-4 2019 Upon incubation of Lcn2-/- and wild type (wt) primary hepatocytes with tunicamycin (TM) or thapsigargin (TG) we found the Lcn2-/- hepatocytes to react with strong UPR to the ER stress, as evidenced by significantly increased levels of Grp94, Bip and Chop mRNA and protein compared to the wt. Tunicamycin 84-86 lipocalin 2 Mus musculus 122-126 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 31-36 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 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 tribbles pseudokinase 3 Homo sapiens 72-77 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 mechanistic target of rapamycin kinase Homo sapiens 214-218 30566828-6 2019 When N-linked glycosylation was inhibited by tunicamycin or abolished by the N39Q, N39A, or T41A mutation, CTRP12 cleavage was enhanced. Tunicamycin 45-56 C1q and TNF related 12 Homo sapiens 107-113 30820153-0 2019 Involvement of Orai1 in tunicamycin-induced endothelial dysfunction. Tunicamycin 24-35 ORAI calcium release-activated calcium modulator 1 Homo sapiens 15-20 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 100-103 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 30820153-8 2019 Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction. Tunicamycin 14-25 ORAI calcium release-activated calcium modulator 1 Homo sapiens 47-52 30820153-8 2019 Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction. Tunicamycin 14-25 ORAI calcium release-activated calcium modulator 1 Homo sapiens 84-89 30770792-9 2019 Thus, our study is the first to show that Smac mimetic protects from TM-triggered apoptosis by resolving the UPR and ER stress. Tunicamycin 69-71 diablo IAP-binding mitochondrial protein Homo sapiens 42-46 30448406-7 2019 Treating EVT-like JEG-3 and HTR8/SVneo cells with ER stress inducers (tunicamycin and thapsigargin) suppressed MMP2 mRNA and protein expression, secretion, and activity and reduced their invasiveness. Tunicamycin 70-81 matrix metallopeptidase 2 Homo sapiens 111-115 30770792-0 2019 Smac mimetic suppresses tunicamycin-induced apoptosis via resolution of ER stress. Tunicamycin 24-35 diablo IAP-binding mitochondrial protein Homo sapiens 0-4 30770792-2 2019 Here, we discover that Smac mimetic suppresses tunicamycin (TM)-induced apoptosis via resolution of the unfolded protein response (UPR) and ER stress. Tunicamycin 47-58 diablo IAP-binding mitochondrial protein Homo sapiens 23-27 30770792-2 2019 Here, we discover that Smac mimetic suppresses tunicamycin (TM)-induced apoptosis via resolution of the unfolded protein response (UPR) and ER stress. Tunicamycin 60-62 diablo IAP-binding mitochondrial protein Homo sapiens 23-27 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 83-111 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 113-118 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 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 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 168-201 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 203-207 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 X-box binding protein 1 Homo sapiens 229-252 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 X-box binding protein 1 Homo sapiens 254-258 30539651-5 2019 Concomitant treatment of tunicamycin and transfection of cells with MIOX-pcDNA led to a marked generation of ROS, which was reduced by MIOX-siRNA. Tunicamycin 25-36 myo-inositol oxygenase Mus musculus 68-72 30539651-5 2019 Concomitant treatment of tunicamycin and transfection of cells with MIOX-pcDNA led to a marked generation of ROS, which was reduced by MIOX-siRNA. Tunicamycin 25-36 myo-inositol oxygenase Mus musculus 135-139 30539651-11 2019 Also, their tunicamycin-induced accentuated expression in tubular cells was notably reduced with MIOX-siRNA. Tunicamycin 12-23 myo-inositol oxygenase Mus musculus 97-101 30641938-5 2019 Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo. Tunicamycin 158-169 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 37-57 30483742-0 2019 Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-kappaB signaling pathway. Tunicamycin 0-11 pentraxin 3 Homo sapiens 88-92 30483742-0 2019 Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-kappaB signaling pathway. Tunicamycin 0-11 AKT serine/threonine kinase 1 Homo sapiens 111-114 30483742-7 2019 Furthermore, we found that deglycosylated PTX3 (dePTX3) by tunicamycin (TM), which is N-glycan precursor biosynthesis blocker, and PNGase F significantly reduced the survival and migration of lung cancer cells. Tunicamycin 59-70 pentraxin 3 Homo sapiens 42-46 30483742-7 2019 Furthermore, we found that deglycosylated PTX3 (dePTX3) by tunicamycin (TM), which is N-glycan precursor biosynthesis blocker, and PNGase F significantly reduced the survival and migration of lung cancer cells. Tunicamycin 72-74 pentraxin 3 Homo sapiens 42-46 30475171-0 2019 Both thapsigargin- and tunicamycin-induced endoplasmic reticulum stress increases expression of Hrd1 in IRE1-dependent fashion. Tunicamycin 23-34 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 104-108 30475171-3 2019 RESULTS: We demonstrate that ER stress, induced by thapsigargin or tunicamycin, correlates with the increased expression of Hrd1 in both SH-SY5Y and SK-N-SH cells. Tunicamycin 67-78 synoviolin 1 Homo sapiens 124-128 30475171-6 2019 Inhibition of IRE1 associated with the inhibition of XBP1 splicing does not affect the survival of SH-SY5Y cells treated with either thapsigargin or tunicamycin but results in the complete suppression of both the thapsigargin- and tunicamycin-induced expression of Hrd1. Tunicamycin 231-242 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 14-18 30475171-6 2019 Inhibition of IRE1 associated with the inhibition of XBP1 splicing does not affect the survival of SH-SY5Y cells treated with either thapsigargin or tunicamycin but results in the complete suppression of both the thapsigargin- and tunicamycin-induced expression of Hrd1. Tunicamycin 231-242 X-box binding protein 1 Homo sapiens 53-57 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 caspase 3 Homo sapiens 148-157 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 30475171-0 2019 Both thapsigargin- and tunicamycin-induced endoplasmic reticulum stress increases expression of Hrd1 in IRE1-dependent fashion. Tunicamycin 23-34 synoviolin 1 Homo sapiens 96-100 30692541-4 2019 Oleic acid with or without tunicamycin significantly increases the formation of nucleoplasmic LDs, to which CDP-choline diacylglycerol phosphotransferase alpha (CCTalpha) is recruited, resulting in activation of phosphatidylcholine (PC) synthesis. Tunicamycin 27-38 phosphate cytidylyltransferase 1A, choline Homo sapiens 161-169 30429217-6 2019 Interestingly, calreticulin was sufficient for attenuating ER stress in tunicamycin- or thapsigargin-treated HeLa cells, whereas lentivirus-mediated shRNA calreticulin knockdown exacerbated ER stress. Tunicamycin 72-83 calreticulin Homo sapiens 15-27 30641938-5 2019 Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo. Tunicamycin 158-169 uncoupling protein 1 (mitochondrial, proton carrier) Mus musculus 59-63 30588337-7 2018 Our screens confirmed that MFSD2A and ARF4, which were identified in previous screens, are necessary for tunicamycin- and brefeldin A-induced cytotoxicity, respectively. Tunicamycin 105-116 major facilitator superfamily domain containing 2A Homo sapiens 27-33 30133247-5 2018 However, degradation of cytidylate kinase (CMK), which catalyzes reactions involved in the synthesis of both ribonucleotides and deoxyribonucleotides, blocks both DNA replication and wall teichoic acid biosynthesis, producing cytological effects identical to those created by simultaneously inhibiting both processes with the antibiotics ciprofloxacin and tunicamycin. Tunicamycin 356-367 cytidine/uridine monophosphate kinase 1 Homo sapiens 24-41 30133247-5 2018 However, degradation of cytidylate kinase (CMK), which catalyzes reactions involved in the synthesis of both ribonucleotides and deoxyribonucleotides, blocks both DNA replication and wall teichoic acid biosynthesis, producing cytological effects identical to those created by simultaneously inhibiting both processes with the antibiotics ciprofloxacin and tunicamycin. Tunicamycin 356-367 cytidine/uridine monophosphate kinase 1 Homo sapiens 43-46 30619478-10 2018 Moreover, induction of ER stress by tunicamycin and thapsigargin markedly increases Nrf2 expression, which is abolished in cells pretreated with XBP1 splicing inhibitors 4mu8C and quinotrierixin. Tunicamycin 36-47 NFE2 like bZIP transcription factor 2 Homo sapiens 84-88 30619478-10 2018 Moreover, induction of ER stress by tunicamycin and thapsigargin markedly increases Nrf2 expression, which is abolished in cells pretreated with XBP1 splicing inhibitors 4mu8C and quinotrierixin. Tunicamycin 36-47 X-box binding protein 1 Homo sapiens 145-149 30063946-3 2018 Because obesity promotes endoplasmic reticulum (ER) stress, we sought to determine how tunicamycin-induced ER stress affected Gnrh1 gene expression in the mouse hypothalamic cell line GT1-7. Tunicamycin 87-98 gonadotropin releasing hormone 1 Mus musculus 126-131 30063946-4 2018 Tunicamycin repressed expression of Gnrh1 in a PKC- and JNK-dependent manner, while upregulating expression of a known Gnrh1 repressor, Fos. Tunicamycin 0-11 gonadotropin releasing hormone 1 Mus musculus 36-41 30063946-4 2018 Tunicamycin repressed expression of Gnrh1 in a PKC- and JNK-dependent manner, while upregulating expression of a known Gnrh1 repressor, Fos. Tunicamycin 0-11 mitogen-activated protein kinase 8 Mus musculus 56-59 30063946-4 2018 Tunicamycin repressed expression of Gnrh1 in a PKC- and JNK-dependent manner, while upregulating expression of a known Gnrh1 repressor, Fos. Tunicamycin 0-11 gonadotropin releasing hormone 1 Mus musculus 119-124 30063946-4 2018 Tunicamycin repressed expression of Gnrh1 in a PKC- and JNK-dependent manner, while upregulating expression of a known Gnrh1 repressor, Fos. Tunicamycin 0-11 FBJ osteosarcoma oncogene Mus musculus 136-139 30063946-7 2018 Using a small molecule inhibitor, we determined that AP-1 was required for Gnrh1 repression by high-dose palmitate or tunicamycin-induced ER stress. Tunicamycin 118-129 jun proto-oncogene Mus musculus 53-57 30063946-7 2018 Using a small molecule inhibitor, we determined that AP-1 was required for Gnrh1 repression by high-dose palmitate or tunicamycin-induced ER stress. Tunicamycin 118-129 gonadotropin releasing hormone 1 Mus musculus 75-80 30420428-7 2019 However, RyR blockade distinctly prevented beta-cell death, propagation of the unfolded protein response (UPR), and dysfunctional glucose-induced Ca2+ oscillations in tunicamycin-treated INS-1 beta cells and mouse islets and Akita islets. Tunicamycin 167-178 ryanodine receptor 2 Rattus norvegicus 9-12 31111119-4 2019 We provide further evidence that ER stress inducing agents (Tunicamycin and Brefeldin A) disrupts Ca2+ homeostasis by directly inhibiting TRPC1-mediated Ca2+ entry, which led to ER stress in salivary gland cells. Tunicamycin 60-71 transient receptor potential cation channel, subfamily C, member 1 Mus musculus 138-143 31216950-6 2019 Since VAMP721/722 amounts were reported not to be increased by an ER stress inducer, tunicamycin in crt1/2 plants, our results suggest that ER stress and immune signalings distinctly control cellular abundance of VAMP721/722. Tunicamycin 85-96 compromized recognition of TCV 1 Arabidopsis thaliana 100-106 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 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 75-80 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 30567393-3 2018 Tunicamycin (TM) treatment significantly increased mRNA levels of CHOP and GRP78, and induced lipid accumulation in the liver. Tunicamycin 13-15 heat shock protein family A (Hsp70) member 5 Homo sapiens 75-80 30556167-4 2018 We found that 17-AAG (tanespimycin), an HSP90 (heat shock protein 90) inhibitor often used to kill cancer cells, could potently inhibit tunicamycin-induced ERS and the downstream nuclear factor kappa B activity in neonatal rat cardiomyocytes, leading to diminished apoptotic signaling and thus enhanced cell survival. Tunicamycin 136-147 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 40-45 30556167-4 2018 We found that 17-AAG (tanespimycin), an HSP90 (heat shock protein 90) inhibitor often used to kill cancer cells, could potently inhibit tunicamycin-induced ERS and the downstream nuclear factor kappa B activity in neonatal rat cardiomyocytes, leading to diminished apoptotic signaling and thus enhanced cell survival. Tunicamycin 136-147 heat shock protein 90 alpha family class A member 1 Rattus norvegicus 47-68 30588337-7 2018 Our screens confirmed that MFSD2A and ARF4, which were identified in previous screens, are necessary for tunicamycin- and brefeldin A-induced cytotoxicity, respectively. Tunicamycin 105-116 ADP ribosylation factor 4 Homo sapiens 38-42 30647729-4 2018 ER stress induced by tunicamycin administration increased TG2 protein levels in the mouse prefrontal cortex (PFC). Tunicamycin 21-32 transglutaminase 2, C polypeptide Mus musculus 58-61 30291216-8 2018 Desmogleins (Dsgs) 1 and 3, which constitute the core structure of desmosomes, were well transported to the cell-cell borders, but the amount decreased and showed an aberrant distribution at the cell borders in tunicamycin-treated keratinocytes. Tunicamycin 211-222 desmoglein 1 Homo sapiens 0-26 30253173-7 2018 In particular, EX-4 treatment restored HFD- and tunicamycin-induced Nrf2 nuclear translocation to control levels. Tunicamycin 48-59 nuclear factor, erythroid derived 2, like 2 Mus musculus 68-72 30287474-4 2018 Further characterization of FKH-9 suggests that loss of FKH-9 enhances resistance to the ER toxin tunicamycin and results in enhanced ER-associated degradation (ERAD). Tunicamycin 98-109 Fork-head domain-containing protein Caenorhabditis elegans 28-33 30287474-4 2018 Further characterization of FKH-9 suggests that loss of FKH-9 enhances resistance to the ER toxin tunicamycin and results in enhanced ER-associated degradation (ERAD). Tunicamycin 98-109 Fork-head domain-containing protein Caenorhabditis elegans 56-61 30173922-6 2018 We showed that disruption of ER homeostasis by treating adult rat cardiomyocytes in culture with tunicamycin leads to contractile dysfunction through JNK signaling pathway. Tunicamycin 97-108 mitogen-activated protein kinase 8 Rattus norvegicus 150-153 30533198-14 2018 Tunicamycin upregulated p62 and protected synovial fibroblasts from BAY 11-7085-induced cell death. Tunicamycin 0-11 sequestosome 1 Homo sapiens 24-27 30451898-5 2018 Indeed, in ER stressors-treated cells with thapsigargin, brefeldin A or tunicamycin, a greater increase in necrosis and decrease of ATP content was observed in NUPR1-defficent cells. Tunicamycin 72-83 nuclear protein transcription regulator 1 Mus musculus 160-165 30056252-10 2018 Subsequently, incubation with either MCR antagonists significantly augmented NO2/NO3 levels (stable NO metabolites) and this was attenuated by silencing of MCR or tunicamycin. Tunicamycin 163-174 nuclear receptor subfamily 3 group C member 2 Homo sapiens 37-40 30417434-19 2018 Taken together, adenosine upregulated Bcl-2 and GADD34 to protect PBCs against Tu-induced apoptosis and increase Insulin secretion. Tunicamycin 79-81 B cell leukemia/lymphoma 2 Mus musculus 38-43 30417434-19 2018 Taken together, adenosine upregulated Bcl-2 and GADD34 to protect PBCs against Tu-induced apoptosis and increase Insulin secretion. Tunicamycin 79-81 protein phosphatase 1, regulatory subunit 15A Mus musculus 48-54 30533221-9 2018 Stimulation with IL-1beta or tunicamycin induced hepatic GDF15 expression in hepatocytes. Tunicamycin 29-40 growth differentiation factor 15 Homo sapiens 57-62 30017234-7 2018 ER stress inducer, tunicamycin (200 ng/mL) significantly increased the level of autophagy and reduced expression of fibronectin in HCFs, both of which were reversed by 4 Phenylbutyric acid. Tunicamycin 19-30 fibronectin 1 Homo sapiens 116-127 30017234-9 2018 LC3 co-localized with fibronectin when stimulated HCFs with tunicamycin. Tunicamycin 60-71 microtubule associated protein 1 light chain 3 alpha Homo sapiens 0-3 30017234-9 2018 LC3 co-localized with fibronectin when stimulated HCFs with tunicamycin. Tunicamycin 60-71 fibronectin 1 Homo sapiens 22-33 30360492-5 2018 In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant. Tunicamycin 26-28 transcription factor HAC1 Saccharomyces cerevisiae S288C 38-42 30360492-5 2018 In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant. Tunicamycin 26-28 Elongator subunit ELP3 Saccharomyces cerevisiae S288C 80-84 30360492-5 2018 In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant. Tunicamycin 13-24 transcription factor HAC1 Saccharomyces cerevisiae S288C 38-42 30360492-5 2018 In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant. Tunicamycin 26-28 pseudouridine synthase DEG1 Saccharomyces cerevisiae S288C 85-89 30360492-5 2018 In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant. Tunicamycin 13-24 Elongator subunit ELP3 Saccharomyces cerevisiae S288C 80-84 29894845-5 2018 Trodusquemine also prevented the Tunicamycin -induced increased arterial levels of the molecular ERS actors 78 kDa glucose-regulated protein (GRP78) and Activating Transcription Factor 6 (ATF6alpha). Tunicamycin 33-44 heat shock protein 5 Mus musculus 142-147 30360492-5 2018 In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant. Tunicamycin 13-24 pseudouridine synthase DEG1 Saccharomyces cerevisiae S288C 85-89 30063110-6 2018 In addition, we demonstrated that tunicamycin-induced ER stress in vitro upregulated ATF6 and CIP2A. Tunicamycin 34-45 activating transcription factor 6 Homo sapiens 85-89 30063110-6 2018 In addition, we demonstrated that tunicamycin-induced ER stress in vitro upregulated ATF6 and CIP2A. Tunicamycin 34-45 cellular inhibitor of PP2A Homo sapiens 94-99 29894845-4 2018 Induction of ERS (Tunicamycin) in vivo in mice or ex vivo in mouse arteries led to severe arterial endothelial dysfunction (i.e. reduced flow-dependent, NO mediated dilatation in isolated small mesenteric arteries), and this was prevented by the PTP1B inhibitor trodusquemine and absent in PTP1B-/- mice. Tunicamycin 18-29 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 246-251 30096296-6 2018 Then we identified compound 20(S)-25-methoxyl-dammarane-3beta,12beta,20-triol (25-OCH3-PPD) could inhibit the promoter activity of SelS, further results showed that 25-OCH3-PPD effectively inhibited tunicamycin (TM) induced up-regulation of SelS expression in both mRNA and protein levels. Tunicamycin 199-210 selenoprotein S Homo sapiens 131-135 30096296-7 2018 Moreover, 25-OCH3-PPD significantly inhibited glucose-regulated protein 78 (GRP78; the major ER stress marker) expression in TM-induced ER stress in HepG2 and HEK293T cells, suggesting that 25-OCH3-PPD could attenuate ER stress in these cells. Tunicamycin 125-127 heat shock protein family A (Hsp70) member 5 Homo sapiens 46-74 30096296-7 2018 Moreover, 25-OCH3-PPD significantly inhibited glucose-regulated protein 78 (GRP78; the major ER stress marker) expression in TM-induced ER stress in HepG2 and HEK293T cells, suggesting that 25-OCH3-PPD could attenuate ER stress in these cells. Tunicamycin 125-127 heat shock protein family A (Hsp70) member 5 Homo sapiens 76-81 29894845-4 2018 Induction of ERS (Tunicamycin) in vivo in mice or ex vivo in mouse arteries led to severe arterial endothelial dysfunction (i.e. reduced flow-dependent, NO mediated dilatation in isolated small mesenteric arteries), and this was prevented by the PTP1B inhibitor trodusquemine and absent in PTP1B-/- mice. Tunicamycin 18-29 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 290-295 29894845-5 2018 Trodusquemine also prevented the Tunicamycin -induced increased arterial levels of the molecular ERS actors 78 kDa glucose-regulated protein (GRP78) and Activating Transcription Factor 6 (ATF6alpha). Tunicamycin 33-44 activating transcription factor 6 Mus musculus 188-197 29894845-6 2018 Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay). Tunicamycin 0-11 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 51-56 29894845-6 2018 Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay). Tunicamycin 0-11 heat shock protein 5 Mus musculus 62-67 29894845-6 2018 Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay). Tunicamycin 0-11 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 95-147 29894845-6 2018 Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay). Tunicamycin 0-11 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 149-153 29894845-6 2018 Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay). Tunicamycin 0-11 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 159-168 30107908-5 2018 We demonstrated here that oxicam-NSAIDs suppressed the activation of caspase-3 and cell death caused by MPP+ or ER stress-inducer, tunicamycin, in SH-SY5Y cells. Tunicamycin 131-142 caspase 3 Homo sapiens 69-78 30185560-6 2018 Among these genes, overexpression of UDP-N-acetylglucosamine-1-P transferase (ALG7), a subunit of the 20S proteasome (PRE7), and YBR085C-A induced tunicamycin resistance in wild-type cells, whereas deletion of all three genes completely reversed the tunicamycin-resistance phenotype. Tunicamycin 147-158 UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase Saccharomyces cerevisiae S288C 78-82 30185560-6 2018 Among these genes, overexpression of UDP-N-acetylglucosamine-1-P transferase (ALG7), a subunit of the 20S proteasome (PRE7), and YBR085C-A induced tunicamycin resistance in wild-type cells, whereas deletion of all three genes completely reversed the tunicamycin-resistance phenotype. Tunicamycin 147-158 proteasome core particle subunit beta 6 Saccharomyces cerevisiae S288C 118-122 30185560-6 2018 Among these genes, overexpression of UDP-N-acetylglucosamine-1-P transferase (ALG7), a subunit of the 20S proteasome (PRE7), and YBR085C-A induced tunicamycin resistance in wild-type cells, whereas deletion of all three genes completely reversed the tunicamycin-resistance phenotype. Tunicamycin 250-261 UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase Saccharomyces cerevisiae S288C 78-82 30185560-6 2018 Among these genes, overexpression of UDP-N-acetylglucosamine-1-P transferase (ALG7), a subunit of the 20S proteasome (PRE7), and YBR085C-A induced tunicamycin resistance in wild-type cells, whereas deletion of all three genes completely reversed the tunicamycin-resistance phenotype. Tunicamycin 250-261 proteasome core particle subunit beta 6 Saccharomyces cerevisiae S288C 118-122 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 30245625-5 2018 In vitro, p58IPK-deficient RGCs show reduced viability and are more susceptible to cell death induced by the ER stress inducer tunicamycin (TM). Tunicamycin 140-142 DnaJ heat shock protein family (Hsp40) member C3 Mus musculus 10-16 30209265-5 2018 Reduction in GRP78 expression during tunicamycin-induced endoplasmic reticulum stress also suppressed MTII-mediated internalization of MC4R and cAMP-mediated transcriptional activity. Tunicamycin 37-48 heat shock protein 5 Mus musculus 13-18 30209265-5 2018 Reduction in GRP78 expression during tunicamycin-induced endoplasmic reticulum stress also suppressed MTII-mediated internalization of MC4R and cAMP-mediated transcriptional activity. Tunicamycin 37-48 metallothionein 2 Mus musculus 102-106 30209265-5 2018 Reduction in GRP78 expression during tunicamycin-induced endoplasmic reticulum stress also suppressed MTII-mediated internalization of MC4R and cAMP-mediated transcriptional activity. Tunicamycin 37-48 melanocortin 4 receptor Mus musculus 135-139 30206979-5 2018 Furthermore, tunicamycin treatment downregulated GPR177 expression in a dose-dependent manner. Tunicamycin 13-24 Wnt ligand secretion mediator Homo sapiens 49-55 30206979-8 2018 Small interfering RNA-mediated knockdown of GPR177 leads to sensitization to ER stress and induces apoptosis of cancer cells along with tunicamycin treatment. Tunicamycin 136-147 Wnt ligand secretion mediator Homo sapiens 44-50 30206979-11 2018 Efficacy of tunicamycin chemotherapy treatments depended on GPR177 expression in gastric cancer cell lines. Tunicamycin 12-23 Wnt ligand secretion mediator Homo sapiens 60-66 30245625-5 2018 In vitro, p58IPK-deficient RGCs show reduced viability and are more susceptible to cell death induced by the ER stress inducer tunicamycin (TM). Tunicamycin 127-138 DnaJ heat shock protein family (Hsp40) member C3 Mus musculus 10-16 30127865-0 2018 MEG-3-mediated Wnt/beta-catenin signaling pathway controls the inhibition of tunicamycin-mediated viability in glioblastoma. Tunicamycin 77-88 maternally expressed 3 Homo sapiens 0-5 30127865-0 2018 MEG-3-mediated Wnt/beta-catenin signaling pathway controls the inhibition of tunicamycin-mediated viability in glioblastoma. Tunicamycin 77-88 catenin beta 1 Homo sapiens 19-31 30127865-6 2018 Results demonstrated that tunicamycin administration promoted apoptosis of glioblastoma cells through the upregulation of poly(ADP-ribose) polymerase and caspase-9. Tunicamycin 26-37 poly(ADP-ribose) polymerase 1 Homo sapiens 122-149 30127865-6 2018 Results demonstrated that tunicamycin administration promoted apoptosis of glioblastoma cells through the upregulation of poly(ADP-ribose) polymerase and caspase-9. Tunicamycin 26-37 caspase 9 Homo sapiens 154-163 30127865-8 2018 Additionally, tunicamycin increased the expression of maternally expressed gene-3 (MEG-3) and wingless/integrated (Wnt)/beta-catenin in glioblastoma cells. Tunicamycin 14-25 maternally expressed 3 Homo sapiens 54-81 30127865-8 2018 Additionally, tunicamycin increased the expression of maternally expressed gene-3 (MEG-3) and wingless/integrated (Wnt)/beta-catenin in glioblastoma cells. Tunicamycin 14-25 maternally expressed 3 Homo sapiens 83-88 29430617-5 2018 In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment. Tunicamycin 30-41 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 153-157 30127865-8 2018 Additionally, tunicamycin increased the expression of maternally expressed gene-3 (MEG-3) and wingless/integrated (Wnt)/beta-catenin in glioblastoma cells. Tunicamycin 14-25 catenin beta 1 Homo sapiens 120-132 29430617-5 2018 In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment. Tunicamycin 30-41 X-box binding protein 1 Mus musculus 173-196 30127865-9 2018 Results also indicated that tunicamycin administration promoted the Wnt/beta-catenin signaling pathway in glioblastoma cells. Tunicamycin 28-39 catenin beta 1 Homo sapiens 72-84 29430617-5 2018 In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment. Tunicamycin 30-41 X-box binding protein 1 Mus musculus 198-202 29430617-5 2018 In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment. Tunicamycin 30-41 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 267-271 29430617-5 2018 In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment. Tunicamycin 30-41 X-box binding protein 1 Mus musculus 272-276 29430617-5 2018 In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment. Tunicamycin 369-380 X-box binding protein 1 Mus musculus 198-202 29430617-6 2018 Reduced estrogen receptor beta (ERbeta) protein levels were found in the PFC of male mice following tunicamycin treatment. Tunicamycin 100-111 estrogen receptor 2 (beta) Mus musculus 8-30 29430617-6 2018 Reduced estrogen receptor beta (ERbeta) protein levels were found in the PFC of male mice following tunicamycin treatment. Tunicamycin 100-111 estrogen receptor 2 (beta) Mus musculus 32-38 29430617-7 2018 Pretreatment with an ERbeta specific agonist, ERB-041 significantly attenuated tunicamycin-induced deficits in social behavior, and activation of IRE1/XBP1 pathway in mouse PFC. Tunicamycin 79-90 estrogen receptor 2 (beta) Mus musculus 21-27 29430617-7 2018 Pretreatment with an ERbeta specific agonist, ERB-041 significantly attenuated tunicamycin-induced deficits in social behavior, and activation of IRE1/XBP1 pathway in mouse PFC. Tunicamycin 79-90 estrogen receptor 2 (beta) Mus musculus 46-49 29430617-8 2018 Moreover, ERB-041 inhibited tunicamycin-induced increases in functional connectivity between PFC and hippocampus in male mice. Tunicamycin 28-39 estrogen receptor 2 (beta) Mus musculus 10-13 30127865-10 2018 Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/beta-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma. Tunicamycin 29-40 maternally expressed 3 Homo sapiens 13-18 30127865-10 2018 Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/beta-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma. Tunicamycin 29-40 catenin beta 1 Homo sapiens 76-88 30127865-10 2018 Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/beta-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma. Tunicamycin 139-150 maternally expressed 3 Homo sapiens 13-18 30127865-10 2018 Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/beta-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma. Tunicamycin 139-150 catenin beta 1 Homo sapiens 76-88 30127865-12 2018 In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/beta-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy. Tunicamycin 43-54 maternally expressed 3 Homo sapiens 114-119 30127865-12 2018 In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/beta-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy. Tunicamycin 43-54 catenin beta 1 Homo sapiens 133-145 30127865-12 2018 In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/beta-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy. Tunicamycin 173-184 maternally expressed 3 Homo sapiens 114-119 29936187-10 2018 mRNA and protein ratios of apoptotic modulators (Bax/Bcl2) are higher in 158JP oligodendrocytes which are also more vulnerable than 158N cells to tunicamycin-induced ER-stress. Tunicamycin 146-157 BCL2 associated X, apoptosis regulator Homo sapiens 49-52 30127865-12 2018 In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/beta-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy. Tunicamycin 173-184 catenin beta 1 Homo sapiens 133-145 30111858-5 2018 CRELD2 expression in Neuro2a cells was induced at the late phase after treatment with tunicamycin (Tm) compared with rapid induction of growth arrest and DNA damage inducible gene 153 (GADD153). Tunicamycin 86-97 cysteine-rich with EGF-like domains 2 Mus musculus 0-6 29936187-10 2018 mRNA and protein ratios of apoptotic modulators (Bax/Bcl2) are higher in 158JP oligodendrocytes which are also more vulnerable than 158N cells to tunicamycin-induced ER-stress. Tunicamycin 146-157 BCL2 apoptosis regulator Homo sapiens 53-57 30147026-4 2018 Increased expression of ER stress markers, inflammation and apoptosis of alveolar epithelial cells were observed in Atg4b-deficient mice compared to WT mice, when treated with the ER stress inducer tunicamycin. Tunicamycin 198-209 autophagy related 4B, cysteine peptidase Mus musculus 116-121 30147026-5 2018 After tunicamycin treatment, Atg4b null lungs showed accumulation of its substrate LC3-I, demonstrating that these mice failed to induce autophagy despite the ER stress conditions. Tunicamycin 6-17 autophagy related 4B, cysteine peptidase Mus musculus 29-34 30147026-6 2018 We also showed that compromised autophagy in lungs from Atg4b null mice is associated with exacerbated lung damage, epithelial apoptosis and the development of lung fibrosis at 21 days after tunicamycin treatment. Tunicamycin 191-202 autophagy related 4B, cysteine peptidase Mus musculus 56-61 30147026-7 2018 Our findings indicate that ATG4B protein and autophagy are essential to mitigate ER stress and to prevent tunicamycin-induced epithelial apoptosis and lung fibrosis. Tunicamycin 106-117 autophagy related 4B, cysteine peptidase Mus musculus 27-32 29871846-1 2018 A series of compounds was discovered that induce the production of VGF mRNA in SH-SY5Y cells and exhibit cytoprotection under tunicamycin induced endoplasmic reticulum (ER) stress. Tunicamycin 126-137 VGF nerve growth factor inducible Homo sapiens 67-70 30081561-0 2018 Induction of Liver Steatosis in BAP31-Deficient Mice Burdened with Tunicamycin-Induced Endoplasmic Reticulum Stress. Tunicamycin 67-78 B cell receptor associated protein 31 Mus musculus 32-37 30081561-4 2018 In this study, wild-type and liver-specific BAP31-depleted mice were administrated with ER stress activator of Tunicamycin, the markers of ER stress, liver steatosis, and the underlying molecular mechanisms were determined. Tunicamycin 111-122 B cell receptor associated protein 31 Mus musculus 44-49 30081561-5 2018 BAP31 deficiency increased Tunicamycin-induced hepatic lipid accumulation, aggravated liver dysfunction, and increased the mRNA levels of ER stress markers, including glucose-regulated protein 78 (GRP78), X-box binding protein 1 (XBP1), inositol-requiring protein-1alpha (IRE1alpha) and C/EBP homologous protein (CHOP), thus promoting ER stress in vivo and in vitro. Tunicamycin 27-38 B cell receptor associated protein 31 Mus musculus 0-5 30081561-8 2018 Finally, BAP31 deficiency increased Tunicamycin-induced hepatic inflammatory response. Tunicamycin 36-47 B cell receptor associated protein 31 Mus musculus 9-14 30081561-9 2018 These results demonstrate that BAP31 deficiency increased Tunicamycin-induced ER stress, impaired VLDL secretion and exogenous lipid clearance, and reduced fatty acid beta-oxidation, which eventually resulted in liver steatosis. Tunicamycin 58-69 B cell receptor associated protein 31 Mus musculus 31-36 29800817-3 2018 Werner (WRN) mutant cell lines AG11395, AG05229 and normal aged fibroblast AG13129 display a deficient response to tunicamycin mediated endoplasmic reticulum (ER) stress induced autophagy compared to clinically unaffected GM00637 and normal young fibroblast GM03440. Tunicamycin 115-126 WRN RecQ like helicase Homo sapiens 8-11 29553832-7 2018 Tunicamycin-induced deglycosylation inhibited TRPV4 activity and compromised [Ca2+]i signaling in NHK cells. Tunicamycin 0-11 transient receptor potential cation channel subfamily V member 4 Homo sapiens 46-51 29845243-4 2018 Notably, tunicamycin treatment, an endoplasmic reticulum (ER) stress inducer, induced the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha), but decreased ATF4 protein levels in the mouse liver. Tunicamycin 9-20 eukaryotic translation initiation factor 2A Mus musculus 109-156 29845243-4 2018 Notably, tunicamycin treatment, an endoplasmic reticulum (ER) stress inducer, induced the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha), but decreased ATF4 protein levels in the mouse liver. Tunicamycin 9-20 eukaryotic translation initiation factor 2A Mus musculus 158-167 29845243-4 2018 Notably, tunicamycin treatment, an endoplasmic reticulum (ER) stress inducer, induced the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha), but decreased ATF4 protein levels in the mouse liver. Tunicamycin 9-20 activating transcription factor 4 Mus musculus 184-188 29876740-5 2018 MANF-deficient N2a significantly elevated OS-9 protein after tunicamycin treatment; however, no specific differences in intra- and extracellular status of NHK protein were observed between wild-type and MANF-deficient cells. Tunicamycin 61-72 mesencephalic astrocyte-derived neurotrophic factor Mus musculus 0-4 29684334-4 2018 We found that treatment with the ER stress inducer tunicamycin (TM) increased the phosphorylation of JNK and MKK7 in HT22 cells, which was nullified by GADD45beta-I. Tunicamycin 51-62 mitogen-activated protein kinase 8 Mus musculus 101-104 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 29684334-4 2018 We found that treatment with the ER stress inducer tunicamycin (TM) increased the phosphorylation of JNK and MKK7 in HT22 cells, which was nullified by GADD45beta-I. Tunicamycin 51-62 mitogen-activated protein kinase kinase 7 Mus musculus 109-113 29684334-4 2018 We found that treatment with the ER stress inducer tunicamycin (TM) increased the phosphorylation of JNK and MKK7 in HT22 cells, which was nullified by GADD45beta-I. Tunicamycin 64-66 mitogen-activated protein kinase 8 Mus musculus 101-104 29684334-4 2018 We found that treatment with the ER stress inducer tunicamycin (TM) increased the phosphorylation of JNK and MKK7 in HT22 cells, which was nullified by GADD45beta-I. Tunicamycin 64-66 mitogen-activated protein kinase kinase 7 Mus musculus 109-113 29684334-5 2018 GADD45beta-I significantly attenuated TM-induced toxicity via inhibiting apoptotic cell death, as evidenced by decreased number of TUNEL-positive cells and reduced caspase-3 activity. Tunicamycin 38-40 caspase 3 Mus musculus 164-173 30034224-16 2018 In vitro, emodin treatment was further found to decrease the GRP78 level induced by high glucose or tunicamycin (TM). Tunicamycin 100-111 heat shock protein 5 Mus musculus 61-66 29988028-7 2018 Pharmacological activation of AMPK by metformin significantly abrogated the loss of RUNX2-S118 phosphorylation and protected from tunicamycin-induced endoplasmic reticulum stress, high glucose-induced in vitro adipogenesis and streptozotocin-induced in vivo bone adiposity and bone phenotype. Tunicamycin 130-141 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 30-34 30034224-16 2018 In vitro, emodin treatment was further found to decrease the GRP78 level induced by high glucose or tunicamycin (TM). Tunicamycin 113-115 heat shock protein 5 Mus musculus 61-66 29675957-2 2018 Here, we injected tunicamycin (TM), a recognized ER stress inducer, into the brain ventricle of Sprague-Dawley (SD) rats to induce the unfolded protein response (UPR), demonstrated by the enhanced phosphorylation of pancreatic ER kinase (PERK), inositol-requiring enzyme-1 (IRE-1) and activating transcription factor-6 (ATF-6). Tunicamycin 18-29 activating transcription factor 6 Rattus norvegicus 320-325 30034372-8 2018 Tunicamycin-treated bacteria or the bacterial WTA preparation suppressed NF-kappaB and inflammatory cytokine production (TNFalpha, and IL-6) from murine macrophage cell line (RAW 264.7) indicating the reduced WTA level possibly attenuates an inflammatory response. Tunicamycin 0-11 tumor necrosis factor Mus musculus 121-129 30034372-8 2018 Tunicamycin-treated bacteria or the bacterial WTA preparation suppressed NF-kappaB and inflammatory cytokine production (TNFalpha, and IL-6) from murine macrophage cell line (RAW 264.7) indicating the reduced WTA level possibly attenuates an inflammatory response. Tunicamycin 0-11 interleukin 6 Mus musculus 135-139 29575057-6 2018 Mice subjected to acute ER stress by pioglitazone administration and a low-dose tunicamycin injection presented a maladaptive UPR activation in SAT along with reduced adiponectin synthesis and secretion and increased lipolysis with respect to VAT, associated with lipid accumulation in skeletal muscle and liver. Tunicamycin 80-91 adiponectin, C1Q and collagen domain containing Mus musculus 167-178 29675957-2 2018 Here, we injected tunicamycin (TM), a recognized ER stress inducer, into the brain ventricle of Sprague-Dawley (SD) rats to induce the unfolded protein response (UPR), demonstrated by the enhanced phosphorylation of pancreatic ER kinase (PERK), inositol-requiring enzyme-1 (IRE-1) and activating transcription factor-6 (ATF-6). Tunicamycin 18-29 activating transcription factor 6 Rattus norvegicus 285-318 29675957-5 2018 Simultaneous inhibition of GSK-3beta by hippocampal infusion of SB216763 (SB) attenuated TM-induced UPR and spatial memory impairment with restoration of pS129-CREB and synaptic plasticity. Tunicamycin 89-91 glycogen synthase kinase 3 alpha Rattus norvegicus 27-36 29758225-6 2018 Indeed, we found that ER stress induced by thapsigargin and tunicamycin led to increased expression of TRPV6 via ATF6alpha signaling branch. Tunicamycin 60-71 transient receptor potential cation channel subfamily V member 6 Homo sapiens 103-108 29758225-6 2018 Indeed, we found that ER stress induced by thapsigargin and tunicamycin led to increased expression of TRPV6 via ATF6alpha signaling branch. Tunicamycin 60-71 activating transcription factor 6 Homo sapiens 113-122 29688606-7 2018 Interestingly, although the degree of endogenous BiP3 protein accumulation in the ssi2 mutant was comparable to that in wild-type plants treated with the ER stress inducer tunicamycin, much less BiP3 transcripts were detected in the ssi2 mutant compared to tunicamycin-treated wild-type plants. Tunicamycin 172-183 Plant stearoyl-acyl-carrier-protein desaturase family protein Arabidopsis thaliana 82-86 29891966-7 2018 The inhibition of N-glycosylation by tunicamycin or glucose starvation markedly reduced proIGF-1Ea and mature IGF-1 production. Tunicamycin 37-48 insulin like growth factor 1 Homo sapiens 91-96 29879176-3 2018 METHOD: ERS in INS-1-3 cells was induced by exposure cells to thapsigargin (TG), tunicamycin (TM) or palmitic acid (PA) +high glucose (HG). Tunicamycin 81-92 forkhead box M1 Homo sapiens 15-20 29879176-3 2018 METHOD: ERS in INS-1-3 cells was induced by exposure cells to thapsigargin (TG), tunicamycin (TM) or palmitic acid (PA) +high glucose (HG). Tunicamycin 94-96 forkhead box M1 Homo sapiens 15-20 29650257-5 2018 An ER stress-inducing chemical, tunicamycin, increased the activities of caspase-3 and -4, whereas pretreatment with NPY decreased caspase-3 and -4 activities during the ER stress response. Tunicamycin 32-43 caspase 3 Homo sapiens 73-89 29650257-6 2018 In addition, NPY suppressed the activation of three major ER stress sensors during the tunicamycin-induced ER stress response. Tunicamycin 87-98 neuropeptide Y Homo sapiens 13-16 29805584-0 2018 Tunicamycin inhibits progression of glioma cells through downregulation of the MEG-3-regulated wnt/beta-catenin signaling pathway. Tunicamycin 0-11 maternally expressed 3 Homo sapiens 79-84 29620275-7 2018 Compared with in cells prior to treatment, human leukemia cells treated with tunicamycin exhibited increased expression of p-PERK, p-eIF2alpha and GRP78 after 72 h (P<0.05). Tunicamycin 77-88 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 125-129 29620275-7 2018 Compared with in cells prior to treatment, human leukemia cells treated with tunicamycin exhibited increased expression of p-PERK, p-eIF2alpha and GRP78 after 72 h (P<0.05). Tunicamycin 77-88 eukaryotic translation initiation factor 2A Homo sapiens 133-142 29620275-7 2018 Compared with in cells prior to treatment, human leukemia cells treated with tunicamycin exhibited increased expression of p-PERK, p-eIF2alpha and GRP78 after 72 h (P<0.05). Tunicamycin 77-88 heat shock protein family A (Hsp70) member 5 Homo sapiens 147-152 28444413-4 2018 MATERIAL AND METHODS: Initially, the expression of CDNF was tested by treating H9c2 cells with various concentrations of tunicamycin (TM) and performing reverse-transcriptase polymerase chain reaction and Western blotting. Tunicamycin 121-132 cerebral dopamine neurotrophic factor Rattus norvegicus 51-55 29649564-4 2018 Both overexpression of XBP1s and tunicamycin treatment were able to enhance MANF transcription. Tunicamycin 33-44 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 76-80 29805584-0 2018 Tunicamycin inhibits progression of glioma cells through downregulation of the MEG-3-regulated wnt/beta-catenin signaling pathway. Tunicamycin 0-11 catenin beta 1 Homo sapiens 99-111 29784903-7 2018 L-NAME, tunicamycin, and Genipin attenuated vasodilation in WT, WT-EX and ApoE KO-EX, but not in ApoE KO. Tunicamycin 8-19 apolipoprotein E Mus musculus 74-78 29764928-6 2018 Our results show that ER stress maker GRP78 expression was increased in human endometrial Ishikawa and endometrial stromal cells (ESCs) treated with tunicamycin. Tunicamycin 149-160 heat shock protein family A (Hsp70) member 5 Homo sapiens 38-43 29764928-7 2018 Addition of estrogen decreased tunicamycin-induced GRP78 expression. Tunicamycin 31-42 heat shock protein family A (Hsp70) member 5 Homo sapiens 51-56 29626480-5 2018 TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice. Tunicamycin 18-29 insulin receptor Mus musculus 46-62 29626480-5 2018 TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice. Tunicamycin 18-29 insulin receptor Mus musculus 64-66 29626480-5 2018 TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice. Tunicamycin 18-29 activating transcription factor 6 Mus musculus 92-101 29626480-5 2018 TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice. Tunicamycin 31-33 insulin receptor Mus musculus 46-62 29626480-5 2018 TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice. Tunicamycin 31-33 insulin receptor Mus musculus 64-66 29626480-5 2018 TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice. Tunicamycin 31-33 activating transcription factor 6 Mus musculus 92-101 29545069-6 2018 We defined that the post-acute response was dependent on SVCT2 located in early secretory compartments, and its trafficking was abolished with Tunicamycin and Brefeldin A treatment. Tunicamycin 143-154 solute carrier family 23 member 2 Homo sapiens 57-62 29634759-6 2018 The aim of this study is to investigate how tunicamycin treatment, that induces eIF2 phosphorylation, affects mRNA translation in erythroblasts. Tunicamycin 44-55 eukaryotic translation initiation factor 2 subunit beta Homo sapiens 80-84 29555819-3 2018 Here we show that the Grb10 gene could be reactivated in adult mouse liver by acute endoplasmic reticulum stress (ER stress) such as tunicamycin or a short-term high-fat diet (HFD) challenge, concurrently with increased unfolded protein response (UPR) and hepatosteatosis. Tunicamycin 133-144 growth factor receptor bound protein 10 Mus musculus 22-27 29744053-3 2018 Results: In the present study, we showed that intestinal epithelial cells (IEC-6) incubated with tunicamycin led to caspase-3-dependent apoptotic cell death. Tunicamycin 97-108 caspase 3 Homo sapiens 116-125 29744053-5 2018 Further study demonstrated that tunicamycin-induced cell death was enhanced by rapamycin, a specific inhibitor of mTORC1. Tunicamycin 32-43 CREB regulated transcription coactivator 1 Mus musculus 114-120 29744053-7 2018 These effects of tunicamycin were exacerbated by mTORC1 inhibitor. Tunicamycin 17-28 CREB regulated transcription coactivator 1 Mus musculus 49-55 29717117-5 2018 We found that tunicamycin (TU), but no other ER stress inducers, sensitized mouse fibroblasts and hippocampal neuronal cells to TRAIL-induced apoptosis. Tunicamycin 14-25 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 128-133 29717117-5 2018 We found that tunicamycin (TU), but no other ER stress inducers, sensitized mouse fibroblasts and hippocampal neuronal cells to TRAIL-induced apoptosis. Tunicamycin 27-29 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 128-133 29454702-6 2018 The CCL2 in MAC-T cells attenuates endoplasmic reticulum stress induced by tunicamycin, suggesting that CCL2 regulates intracellular synthesis of proteins and lipids and prevents activation of apoptotic pathways initiated in response to endoplasmic reticulum stress. Tunicamycin 75-86 C-C motif chemokine 2 Bos taurus 4-8 29454702-6 2018 The CCL2 in MAC-T cells attenuates endoplasmic reticulum stress induced by tunicamycin, suggesting that CCL2 regulates intracellular synthesis of proteins and lipids and prevents activation of apoptotic pathways initiated in response to endoplasmic reticulum stress. Tunicamycin 75-86 C-C motif chemokine 2 Bos taurus 104-108 29488603-8 2018 Flow cytometry assays indicated that miR-124 transfection attenuated apoptosis resistance of osteosarcoma to tunicamycin, potentially via the downregulation of P53 and Bcl-2 apoptosis regulator expression. Tunicamycin 109-120 tumor protein p53 Homo sapiens 160-163 28847729-5 2018 Administration of chemical ER stressor tunicamycin to activate the UPR pathway resulted in robust increase of hepatic and circulating GDF15 levels. Tunicamycin 39-50 growth differentiation factor 15 Mus musculus 134-139 29634759-8 2018 Treatment of erythroblasts with Tunicamycin (Tm) increased phosphorylation of eIF2 2-fold. Tunicamycin 32-43 eukaryotic translation initiation factor 2 subunit beta Homo sapiens 78-82 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 29343429-6 2018 The endoplasmic reticulum (ER) stress condition and the related unfolded protein response (UPR), triggered by treatment with thapsigargin and tunicamycin, cause an increase of the cap-independent translation of ACC1 mRNA in HepG2 cells, despite the overall reduction in global protein synthesis. Tunicamycin 142-153 acetyl-CoA carboxylase alpha Homo sapiens 211-215 29377347-0 2018 Tunicamycin inhibits cell proliferation and migration in hepatocellular carcinoma through suppression of CD44s and the ERK1/2 pathway. Tunicamycin 0-11 CD44 molecule (Indian blood group) Homo sapiens 105-109 29377347-0 2018 Tunicamycin inhibits cell proliferation and migration in hepatocellular carcinoma through suppression of CD44s and the ERK1/2 pathway. Tunicamycin 0-11 mitogen-activated protein kinase 3 Homo sapiens 119-125 28885691-8 2018 Consistent with this result, the stimulated unfolded protein response (UPR) regulatory proteins induced by tunicamycin were down-regulated by FGF2. Tunicamycin 107-118 fibroblast growth factor 2 Bos taurus 142-146 29385296-6 2018 Both allelic ire1 knock-down mutants ire1-1 and ire1-2 were much more sensitive than their parental strain CC-4533 to the ER stress inducers tunicamycin, dithiothreitol and brefeldin A. Tunicamycin 141-152 uncharacterized protein Chlamydomonas reinhardtii 13-17 29385296-6 2018 Both allelic ire1 knock-down mutants ire1-1 and ire1-2 were much more sensitive than their parental strain CC-4533 to the ER stress inducers tunicamycin, dithiothreitol and brefeldin A. Tunicamycin 141-152 uncharacterized protein Chlamydomonas reinhardtii 37-43 29385296-6 2018 Both allelic ire1 knock-down mutants ire1-1 and ire1-2 were much more sensitive than their parental strain CC-4533 to the ER stress inducers tunicamycin, dithiothreitol and brefeldin A. Tunicamycin 141-152 uncharacterized protein Chlamydomonas reinhardtii 37-41 29385296-7 2018 Treatment with a low concentration of tunicamycin resulted in growth arrest and cytolysis in ire1 mutants, but not in CC-4533 cells. Tunicamycin 38-49 uncharacterized protein Chlamydomonas reinhardtii 93-97 29385296-9 2018 The survival of ire1 mutants treated with tunicamycin improved in the presence of the ROS scavenger glutathione, suggesting that ire1 mutants failed to maintain ROS levels under ER stress. Tunicamycin 42-53 uncharacterized protein Chlamydomonas reinhardtii 16-20 29385296-9 2018 The survival of ire1 mutants treated with tunicamycin improved in the presence of the ROS scavenger glutathione, suggesting that ire1 mutants failed to maintain ROS levels under ER stress. Tunicamycin 42-53 uncharacterized protein Chlamydomonas reinhardtii 129-133 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 192-197 29541178-7 2018 Mechanism analysis demonstrated that Tunicamycin inhibited the protein kinase B (Akt) and nuclear factor-kappaB (NF-kappaB) signaling pathways, whilst Akt overexpression significantly cancelled out the Tunicamycin-inhibited growth and aggressiveness of breast cancer cells, as compared with control cells. Tunicamycin 37-48 thymoma viral proto-oncogene 1 Mus musculus 81-84 29541178-7 2018 Mechanism analysis demonstrated that Tunicamycin inhibited the protein kinase B (Akt) and nuclear factor-kappaB (NF-kappaB) signaling pathways, whilst Akt overexpression significantly cancelled out the Tunicamycin-inhibited growth and aggressiveness of breast cancer cells, as compared with control cells. Tunicamycin 202-213 thymoma viral proto-oncogene 1 Mus musculus 151-154 29541178-9 2018 In conclusion, these results indicate that Tunicamycin may inhibit the growth and aggressiveness of breast cancer cells via regulation of the Akt/NF-kappaB signaling pathway. Tunicamycin 43-54 thymoma viral proto-oncogene 1 Mus musculus 142-145 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 X-box binding protein 1 Homo sapiens 90-113 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 activating transcription factor 4 Homo sapiens 122-155 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 activating transcription factor 4 Homo sapiens 156-160 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 29707686-5 2018 Before commencing SCNT, somatic cells treated with tunicamycin (TM), an ER stress inducer, confirmed the splicing of Xbp1 mRNA and increased expressions of ER stress-associated genes. Tunicamycin 51-62 X-box binding protein 1 Homo sapiens 117-121 28822264-8 2018 RESULT: Tunicamycin greatly increased protein levels of GRP94. Tunicamycin 8-19 heat shock protein 90, beta (Grp94), member 1 Mus musculus 56-61 29323465-3 2018 Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response. Tunicamycin 42-53 sequestosome-1 Cricetulus griseus 103-109 29323465-3 2018 Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response. Tunicamycin 42-53 endoplasmic reticulum chaperone BiP Cricetulus griseus 111-116 29323465-3 2018 Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response. Tunicamycin 42-53 homocysteine-responsive endoplasmic reticulum-resident ubiquitin-like domain member 1 protein Cricetulus griseus 122-129 29323465-3 2018 Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response. Tunicamycin 42-53 cyclic AMP-dependent transcription factor ATF-5 Cricetulus griseus 204-208 29323465-3 2018 Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response. Tunicamycin 42-53 teneurin-4 Cricetulus griseus 210-214 29323465-3 2018 Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response. Tunicamycin 42-53 survivin Cricetulus griseus 220-225 29344654-0 2018 Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway. Tunicamycin 0-11 mitogen-activated protein kinase 1 Homo sapiens 85-88 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 44-55 mechanistic target of rapamycin kinase Homo sapiens 139-143 28825160-5 2018 Next, we established Neuro2a cells with edited GADD34 and ATF4/GADD34 genes and found that ATF4 acts as a proapoptotic factor, but GADD34 depletion did not attenuate the expression of cleaved caspase-3 induced by tunicamycin treatment. Tunicamycin 213-224 activating transcription factor 4 Mus musculus 91-95 29344654-0 2018 Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway. Tunicamycin 0-11 mitogen-activated protein kinase 8 Homo sapiens 89-92 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 182-193 mitogen-activated protein kinase 1 Homo sapiens 118-121 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 182-193 mitogen-activated protein kinase 8 Homo sapiens 122-125 29344654-0 2018 Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway. Tunicamycin 0-11 AKT serine/threonine kinase 1 Homo sapiens 102-105 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 182-193 AKT serine/threonine kinase 1 Homo sapiens 135-138 29344654-0 2018 Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway. Tunicamycin 0-11 mechanistic target of rapamycin kinase Homo sapiens 106-110 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 182-193 mechanistic target of rapamycin kinase Homo sapiens 139-143 29344654-4 2018 Western blotting, immunohistochemistry, apoptotic assays and immunofluorescence were used to analyze the therapeutic effects of tunicamycin on apoptosis, growth, aggressiveness and cell cycle of colon tumor cells, by downregulation of fibronectin, vimentin and E-cadherin expression levels. Tunicamycin 128-139 fibronectin 1 Homo sapiens 235-246 29344654-4 2018 Western blotting, immunohistochemistry, apoptotic assays and immunofluorescence were used to analyze the therapeutic effects of tunicamycin on apoptosis, growth, aggressiveness and cell cycle of colon tumor cells, by downregulation of fibronectin, vimentin and E-cadherin expression levels. Tunicamycin 128-139 vimentin Homo sapiens 248-256 29344654-4 2018 Western blotting, immunohistochemistry, apoptotic assays and immunofluorescence were used to analyze the therapeutic effects of tunicamycin on apoptosis, growth, aggressiveness and cell cycle of colon tumor cells, by downregulation of fibronectin, vimentin and E-cadherin expression levels. Tunicamycin 128-139 cadherin 1 Homo sapiens 261-271 29344654-6 2018 In addition, tunicamycin administration promoted apoptosis of colon carcinoma cells via upregulation of apoptotic protease activating factor 1 and cytochrome c expression levels, which are proteins that have a role in mitochondrial apoptosis signaling. Tunicamycin 13-24 apoptotic peptidase activating factor 1 Homo sapiens 104-142 29344654-6 2018 In addition, tunicamycin administration promoted apoptosis of colon carcinoma cells via upregulation of apoptotic protease activating factor 1 and cytochrome c expression levels, which are proteins that have a role in mitochondrial apoptosis signaling. Tunicamycin 13-24 cytochrome c, somatic Homo sapiens 147-159 29344654-8 2018 Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells. Tunicamycin 39-50 mitogen-activated protein kinase 1 Homo sapiens 100-137 29344654-8 2018 Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells. Tunicamycin 39-50 mitogen-activated protein kinase 1 Homo sapiens 139-142 29344654-8 2018 Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells. Tunicamycin 39-50 mitogen-activated protein kinase 8 Homo sapiens 145-174 29344654-8 2018 Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells. Tunicamycin 39-50 AKT serine/threonine kinase 1 Homo sapiens 197-200 29344654-8 2018 Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells. Tunicamycin 39-50 mechanistic target of rapamycin kinase Homo sapiens 217-246 29344654-8 2018 Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells. Tunicamycin 39-50 mechanistic target of rapamycin kinase Homo sapiens 248-252 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 43-54 mitogen-activated protein kinase 1 Homo sapiens 29-32 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 43-54 mitogen-activated protein kinase 8 Homo sapiens 82-85 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 43-54 AKT serine/threonine kinase 1 Homo sapiens 87-90 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 43-54 mechanistic target of rapamycin kinase Homo sapiens 95-99 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 134-145 mitogen-activated protein kinase 1 Homo sapiens 29-32 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 134-145 mitogen-activated protein kinase 8 Homo sapiens 82-85 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 134-145 AKT serine/threonine kinase 1 Homo sapiens 87-90 29344654-9 2018 Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma. Tunicamycin 134-145 mechanistic target of rapamycin kinase Homo sapiens 95-99 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 44-55 mitogen-activated protein kinase 1 Homo sapiens 118-121 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 44-55 mitogen-activated protein kinase 8 Homo sapiens 122-125 29344654-11 2018 In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy. Tunicamycin 44-55 AKT serine/threonine kinase 1 Homo sapiens 135-138 29273683-6 2018 Inhibiting glycosylation by tunicamycin also markedly reduced human and rat CBG steroid-binding activities. Tunicamycin 28-39 serpin family A member 6 Rattus norvegicus 76-79 29459785-6 2018 Structural and functional analyses reveal the difference between GPT and MraY in their mechanisms of inhibition by tunicamycin. Tunicamycin 115-126 glutamic--pyruvic transaminase Homo sapiens 65-68 29212664-8 2018 Failure to induce the unfolded protein response in trl1Delta cells grown with tunicamycin is lethal owing to their inability to ligate HAC1 after its cleavage by Ire1. Tunicamycin 78-89 transcription factor HAC1 Saccharomyces cerevisiae S288C 135-139 29212664-8 2018 Failure to induce the unfolded protein response in trl1Delta cells grown with tunicamycin is lethal owing to their inability to ligate HAC1 after its cleavage by Ire1. Tunicamycin 78-89 bifunctional endoribonuclease/protein kinase IRE1 Saccharomyces cerevisiae S288C 162-166 29495436-5 2018 In the present study, tunicamycin, an N-glycosyltransferase inhibitor, was employed to treat CHO cells (CHO-CRT) stably expressing full-length recombinant mouse CRT in secreted form for preparation of aberrantly glycosylated eCRT (tun-eCRT). Tunicamycin 22-33 calreticulin Homo sapiens 108-111 29495436-5 2018 In the present study, tunicamycin, an N-glycosyltransferase inhibitor, was employed to treat CHO cells (CHO-CRT) stably expressing full-length recombinant mouse CRT in secreted form for preparation of aberrantly glycosylated eCRT (tun-eCRT). Tunicamycin 22-33 calreticulin Mus musculus 161-164 29275936-3 2018 This study investigated the effect of Akt2 knockdown on tunicamycin (TM)-induced cytotoxicity in cardiomyocytes and the underlying mechanisms with a focus on the JNK-Wnt pathway. Tunicamycin 56-67 AKT serine/threonine kinase 2 Homo sapiens 38-42 29275936-3 2018 This study investigated the effect of Akt2 knockdown on tunicamycin (TM)-induced cytotoxicity in cardiomyocytes and the underlying mechanisms with a focus on the JNK-Wnt pathway. Tunicamycin 69-71 AKT serine/threonine kinase 2 Homo sapiens 38-42 29206917-3 2018 Paraffin sections from N-glycosylation inhibitor tunicamycin treated ER-/PR-/HER2+ (double negative) breast tumor in athymic nude mice exhibited reduced N-glycan but increased GRP78 expression. Tunicamycin 49-60 erb-b2 receptor tyrosine kinase 2 Homo sapiens 77-81 29206917-3 2018 Paraffin sections from N-glycosylation inhibitor tunicamycin treated ER-/PR-/HER2+ (double negative) breast tumor in athymic nude mice exhibited reduced N-glycan but increased GRP78 expression. Tunicamycin 49-60 heat shock protein 5 Mus musculus 176-181 29206917-4 2018 We have evaluated the effect of tunicamycin on cellular localization of GRP78 in metastatic human breast cancer cells MDA-MB-231 (ER-/PR-/HER2-). Tunicamycin 32-43 heat shock protein family A (Hsp70) member 5 Homo sapiens 72-77 29206917-7 2018 GRP78 expression (protein and mRNA) was higher in tunicamycin (1.0 mug/mL) treated MCF-7 and MDA-MB-231 cells. Tunicamycin 50-61 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 29206917-12 2018 The conclusion, GRP78 is expressed neither on the outer-leaflet of the (ER-/PR-/HER2-) human breast cancer cells nor it is secreted into the culture media during tunicamycin-induced ER stress. Tunicamycin 162-173 heat shock protein family A (Hsp70) member 5 Homo sapiens 16-21 29459785-2 2018 The enzyme UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosaminephosphotransferase (GlcNAc-1-P-transferase or GPT) catalyzes the first and committed step of N-linked glycosylation in the endoplasmic reticulum membrane, and it is the target of the natural product tunicamycin. Tunicamycin 272-283 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 11-91 29459785-2 2018 The enzyme UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosaminephosphotransferase (GlcNAc-1-P-transferase or GPT) catalyzes the first and committed step of N-linked glycosylation in the endoplasmic reticulum membrane, and it is the target of the natural product tunicamycin. Tunicamycin 272-283 glutamic--pyruvic transaminase Homo sapiens 119-122 29459785-3 2018 Tunicamycin has potent antibacterial activity, inhibiting the bacterial cell wall synthesis enzyme MraY, but its usefulness as an antibiotic is limited by off-target inhibition of human GPT. Tunicamycin 0-11 glutamic--pyruvic transaminase Homo sapiens 186-189 29459785-5 2018 Here we present crystal structures of human GPT in complex with tunicamycin. Tunicamycin 64-75 glutamic--pyruvic transaminase Homo sapiens 44-47 29382365-12 2018 Tunicamycin induced apoptosis of MZB1+ cells in target organs, resulting in decreased serum anti-dsDNA antibody levels. Tunicamycin 0-11 marginal zone B and B1 cell specific protein Homo sapiens 33-37 29307512-11 2018 ER stress was readily induced by Tunicamycin and resulted in a reduction of insulin mRNA. Tunicamycin 33-44 insulin Homo sapiens 76-83 29079428-0 2018 Globular adiponectin protects hepatocytes from tunicamycin-induced cell death via modulation of the inflammasome and heme oxygenase-1 induction. Tunicamycin 47-58 adiponectin, C1Q and collagen domain containing Rattus norvegicus 9-20 29079428-0 2018 Globular adiponectin protects hepatocytes from tunicamycin-induced cell death via modulation of the inflammasome and heme oxygenase-1 induction. Tunicamycin 47-58 heme oxygenase 1 Rattus norvegicus 117-133 29079428-5 2018 In the present study, we examined the protective effect of globular adiponectin (gAcrp) on tunicamycin-induced cell death and further investigated its potential underlying mechanisms in rat hepatocytes. Tunicamycin 91-102 adiponectin, C1Q and collagen domain containing Rattus norvegicus 68-79 29079428-7 2018 Interestingly, gAcrp prevented the tunicamycin-induced activation of the inflammasome, a key platform involved in the production of inflammatory cytokines that induces pyroptosis, determined by suppression of interleukin-1beta (IL-1beta) maturation, apoptosis-associated speck-like protein containing a carboxy-terminal CARD (ASC) speck formation, and caspase-1 activation. Tunicamycin 35-46 interleukin 1 beta Rattus norvegicus 209-226 29079428-7 2018 Interestingly, gAcrp prevented the tunicamycin-induced activation of the inflammasome, a key platform involved in the production of inflammatory cytokines that induces pyroptosis, determined by suppression of interleukin-1beta (IL-1beta) maturation, apoptosis-associated speck-like protein containing a carboxy-terminal CARD (ASC) speck formation, and caspase-1 activation. Tunicamycin 35-46 interleukin 1 beta Rattus norvegicus 228-236 29079428-7 2018 Interestingly, gAcrp prevented the tunicamycin-induced activation of the inflammasome, a key platform involved in the production of inflammatory cytokines that induces pyroptosis, determined by suppression of interleukin-1beta (IL-1beta) maturation, apoptosis-associated speck-like protein containing a carboxy-terminal CARD (ASC) speck formation, and caspase-1 activation. Tunicamycin 35-46 caspase 1 Rattus norvegicus 352-361 29079428-9 2018 In addition, inhibition of heme oxygenase-1 (HO-1) signaling by pretreatment with SnPP, a pharmacological inhibitor of HO-1, or transfection with an siRNA targeting HO-1, abrogated the protective effects of gAcrp against tunicamycin-induced cell death and abolished the suppressive effect on the inflammasome activation, demonstrating that HO-1 signaling plays a crucial role in the protective effect of gAcrp against tunicamycin-induced damage in liver cells. Tunicamycin 221-232 heme oxygenase 1 Rattus norvegicus 27-43 29079428-9 2018 In addition, inhibition of heme oxygenase-1 (HO-1) signaling by pretreatment with SnPP, a pharmacological inhibitor of HO-1, or transfection with an siRNA targeting HO-1, abrogated the protective effects of gAcrp against tunicamycin-induced cell death and abolished the suppressive effect on the inflammasome activation, demonstrating that HO-1 signaling plays a crucial role in the protective effect of gAcrp against tunicamycin-induced damage in liver cells. Tunicamycin 221-232 heme oxygenase 1 Rattus norvegicus 45-49 29079428-9 2018 In addition, inhibition of heme oxygenase-1 (HO-1) signaling by pretreatment with SnPP, a pharmacological inhibitor of HO-1, or transfection with an siRNA targeting HO-1, abrogated the protective effects of gAcrp against tunicamycin-induced cell death and abolished the suppressive effect on the inflammasome activation, demonstrating that HO-1 signaling plays a crucial role in the protective effect of gAcrp against tunicamycin-induced damage in liver cells. Tunicamycin 418-429 heme oxygenase 1 Rattus norvegicus 27-43 29079428-9 2018 In addition, inhibition of heme oxygenase-1 (HO-1) signaling by pretreatment with SnPP, a pharmacological inhibitor of HO-1, or transfection with an siRNA targeting HO-1, abrogated the protective effects of gAcrp against tunicamycin-induced cell death and abolished the suppressive effect on the inflammasome activation, demonstrating that HO-1 signaling plays a crucial role in the protective effect of gAcrp against tunicamycin-induced damage in liver cells. Tunicamycin 418-429 heme oxygenase 1 Rattus norvegicus 45-49 29303997-7 2018 A role for glycosylation in cell-surface tetherin expression is supported by tunicamycin treatment, which inhibits the first step of N-linked glycosylation and impairs both cell-surface expression and antiviral activity. Tunicamycin 77-88 bone marrow stromal cell antigen 2 Homo sapiens 41-49 29531800-3 2018 To this end, we investigated the effects of a subcytotoxic concentration of Tunicamycin in IRE1alpha-proficient and in IRE1alpha-deficient cells, by pharmacological inhibition with 4mu8 C or down-regulation by specific siRNA. Tunicamycin 76-87 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 91-100 29105510-10 2018 In vitro, T6 cells exposed to tunicamycin by increasing abundances of CHOP, sXBP1, cleaved caspase-3, and LC3BII were diminished in the cell cultures transfected with the miR-29a mimic. Tunicamycin 30-41 DNA-damage inducible transcript 3 Mus musculus 70-74 30637701-12 2018 Inhibition of GPT with tunicamycin downregulates the DPMS catalytic activity quantitatively. Tunicamycin 23-34 glutamic--pyruvic transaminase Homo sapiens 14-17 30637701-12 2018 Inhibition of GPT with tunicamycin downregulates the DPMS catalytic activity quantitatively. Tunicamycin 23-34 dolichyl-phosphate mannosyltransferase subunit 1, catalytic Bos taurus 53-57 30637701-14 2018 Interestingly, nano-formulated tunicamycin is three times more potent in inhibiting the cell cycle progression than the native tunicamycin and is supported by downregulation of the ratio of phospho-p53 to total-p53 as well as phospho-Rb to total Rb. Tunicamycin 31-42 tumor protein p53 Homo sapiens 198-201 30637701-14 2018 Interestingly, nano-formulated tunicamycin is three times more potent in inhibiting the cell cycle progression than the native tunicamycin and is supported by downregulation of the ratio of phospho-p53 to total-p53 as well as phospho-Rb to total Rb. Tunicamycin 31-42 tumor protein p53 Homo sapiens 211-214 29705800-7 2018 RESULTS: A549 cells switched from a cobblestone-like appearance to an elongated fibroblast like appearance after exposure to tunicamycin or bleomycin, accompanied by increased expression of N-cadherin, alpha-SMA and Collagen I. Tunicamycin 125-136 cadherin 2 Homo sapiens 190-200 29705800-8 2018 Meanwhile, GRP78 was upregulated in A549 cells exposed to tunicamycin or bleomycin. Tunicamycin 58-69 heat shock protein family A (Hsp70) member 5 Homo sapiens 11-16 29705800-10 2018 Moreover, tunicamycin and bleomycin promoted the expression of HDAC2 and HDAC6, and HDACs inhibitor SAHA abrogated the morphological and biochemical changes in A549 cells. Tunicamycin 10-21 histone deacetylase 2 Homo sapiens 63-68 29705800-10 2018 Moreover, tunicamycin and bleomycin promoted the expression of HDAC2 and HDAC6, and HDACs inhibitor SAHA abrogated the morphological and biochemical changes in A549 cells. Tunicamycin 10-21 histone deacetylase 6 Homo sapiens 73-78 29105510-10 2018 In vitro, T6 cells exposed to tunicamycin by increasing abundances of CHOP, sXBP1, cleaved caspase-3, and LC3BII were diminished in the cell cultures transfected with the miR-29a mimic. Tunicamycin 30-41 microRNA 29a Mus musculus 171-178 29154199-6 2018 Importantly, UVB treatment perturbs the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and LC3-II turnover in response to treatment with MTOR inhibitors (Torin 1 and pp242), as well as endoplasmic reticular stress (A23187 and tunicamycin), inositol pathway (L690,330) and autophagy inducers (resveratrol and STF62247). Tunicamycin 258-269 microtubule associated protein 1 light chain 3 alpha Homo sapiens 102-105 29962431-6 2018 In mice, postprandial and tunicamycin-induced ER stress was significantly reduced by overexpression of FGF21 using a recombinant adenovirus. Tunicamycin 26-37 fibroblast growth factor 21 Mus musculus 103-108 29154199-6 2018 Importantly, UVB treatment perturbs the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and LC3-II turnover in response to treatment with MTOR inhibitors (Torin 1 and pp242), as well as endoplasmic reticular stress (A23187 and tunicamycin), inositol pathway (L690,330) and autophagy inducers (resveratrol and STF62247). Tunicamycin 258-269 mechanistic target of rapamycin kinase Homo sapiens 169-173 29212948-4 2017 For the first time to our knowledge, we demonstrate that CRELD2 can serve as a sensitive urinary biomarker for detecting ER stress in podocytes or renal tubular cells in murine models of podocyte ER stress-induced nephrotic syndrome and tunicamycin- or ischemia-reperfusion-induced acute kidney injury (AKI), respectively. Tunicamycin 237-248 cysteine-rich with EGF-like domains 2 Mus musculus 57-63 29234100-5 2017 The total number of ER-mitochondria associations detected by this approach increases in response to tunicamycin-induced ER stress, serum deprivation or reduced levels of mitofusin 2 (MFN2). Tunicamycin 100-111 mitofusin 2 Homo sapiens 170-181 29234100-5 2017 The total number of ER-mitochondria associations detected by this approach increases in response to tunicamycin-induced ER stress, serum deprivation or reduced levels of mitofusin 2 (MFN2). Tunicamycin 100-111 mitofusin 2 Homo sapiens 183-187 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 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 90 beta family member 1 Rattus norvegicus 159-164 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 caspase 12 Rattus norvegicus 169-179 28941626-4 2017 WT and PTP1B knockout mice were subjected to the ER stress inducer tunicamycin (1mg/kg). Tunicamycin 67-78 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 7-12 28941626-8 2017 Levels of serine phosphorylation of IRS-1, TRIB3, Atg5/7, LC3B and the autophagy adaptor p62 were significantly upregulated while IRS-1 tyrosine phosphorylation was reduced by tunicamycin, the effect of which were obliterated by PTP1B ablation. Tunicamycin 176-187 insulin receptor substrate 1 Mus musculus 36-41 28150859-8 2017 In addition, cell death resulting from tunicamycin-induced ER stress was prevented when pLE cells were treated with the combination of tunicamycin and BDNF which also decreased cells in the Sub-G1 phase of the cell cycle. Tunicamycin 39-50 brain derived neurotrophic factor Sus scrofa 151-155 29293771-9 2017 Furthermore, adiponectin reduced tunicamycin-induced expression and activation of endoplasmic reticulum stress-related proteins in MAC-T cells and attenuated the repressive effect of tunicamycin on proliferation of MAC-T cells. Tunicamycin 33-44 adiponectin, C1Q and collagen domain containing Bos taurus 13-24 29293771-9 2017 Furthermore, adiponectin reduced tunicamycin-induced expression and activation of endoplasmic reticulum stress-related proteins in MAC-T cells and attenuated the repressive effect of tunicamycin on proliferation of MAC-T cells. Tunicamycin 183-194 adiponectin, C1Q and collagen domain containing Bos taurus 13-24 28951205-8 2017 Overexpression of YAP1-5SA significantly inhibited tunicamycin-induced caspase-8 processing without affecting phosphorylation of p-38 and Akt. Tunicamycin 51-62 Yes1 associated transcriptional regulator Homo sapiens 18-26 29226084-4 2017 The N-glycosylation inhibitor tunicamycin reduced the apparent molecular weight of immunoreactivity associated with myc-tagged GPR61 by 1-2 kDa, which was comparable to the evident molecular weight of the myc-tagged N12S GPR61 mutant with disrupted consensus N-glycosylation site. Tunicamycin 30-41 G protein-coupled receptor 61 Homo sapiens 127-132 29226084-4 2017 The N-glycosylation inhibitor tunicamycin reduced the apparent molecular weight of immunoreactivity associated with myc-tagged GPR61 by 1-2 kDa, which was comparable to the evident molecular weight of the myc-tagged N12S GPR61 mutant with disrupted consensus N-glycosylation site. Tunicamycin 30-41 G protein-coupled receptor 61 Homo sapiens 221-226 29226084-5 2017 Analysis of GPR61 expression demonstrated that tunicamycin treatment reduced considerably heterologous expression of GPR61 in the cell membrane despite the N12S GPR61 mutant being readily expressed at the cell surface. Tunicamycin 47-58 G protein-coupled receptor 61 Homo sapiens 12-17 29226084-5 2017 Analysis of GPR61 expression demonstrated that tunicamycin treatment reduced considerably heterologous expression of GPR61 in the cell membrane despite the N12S GPR61 mutant being readily expressed at the cell surface. Tunicamycin 47-58 G protein-coupled receptor 61 Homo sapiens 117-122 29226084-5 2017 Analysis of GPR61 expression demonstrated that tunicamycin treatment reduced considerably heterologous expression of GPR61 in the cell membrane despite the N12S GPR61 mutant being readily expressed at the cell surface. Tunicamycin 47-58 G protein-coupled receptor 61 Homo sapiens 117-122 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 caspase 3 Homo sapiens 78-87 29066182-8 2017 Exposure of PCECs to the chemical ER stress inducer tunicamycin also increased sEH expression. Tunicamycin 52-63 epoxide hydrolase 2 Homo sapiens 79-82 29066182-10 2017 The impairment of endothelium-dependent vasorelaxation induced by Ang-II or tunicamycin was ameliorated by inhibitors of ER stress or sEH. Tunicamycin 76-87 epoxide hydrolase 2 Homo sapiens 134-137 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 28951205-8 2017 Overexpression of YAP1-5SA significantly inhibited tunicamycin-induced caspase-8 processing without affecting phosphorylation of p-38 and Akt. Tunicamycin 51-62 caspase 8 Homo sapiens 71-80 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 28951205-5 2017 YAP1 protein expression was downregulated by tunicamycin and the phosphorylation of YAP1 at the Ser127 site was significantly increased by tunicamycin. Tunicamycin 45-56 Yes1 associated transcriptional regulator Homo sapiens 0-4 28951205-5 2017 YAP1 protein expression was downregulated by tunicamycin and the phosphorylation of YAP1 at the Ser127 site was significantly increased by tunicamycin. Tunicamycin 139-150 Yes1 associated transcriptional regulator Homo sapiens 0-4 28951205-9 2017 Furthermore, the overexpression of YAP1-5SA significantly restored the decrease in ANKRD1 expression induced by tunicamycin. Tunicamycin 112-123 Yes1 associated transcriptional regulator Homo sapiens 35-43 28951205-5 2017 YAP1 protein expression was downregulated by tunicamycin and the phosphorylation of YAP1 at the Ser127 site was significantly increased by tunicamycin. Tunicamycin 139-150 Yes1 associated transcriptional regulator Homo sapiens 84-88 28951205-6 2017 Tunicamycin further decreased cell viability followed by an increase in caspase-3 processing in the absence of YAP1 when compared with treatment only with tunicamycin or siYAP1. Tunicamycin 0-11 caspase 3 Homo sapiens 72-81 28951205-7 2017 On the other hand, overexpression of a constitutively active YAP1 (YAP1-5SA), which lacks five serine phosphorylation sites, significantly prevented the caspase-3 processing and restored the decrease in cell viability induced by tunicamycin. Tunicamycin 229-240 Yes1 associated transcriptional regulator Homo sapiens 61-65 28951205-7 2017 On the other hand, overexpression of a constitutively active YAP1 (YAP1-5SA), which lacks five serine phosphorylation sites, significantly prevented the caspase-3 processing and restored the decrease in cell viability induced by tunicamycin. Tunicamycin 229-240 Yes1 associated transcriptional regulator Homo sapiens 67-75 28951205-9 2017 Furthermore, the overexpression of YAP1-5SA significantly restored the decrease in ANKRD1 expression induced by tunicamycin. Tunicamycin 112-123 ankyrin repeat domain 1 Homo sapiens 83-89 28951205-10 2017 The inhibition of tunicamycin-induced caspase-3 cleavage by YAP1-5SA was markedly attenuated in ANKRD1-knockdown cells. Tunicamycin 18-29 caspase 3 Homo sapiens 38-47 28951205-10 2017 The inhibition of tunicamycin-induced caspase-3 cleavage by YAP1-5SA was markedly attenuated in ANKRD1-knockdown cells. Tunicamycin 18-29 Yes1 associated transcriptional regulator Homo sapiens 60-68 28951205-10 2017 The inhibition of tunicamycin-induced caspase-3 cleavage by YAP1-5SA was markedly attenuated in ANKRD1-knockdown cells. Tunicamycin 18-29 ankyrin repeat domain 1 Homo sapiens 96-102 28063235-11 2017 In addition, adiponectin inhibited tunicamycin-induced endoplasmic reticulum (ER)-stress through effects on ER stress regulated proteins in pLE cells. Tunicamycin 35-46 adiponectin, C1Q and collagen domain containing Homo sapiens 13-24 29095946-4 2017 Treatment of FRTL-5 thyrocytes with the ER stress inducer tunicamycin (TM) dose-dependently increased the mRNA and/or protein levels of known UPR target genes, stimulated phosphorylation of the ER stress sensor protein kinase RNA-like ER kinase (PERK) and of the PERK target protein eukaryotic initiation factor 2alpha (eIF2alpha) and caused splicing of the ER stress-sensitive transcription factor X-box binding protein (XBP-1) (P < 0.05). Tunicamycin 58-69 eukaryotic translation initiation factor 2A Rattus norvegicus 320-329 29095946-4 2017 Treatment of FRTL-5 thyrocytes with the ER stress inducer tunicamycin (TM) dose-dependently increased the mRNA and/or protein levels of known UPR target genes, stimulated phosphorylation of the ER stress sensor protein kinase RNA-like ER kinase (PERK) and of the PERK target protein eukaryotic initiation factor 2alpha (eIF2alpha) and caused splicing of the ER stress-sensitive transcription factor X-box binding protein (XBP-1) (P < 0.05). Tunicamycin 58-69 X-box binding protein 1 Rattus norvegicus 422-427 28383761-9 2017 Meanwhile, in mouse liver phosphorylation of eIF2alpha, a factor that regulates NMD, was increased by both tunicamycin and nutritional interventions. Tunicamycin 107-118 eukaryotic translation initiation factor 2A Mus musculus 45-54 28880013-5 2017 Pretreatment with the N-linked glycosylation inhibitor tunicamycin, osimertinib clearly decreased the production of new PD-L1 protein probably due to a reduction in mRNA. Tunicamycin 55-66 CD274 molecule Homo sapiens 120-125 28634818-7 2017 In cells treated with the ER stressors thapsigargin and tunicamycin, expression of SG2NA was increased at both mRNA and protein levels. Tunicamycin 56-67 striatin, calmodulin binding protein 3 Mus musculus 83-88 28580641-4 2017 Melatonin significantly inhibited GCD2 corneal cell death, caspase-3 activation, and poly (ADP-ribose) polymerase 1 cleavage caused by the ER stress inducer, tunicamycin. Tunicamycin 158-169 poly(ADP-ribose) polymerase 1 Homo sapiens 59-115 28949374-4 2017 In the present study, it was demonstrated that mild ER stress resulted in upregulated expression levels of FGF21 and its main receptors, as a response to cell compensation, at the induction of <=5 microM tunicamycin (TM). Tunicamycin 207-218 fibroblast growth factor 21 Rattus norvegicus 107-112 28949374-4 2017 In the present study, it was demonstrated that mild ER stress resulted in upregulated expression levels of FGF21 and its main receptors, as a response to cell compensation, at the induction of <=5 microM tunicamycin (TM). Tunicamycin 220-222 fibroblast growth factor 21 Rattus norvegicus 107-112 29285262-8 2017 Treatment of MV4-11 cells with receptor trafficking inhibitors, tunicamycin and brefeldin A, resulted in deglycosylation of NOX4 and NOX4D. Tunicamycin 64-75 NADPH oxidase 4 Homo sapiens 124-128 28779263-0 2017 Tunicamycin potentiates paclitaxel-induced apoptosis through inhibition of PI3K/AKT and MAPK pathways in breast cancer. Tunicamycin 0-11 thymoma viral proto-oncogene 1 Mus musculus 80-83 28779263-2 2017 However, tunicamycin has the ability to downregulate AKT and MAPK pathways. Tunicamycin 9-20 thymoma viral proto-oncogene 1 Mus musculus 53-56 28779263-11 2017 Both annexin V-FITC/propidium iodide assay and TUNEL assay indicated that the combination of tunicamycin with paclitaxel resulted in significant increased cell apoptosis as compared with individual treatment in vitro and in vivo. Tunicamycin 93-104 annexin A5 Mus musculus 5-14 28779263-13 2017 Western blotting analysis confirmed that tunicamycin decreased paclitaxel-induced upregulation of survival signal pathways such as AKT and MAPK. Tunicamycin 41-52 thymoma viral proto-oncogene 1 Mus musculus 131-134 28779263-14 2017 CONCLUSION: These results revealed that tunicamycin synergistically enhanced the antitumor effects of paclitaxel through potentiating apoptosis via inhibiting paclitaxel-induced elevation of AKT and MAPK pathways. Tunicamycin 40-51 thymoma viral proto-oncogene 1 Mus musculus 191-194 28383761-10 2017 Hepatic expression of GRP78, a central chaperone in ER stress responses, was increased by tunicamycin but not by the nutritional interventions. Tunicamycin 90-101 heat shock protein 5 Mus musculus 22-27 28597972-5 2017 We then found that overexpression of SERP1 could rescue GLP-1R glycosylation after application of tunicamycin to block N-linked glycosylation. Tunicamycin 98-109 stress associated endoplasmic reticulum protein 1 Homo sapiens 37-42 28597972-8 2017 Moreover, as a GLP-1R interactor, SERP1 could also partly reverse the accumulation of tunicamycin-induced ER stress. Tunicamycin 86-97 glucagon like peptide 1 receptor Homo sapiens 15-21 28597972-8 2017 Moreover, as a GLP-1R interactor, SERP1 could also partly reverse the accumulation of tunicamycin-induced ER stress. Tunicamycin 86-97 stress associated endoplasmic reticulum protein 1 Homo sapiens 34-39 28597972-9 2017 Taken together, our findings identify a group of proteins that interact with GLP-1R and show that one specific interacting protein, SERP1, has an important role in facilitating the glycosylation of GLP-1R and rescuing its activities after ER stress induced by tunicamycin. Tunicamycin 260-271 glucagon like peptide 1 receptor Homo sapiens 77-83 28597972-9 2017 Taken together, our findings identify a group of proteins that interact with GLP-1R and show that one specific interacting protein, SERP1, has an important role in facilitating the glycosylation of GLP-1R and rescuing its activities after ER stress induced by tunicamycin. Tunicamycin 260-271 stress associated endoplasmic reticulum protein 1 Homo sapiens 132-137 28597972-9 2017 Taken together, our findings identify a group of proteins that interact with GLP-1R and show that one specific interacting protein, SERP1, has an important role in facilitating the glycosylation of GLP-1R and rescuing its activities after ER stress induced by tunicamycin. Tunicamycin 260-271 glucagon like peptide 1 receptor Homo sapiens 198-204 28580641-9 2017 Interestingly, melatonin treatments enhanced SEL1L levels and suppressed the inhibition of SEL1L N-glycosylation caused by tunicamycin. Tunicamycin 123-134 SEL1L adaptor subunit of ERAD E3 ubiquitin ligase Homo sapiens 91-96 28688763-7 2017 Interestingly, the level of SLC30A10 mRNA was significantly increased by tunicamycin as an ER stressor, suggesting that the induction of SLC30A10 by MPP+ was caused via ER stress. Tunicamycin 73-84 solute carrier family 30 member 10 Homo sapiens 28-36 27660269-0 2017 ER Stress Induced by Tunicamycin Triggers alpha-Synuclein Oligomerization, Dopaminergic Neurons Death and Locomotor Impairment: a New Model of Parkinson"s Disease. Tunicamycin 21-32 synuclein alpha Rattus norvegicus 42-57 27660269-8 2017 In addition, we observed an extensive alpha-synuclein oligomerization in SNpc of Tm-injected animals when compared with DMSO-injected controls. Tunicamycin 81-83 synuclein alpha Rattus norvegicus 38-53 28980921-7 2017 The glycosylation inhibitor tunicamycin inhibited the recovery of both CD71 and GPA, and BADGP inhibited the recovery of GPA. Tunicamycin 28-39 transferrin receptor Homo sapiens 71-75 28980921-7 2017 The glycosylation inhibitor tunicamycin inhibited the recovery of both CD71 and GPA, and BADGP inhibited the recovery of GPA. Tunicamycin 28-39 glycophorin A (MNS blood group) Homo sapiens 80-83 28935975-10 2017 TSG-6 also blocked both tunicamycin- and palmitate-induced apoptosis of hepatocytes and increased their viability by inducing autophagy formation in these cells. Tunicamycin 24-35 tumor necrosis factor alpha induced protein 6 Mus musculus 0-5 28753226-9 2017 Disruption of endoplasmic reticulum (ER)-to-Golgi transport by co-expression of Sar1(H74L) trapped tunicamycin-released AtFucTc-GFP in the ER, however, without NE localization. Tunicamycin 99-110 synaptobrevin-related protein 1 Arabidopsis thaliana 80-84 28688763-7 2017 Interestingly, the level of SLC30A10 mRNA was significantly increased by tunicamycin as an ER stressor, suggesting that the induction of SLC30A10 by MPP+ was caused via ER stress. Tunicamycin 73-84 solute carrier family 30 member 10 Homo sapiens 137-145 28839162-4 2017 Pharmacologic ER stress induced by tunicamycin upregulates miR-204 and downregulates Sirt1 in the vascular wall/endothelium in vivo and in endothelial cells in vitro. Tunicamycin 35-46 microRNA 204 Mus musculus 59-66 28904368-7 2017 Our TUNEL experiments using tunicamycin, an apoptosis inducer, and GADD34, an inhibitor of eIF2alpha phosphorylation, demonstrated that PC1-5TMC inhibits apoptosis of HEK293T cells in a PKR-eIF2alpha-dependent manner, with concurrent up- and down-regulation of Bcl-2 and Bax, respectively, revealed by Western blotting. Tunicamycin 28-39 polycystin 1, transient receptor potential channel interacting Homo sapiens 136-139 28841673-2 2017 We demonstrated the induction of ER stress in response to tunicamycin stimulation, as evidenced by increased expression of chaperone proteins Grp78, Grp94, and enhanced eukaryotic initiation factor 2 subunit 1 (eIF2alpha) phosphorylation in hepatocellular carcinoma cells. Tunicamycin 58-69 heat shock protein family A (Hsp70) member 5 Homo sapiens 142-147 28841673-2 2017 We demonstrated the induction of ER stress in response to tunicamycin stimulation, as evidenced by increased expression of chaperone proteins Grp78, Grp94, and enhanced eukaryotic initiation factor 2 subunit 1 (eIF2alpha) phosphorylation in hepatocellular carcinoma cells. Tunicamycin 58-69 heat shock protein 90 beta family member 1 Homo sapiens 149-154 28841673-2 2017 We demonstrated the induction of ER stress in response to tunicamycin stimulation, as evidenced by increased expression of chaperone proteins Grp78, Grp94, and enhanced eukaryotic initiation factor 2 subunit 1 (eIF2alpha) phosphorylation in hepatocellular carcinoma cells. Tunicamycin 58-69 eukaryotic translation initiation factor 2A Homo sapiens 211-220 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 28839162-4 2017 Pharmacologic ER stress induced by tunicamycin upregulates miR-204 and downregulates Sirt1 in the vascular wall/endothelium in vivo and in endothelial cells in vitro. Tunicamycin 35-46 sirtuin 1 Mus musculus 85-90 28839162-5 2017 Inhibition of miR-204 protects against tunicamycin-induced vascular/endothelial ER stress, associated impairment of endothelium-dependent vasorelaxation, and preserves endothelial Sirt1. Tunicamycin 39-50 microRNA 204 Mus musculus 14-21 28839162-5 2017 Inhibition of miR-204 protects against tunicamycin-induced vascular/endothelial ER stress, associated impairment of endothelium-dependent vasorelaxation, and preserves endothelial Sirt1. Tunicamycin 39-50 sirtuin 1 Mus musculus 180-185 28955790-6 2017 Using a selected clone, we observed that the expression of HiBiT-tagged ATF4 in the selected cells varied in response to treatment with protein synthesis inhibitors or proteasome inhibitors and tunicamycin. Tunicamycin 194-205 activating transcription factor 4 Mus musculus 72-76 28624282-4 2017 Treatment of MDBK cells with 2 different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), strongly induced ER stress as evident from induction of ER stress target genes, increased phosphorylation of PKR-like ER kinase, and enhanced splicing of X-box binding protein 1. Tunicamycin 83-94 X-box binding protein 1 Bos taurus 255-278 28777337-7 2017 Besides, tunicamycin remarkably increased hepatic triglyceride content and suppressed the expression of apolipoprotein B100. Tunicamycin 9-20 apolipoprotein B Mus musculus 104-123 28777337-8 2017 In addition, tunicamycin-treated mice had lower serum levels of triglyceride, apolipoprotein B, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. Tunicamycin 13-24 apolipoprotein B Mus musculus 78-94 28777337-9 2017 Gene expression of peroxisome proliferator-activated receptor alpha was decreased by tunicamycin, but the protein level was increased. Tunicamycin 85-96 peroxisome proliferator activated receptor alpha Mus musculus 19-67 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 111-122 polo like kinase 2 Homo sapiens 0-4 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 polo like kinase 2 Homo sapiens 0-4 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 polo like kinase 2 Homo sapiens 157-161 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 activating transcription factor 4 Homo sapiens 190-223 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 activating transcription factor 4 Homo sapiens 225-229 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 28067406-7 2017 Ninj1 N-glycosylation was characterized by treatment of tunicamycin and substitution of Asn to Gln or Ala. Tunicamycin 56-67 ninjurin 1 Homo sapiens 0-5 28495589-3 2017 ER stress was induced in brain-derived mouse bEnd5 endothelial cells by thapsigargin or tunicamycin and caused apoptotic cell death over a 72h period. Tunicamycin 88-99 BEN domain containing 5 Mus musculus 45-50 28624282-4 2017 Treatment of MDBK cells with 2 different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), strongly induced ER stress as evident from induction of ER stress target genes, increased phosphorylation of PKR-like ER kinase, and enhanced splicing of X-box binding protein 1. Tunicamycin 96-98 X-box binding protein 1 Bos taurus 255-278 28596490-6 2017 We discovered that interfering with N-linked glycosylation of GPER, either by mutation of the predicted glycosylation sites or pharmacologically with tunicamycin, drives GPER into the nucleus. Tunicamycin 150-161 G protein-coupled estrogen receptor 1 Homo sapiens 62-66 28407373-5 2017 We demonstrated that wild-type and s1p mutant plants produce the active, nuclear form of bZIP28 in response to the ER stress inducer tunicamycin. Tunicamycin 133-144 SITE-1 protease Arabidopsis thaliana 35-38 28407373-5 2017 We demonstrated that wild-type and s1p mutant plants produce the active, nuclear form of bZIP28 in response to the ER stress inducer tunicamycin. Tunicamycin 133-144 Basic-leucine zipper (bZIP) transcription factor family protein Arabidopsis thaliana 89-95 28537902-3 2017 Increasing concentrations of tunicamycin and CDDP activated ERS in SKOV3 cells, reduced cell viability and proliferation, increased apoptosis and autophagy, enhanced expression of ERS-related proteins, and inhibited expression of PI3K/AKT/mTOR pathway-related proteins. Tunicamycin 29-40 AKT serine/threonine kinase 1 Homo sapiens 235-238 28537902-3 2017 Increasing concentrations of tunicamycin and CDDP activated ERS in SKOV3 cells, reduced cell viability and proliferation, increased apoptosis and autophagy, enhanced expression of ERS-related proteins, and inhibited expression of PI3K/AKT/mTOR pathway-related proteins. Tunicamycin 29-40 mechanistic target of rapamycin kinase Homo sapiens 239-243 28482072-9 2017 In response to the ER stress inducer tunicamycin, PGC-1alpha expression was decreased, whereas the ER stress inhibitor 4-phenylbutyric acid blocked high glucose-suppressed PGC-1alpha expression. Tunicamycin 37-48 PPARG coactivator 1 alpha Homo sapiens 50-60 28482072-9 2017 In response to the ER stress inducer tunicamycin, PGC-1alpha expression was decreased, whereas the ER stress inhibitor 4-phenylbutyric acid blocked high glucose-suppressed PGC-1alpha expression. Tunicamycin 37-48 PPARG coactivator 1 alpha Homo sapiens 172-182 28596490-6 2017 We discovered that interfering with N-linked glycosylation of GPER, either by mutation of the predicted glycosylation sites or pharmacologically with tunicamycin, drives GPER into the nucleus. Tunicamycin 150-161 G protein-coupled estrogen receptor 1 Homo sapiens 170-174 28720827-9 2017 In the SH-SY5Y human cells, tunicamycin (TM), a PERK activator, promoted transcription of hsp27; and necrosis induced by glutamate could be rescued by TM, associated with reduced p53 accumulation. Tunicamycin 28-39 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 48-52 28667325-3 2017 The present study reported ER stress induction by tunicamycin treatment that resulted in IRE1alpha-mediated XBP1 mRNA splicing and autophagy. Tunicamycin 50-61 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 89-98 28720827-9 2017 In the SH-SY5Y human cells, tunicamycin (TM), a PERK activator, promoted transcription of hsp27; and necrosis induced by glutamate could be rescued by TM, associated with reduced p53 accumulation. Tunicamycin 28-39 heat shock protein family B (small) member 1 Homo sapiens 90-95 28720827-9 2017 In the SH-SY5Y human cells, tunicamycin (TM), a PERK activator, promoted transcription of hsp27; and necrosis induced by glutamate could be rescued by TM, associated with reduced p53 accumulation. Tunicamycin 28-39 tumor protein p53 Homo sapiens 179-182 28433684-4 2017 Treatment with tunicamycin (Tm) increased SESN2 protein and mRNA levels and reporter gene activity. Tunicamycin 15-26 sestrin 2 Homo sapiens 42-47 28418178-6 2017 In this study, we discovered that UPR-associated transcription factors AtbZIP17, AtbZIP28 and AtbZIP60 responded to tunicamycin (TM) and NaCl induced ER stress and subsequently enhanced Arabidopsis thaliana abiotic stress tolerance. Tunicamycin 116-127 Basic-leucine zipper (bZIP) transcription factor family protein Arabidopsis thaliana 71-79 28418178-6 2017 In this study, we discovered that UPR-associated transcription factors AtbZIP17, AtbZIP28 and AtbZIP60 responded to tunicamycin (TM) and NaCl induced ER stress and subsequently enhanced Arabidopsis thaliana abiotic stress tolerance. Tunicamycin 116-127 basic region/leucine zipper motif 60 Arabidopsis thaliana 94-102 28418178-6 2017 In this study, we discovered that UPR-associated transcription factors AtbZIP17, AtbZIP28 and AtbZIP60 responded to tunicamycin (TM) and NaCl induced ER stress and subsequently enhanced Arabidopsis thaliana abiotic stress tolerance. Tunicamycin 129-131 Basic-leucine zipper (bZIP) transcription factor family protein Arabidopsis thaliana 71-79 28418178-6 2017 In this study, we discovered that UPR-associated transcription factors AtbZIP17, AtbZIP28 and AtbZIP60 responded to tunicamycin (TM) and NaCl induced ER stress and subsequently enhanced Arabidopsis thaliana abiotic stress tolerance. Tunicamycin 129-131 basic region/leucine zipper motif 60 Arabidopsis thaliana 94-102 28487369-5 2017 In N-glycosylation inhibition experiments, we find that treatment with tunicamycin and siRNA-mediated knockdown of the Golgi N-acetylglucosaminyltransferase I gene (MGAT1) induce partial loss of both total and cell-surface levels of the largest mucin, MUC16, and a concomitant reduction in glycocalyx barrier function. Tunicamycin 71-82 alpha-1,3-mannosyl-glycoprotein 2-beta-N-acetylglucosaminyltransferase Homo sapiens 165-170 28487369-5 2017 In N-glycosylation inhibition experiments, we find that treatment with tunicamycin and siRNA-mediated knockdown of the Golgi N-acetylglucosaminyltransferase I gene (MGAT1) induce partial loss of both total and cell-surface levels of the largest mucin, MUC16, and a concomitant reduction in glycocalyx barrier function. Tunicamycin 71-82 LOC100508689 Homo sapiens 245-250 28487369-5 2017 In N-glycosylation inhibition experiments, we find that treatment with tunicamycin and siRNA-mediated knockdown of the Golgi N-acetylglucosaminyltransferase I gene (MGAT1) induce partial loss of both total and cell-surface levels of the largest mucin, MUC16, and a concomitant reduction in glycocalyx barrier function. Tunicamycin 71-82 mucin 16, cell surface associated Homo sapiens 252-257 28978108-0 2017 Tunicamycin induced endoplasmic reticulum stress promotes apoptosis of prostate cancer cells by activating mTORC1. Tunicamycin 0-11 CREB regulated transcription coactivator 1 Mus musculus 107-113 28978108-3 2017 To delineate the role of candidate genes in the apoptotic process under ER stress and to search for new therapeutic strategies to treat metastatic castration resistant prostate cancer, we performed whole genome expression microarray analysis in tunicamycin treated metastatic androgen-insensitive prostate cancer cells, PC-3. Tunicamycin 245-256 proprotein convertase subtilisin/kexin type 1 Homo sapiens 320-324 28978108-8 2017 Overall, our data demonstrate that tunicamycin induced ER stress promotes prostate cancer cell death by activating mTORC1 through eNOS-RagC pathway. Tunicamycin 35-46 CREB regulated transcription coactivator 1 Mus musculus 115-121 28978108-8 2017 Overall, our data demonstrate that tunicamycin induced ER stress promotes prostate cancer cell death by activating mTORC1 through eNOS-RagC pathway. Tunicamycin 35-46 nitric oxide synthase 3 Homo sapiens 130-134 28978108-8 2017 Overall, our data demonstrate that tunicamycin induced ER stress promotes prostate cancer cell death by activating mTORC1 through eNOS-RagC pathway. Tunicamycin 35-46 Ras related GTP binding C Homo sapiens 135-139 28453460-1 2017 OBJECTIVE: The study is to explore the role of tunicamycin-induced endoplasmic reticulum stress (ERS) in human ovarian cancer (OC) SKOV3 cells proliferation, migration and invasion by modulating the activity of PI3K/AKT/mTOR pathway. Tunicamycin 47-58 AKT serine/threonine kinase 1 Homo sapiens 216-219 28453460-1 2017 OBJECTIVE: The study is to explore the role of tunicamycin-induced endoplasmic reticulum stress (ERS) in human ovarian cancer (OC) SKOV3 cells proliferation, migration and invasion by modulating the activity of PI3K/AKT/mTOR pathway. Tunicamycin 47-58 mechanistic target of rapamycin kinase Homo sapiens 220-224 28453460-11 2017 CONCLUSION: The study provides strong evidence that tunicamycin-induced ERS induces the apoptosis of human OC SKOV3 cells through inhibiting PI3K/AKT/mTOR signaling pathway. Tunicamycin 52-63 AKT serine/threonine kinase 1 Homo sapiens 146-149 28453460-11 2017 CONCLUSION: The study provides strong evidence that tunicamycin-induced ERS induces the apoptosis of human OC SKOV3 cells through inhibiting PI3K/AKT/mTOR signaling pathway. Tunicamycin 52-63 mechanistic target of rapamycin kinase Homo sapiens 150-154 28671633-2 2017 Here, we show that the overexpression of P-gp in L1210 cells leads to resistance to tunicamycin and benzyl 2-acetamido-2-deoxy-alpha-d-galactopyranoside (GalNAc-alpha-O-benzyl). Tunicamycin 84-95 phosphoglycolate phosphatase Mus musculus 41-45 28671633-3 2017 Tunicamycin induces both glycosylation depression and ubiquitination improvement of P-gp. Tunicamycin 0-11 phosphoglycolate phosphatase Mus musculus 84-88 28671633-8 2017 Elevation of protein ubiquitination after tunicamycin treatment in these cells leads to protein folding rather than protein degradation, resulting at least in the partial lack of cell sensitivity to tunicamycin in L1210 cells after P-gp expression. Tunicamycin 42-53 phosphoglycolate phosphatase Mus musculus 232-236 28667325-3 2017 The present study reported ER stress induction by tunicamycin treatment that resulted in IRE1alpha-mediated XBP1 mRNA splicing and autophagy. Tunicamycin 50-61 X-box binding protein 1 Homo sapiens 108-112 28978049-4 2017 We showed GRP78/BiP translocation to PC3 cell surface in the presence of tunicamycin, an ER stress inductor, and demonstrated the existence of a GRP78/BiP-dependent non-canonical Nrf2 activation, responsible for increased resistance to ER-stress induced apoptosis. Tunicamycin 73-84 heat shock protein family A (Hsp70) member 5 Homo sapiens 10-15 28978049-4 2017 We showed GRP78/BiP translocation to PC3 cell surface in the presence of tunicamycin, an ER stress inductor, and demonstrated the existence of a GRP78/BiP-dependent non-canonical Nrf2 activation, responsible for increased resistance to ER-stress induced apoptosis. Tunicamycin 73-84 heat shock protein family A (Hsp70) member 5 Homo sapiens 16-19 28978049-5 2017 We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment. Tunicamycin 54-65 NFE2 like bZIP transcription factor 2 Homo sapiens 73-77 28978049-5 2017 We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment. Tunicamycin 54-65 AKT serine/threonine kinase 1 Homo sapiens 104-107 28978049-5 2017 We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment. Tunicamycin 54-65 heat shock protein family A (Hsp70) member 5 Homo sapiens 142-147 28978049-5 2017 We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment. Tunicamycin 54-65 heat shock protein family A (Hsp70) member 5 Homo sapiens 148-151 28630443-6 2017 Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP. Tunicamycin 25-36 eukaryotic translation initiation factor 2A Homo sapiens 50-59 28662078-8 2017 Even so, the fibroblasts of patients with DPAGT1-CDG seemed to be more sensitive to the stressor tunicamycin. Tunicamycin 97-108 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 42-48 28562344-5 2017 We showed PHB accumulated at different levels in melanoma cell lines under stressing stimuli, such as (i) treatment with temozolomide (TMZ), dacarbazine (DTIC) and cisplatin; (ii) serum deprivation; (iii) tunicamycin, an UPR inducer. Tunicamycin 205-216 prohibitin 1 Homo sapiens 10-13 28562344-6 2017 Prohibitin accumulated in the mitochondria of melanoma cells after cisplatin and tunicamycin treatment and its de novo accumulation led to chemoresistance melanoma cell lines. Tunicamycin 81-92 prohibitin 1 Homo sapiens 0-10 28562344-7 2017 In contrast, PHB knock-down sensitized melanoma cells to cisplatin and tunicamycin treatment. Tunicamycin 71-82 prohibitin 1 Homo sapiens 13-16 28630443-6 2017 Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP. Tunicamycin 25-36 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 45-49 28630443-6 2017 Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP. Tunicamycin 25-36 activating transcription factor 4 Homo sapiens 60-64 28674530-7 2017 Additional ER stressors such as tunicamycin and thapsigargin also promoted IL-23 expression by PAMP-stimulated DCs. Tunicamycin 32-43 interleukin 23 subunit alpha Homo sapiens 75-80 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 28674530-7 2017 Additional ER stressors such as tunicamycin and thapsigargin also promoted IL-23 expression by PAMP-stimulated DCs. Tunicamycin 32-43 YME1 like 1 ATPase Homo sapiens 95-99 28630443-6 2017 Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP. Tunicamycin 25-36 growth differentiation factor 10 Homo sapiens 99-102 28522733-9 2017 Similarly, administration of either GSK2656157 or overexpression of PERK-K618A in primary neurons rescues the loss of dendritic outgrowth and number of synapses after treatment with a PERK activator, tunicamycin. Tunicamycin 200-211 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 68-72 28577569-5 2017 METHODS: Human apoA-I was overexpressed in HepG2 hepatocytes, which were then treated with 2 mug/mL tunicamycin or 500 muM palmitic acid. Tunicamycin 100-111 apolipoprotein A1 Homo sapiens 15-21 27941872-7 2017 In vitro, AGR2 expression was stimulated by tunicamycin-induced endoplasmic reticulum (ER) stress in both KRAS wild-type normal pancreas cells, as well as in KRAS mutated pancreatic cancer cells and was essential for ER homoeostasis. Tunicamycin 44-55 anterior gradient 2, protein disulphide isomerase family member Homo sapiens 10-14 27941872-7 2017 In vitro, AGR2 expression was stimulated by tunicamycin-induced endoplasmic reticulum (ER) stress in both KRAS wild-type normal pancreas cells, as well as in KRAS mutated pancreatic cancer cells and was essential for ER homoeostasis. Tunicamycin 44-55 KRAS proto-oncogene, GTPase Homo sapiens 106-110 28631572-7 2017 Tunicamycin led to increased expression of GRP78. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 43-48 28631572-8 2017 With tunicamycin treatment, phosphorylation of PERK and eIF2alpha and CHOP expression increased. Tunicamycin 5-16 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 47-51 28631572-8 2017 With tunicamycin treatment, phosphorylation of PERK and eIF2alpha and CHOP expression increased. Tunicamycin 5-16 eukaryotic translation initiation factor 2A Homo sapiens 56-65 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 28631572-10 2017 With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins. Tunicamycin 19-30 BCL2 associated X, apoptosis regulator Homo sapiens 82-85 28631572-10 2017 With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins. Tunicamycin 19-30 BCL2 apoptosis regulator Homo sapiens 133-138 28631572-10 2017 With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins. Tunicamycin 19-30 AKT serine/threonine kinase 1 Homo sapiens 174-177 28631572-10 2017 With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins. Tunicamycin 19-30 mechanistic target of rapamycin kinase Homo sapiens 178-182 28351617-6 2017 Molecular size of FAM5C was reduced by treatment with N-glycosidase F and in FAM5C-expressing cells cultured in the presence of the N-glycosylation inhibitor tunicamycin. Tunicamycin 158-169 BMP/retinoic acid inducible neural specific 3 Homo sapiens 18-23 28811964-8 2017 Suppression of glycosylation with tunicamycin caused a shift in molecular weight and significant decrease in the expression of PD-L2 protein. Tunicamycin 34-45 programmed cell death 1 ligand 2 Homo sapiens 127-132 28336294-9 2017 Interestingly, we found that ER stress induced by either palmitate, tunicamycin, or thapsigargin led to the degradation of Plin2, an important lipid droplet binding protein. Tunicamycin 68-79 perilipin 2 Rattus norvegicus 123-128 28351617-6 2017 Molecular size of FAM5C was reduced by treatment with N-glycosidase F and in FAM5C-expressing cells cultured in the presence of the N-glycosylation inhibitor tunicamycin. Tunicamycin 158-169 BMP/retinoic acid inducible neural specific 3 Homo sapiens 77-82 28351617-7 2017 FAM5C was secreted by the cells and the secretion of FAM5C was blocked by tunicamycin. Tunicamycin 74-85 BMP/retinoic acid inducible neural specific 3 Homo sapiens 0-5 28351617-7 2017 FAM5C was secreted by the cells and the secretion of FAM5C was blocked by tunicamycin. Tunicamycin 74-85 BMP/retinoic acid inducible neural specific 3 Homo sapiens 53-58 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 caspase 12 Rattus norvegicus 151-161 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 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 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 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 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 caspase 3 Rattus norvegicus 137-146 28521463-11 2017 ERp46 overexpression led to reduced sensitivity to ER stress as indicated by higher half maximal inhibitory concentrations for tunicamycin and thapsigargin in ERp46+ cells. Tunicamycin 127-138 thioredoxin domain containing 5 Homo sapiens 0-5 28521463-11 2017 ERp46 overexpression led to reduced sensitivity to ER stress as indicated by higher half maximal inhibitory concentrations for tunicamycin and thapsigargin in ERp46+ cells. Tunicamycin 127-138 thioredoxin domain containing 5 Homo sapiens 159-164 28399139-6 2017 RESULTS: We demonstrate ibutilide attenuated the up-regulation of ER stress markers GRP78 and GRP94 and rescued the decline in calumenin mRNA and protein levels in tunicamycin treated cardiomyocytes. Tunicamycin 164-175 calumenin Rattus norvegicus 127-136 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 eukaryotic translation initiation factor 2 subunit gamma Homo sapiens 91-95 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 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 AKT serine/threonine kinase 1 Homo sapiens 146-149 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 mechanistic target of rapamycin kinase Homo sapiens 157-161 28459209-14 2017 Our study provide evidence that endoplasmic reticulum stress activated by tunicamycin could promote breast cancer cell autophagy and apoptosis and enhance chemosensitivity of MCF-7 cells by inhibiting the PI3K/AKT/mTOR signaling pathway. Tunicamycin 74-85 AKT serine/threonine kinase 1 Homo sapiens 210-213 28459209-14 2017 Our study provide evidence that endoplasmic reticulum stress activated by tunicamycin could promote breast cancer cell autophagy and apoptosis and enhance chemosensitivity of MCF-7 cells by inhibiting the PI3K/AKT/mTOR signaling pathway. Tunicamycin 74-85 mechanistic target of rapamycin kinase Homo sapiens 214-218 28460451-3 2017 In this study we show that abrogation of FLT3ITD glycoprotein maturation using low doses of the N-glycosylation inhibitor tunicamycin has anti-proliferative and pro-apoptotic effects on FLT3ITD-expressing human and murine cell lines. Tunicamycin 122-133 fms related receptor tyrosine kinase 3 Homo sapiens 41-45 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 110-162 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 164-168 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 28202509-6 2017 Accordingly, SCNN1B sensitized gastric cancer cells to the UPR-inducing drug tunicamycin. Tunicamycin 77-88 sodium channel epithelial 1 subunit beta Homo sapiens 13-19 28399139-0 2017 Ibutilide treatment protects against ER stress induced apoptosis by regulating calumenin expression in tunicamycin treated cardiomyocytes. Tunicamycin 103-114 calumenin Rattus norvegicus 79-88 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 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 90 beta family member 1 Rattus norvegicus 124-129 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 calumenin Rattus norvegicus 134-143 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 caspase 3 Rattus norvegicus 217-226 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 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 activating transcription factor 6 Rattus norvegicus 239-243 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 X-box binding protein 1 Rattus norvegicus 261-266 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 BCL2 associated X, apoptosis regulator Rattus norvegicus 281-284 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 BCL2, apoptosis regulator Rattus norvegicus 285-290 28275095-6 2017 In line with this, Bap1 KO mice are more sensitive to tunicamycin-induced renal damage. Tunicamycin 54-65 Brca1 associated protein 1 Mus musculus 19-23 28131804-5 2017 IFN-lambda1 could also inhibit HCV-induced or tunicamycin (a known inducer of autophagy with similar mechanism to HCV infection) -induced LC3B-II expression and autophagosome formation. Tunicamycin 46-57 interferon alpha 1 Homo sapiens 0-3 28131804-5 2017 IFN-lambda1 could also inhibit HCV-induced or tunicamycin (a known inducer of autophagy with similar mechanism to HCV infection) -induced LC3B-II expression and autophagosome formation. Tunicamycin 46-57 microtubule associated protein 1 light chain 3 beta Homo sapiens 138-142 27341688-3 2017 We aimed to investigate whether ERS induced by oxLDL or tunicamycin (TM) in human macrophages is associated with the stimulation of MMP-9 expression and secretion. Tunicamycin 56-67 matrix metallopeptidase 9 Homo sapiens 132-137 27341688-6 2017 Treatment of oxLDL or TM-incubated cells with ERS inhibitor, sodium phenylbutyrate decreased MMP-9 gene expression, secretion, and activity. Tunicamycin 22-24 matrix metallopeptidase 9 Homo sapiens 93-98 27885588-0 2017 A mouse model reveals that Mfsd2a is critical for unfolded protein response upon exposure to tunicamycin. Tunicamycin 93-104 major facilitator superfamily domain containing 2A Mus musculus 27-33 27885588-2 2017 Mfsd2a functions as a transporter for docosahexaenoic acid and also plays a role in the unfolded protein response (UPR) upon tunicamycin (TM) exposure. Tunicamycin 125-136 major facilitator superfamily domain containing 2A Mus musculus 0-6 27885588-2 2017 Mfsd2a functions as a transporter for docosahexaenoic acid and also plays a role in the unfolded protein response (UPR) upon tunicamycin (TM) exposure. Tunicamycin 138-140 major facilitator superfamily domain containing 2A Mus musculus 0-6 27862269-3 2017 In this study, we demonstrated that the Arp2/3 complex was required for reduction of ribosome protein gene expression in response to defective secretion by addition of tunicamycin. Tunicamycin 168-179 actin-related protein 2 Saccharomyces cerevisiae S288C 40-44 27932512-9 2017 Catalase was induced by the canonical ER stressor, tunicamycin, and by I/R in cardiac myocytes from wild-type but not in cardiac myocytes from ATF6 knockout mice. Tunicamycin 51-62 catalase Mus musculus 0-8 28104755-6 2017 Tunicamycin (TM) treatment resulted in expression of non-glycosylated SMPDL3A that was not secreted, and was largely degraded by the proteasome. Tunicamycin 0-11 sphingomyelin phosphodiesterase acid like 3A Homo sapiens 70-77 28331281-9 2017 Exposure to blue LED light in combination with ER stress inducers (tunicamycin and dithiothreitol) induced the aggregation of S-opsin. Tunicamycin 67-78 opsin 1 (cone pigments), short-wave-sensitive (color blindness, tritan) Mus musculus 126-133 28246389-6 2017 In in vitro experiments, insulin resistance was induced by applying tunicamycin to HUVECs. Tunicamycin 68-79 insulin Homo sapiens 25-32 28246389-9 2017 Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM. Tunicamycin 110-121 bone gamma-carboxyglutamate protein Homo sapiens 149-160 28246389-9 2017 Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM. Tunicamycin 110-121 bone gamma-carboxyglutamate protein Homo sapiens 15-26 28246389-9 2017 Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM. Tunicamycin 110-121 insulin Homo sapiens 46-53 28246389-9 2017 Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM. Tunicamycin 110-121 AKT serine/threonine kinase 1 Homo sapiens 83-86 28246389-9 2017 Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM. Tunicamycin 110-121 nuclear factor kappa B subunit 1 Homo sapiens 87-96 28100484-12 2017 But, after treating with tunicamycin, the levels of Has2, Ptgs2, and Ptgfr increased relatively, whereas Igfbp4 expression decreased. Tunicamycin 25-36 hyaluronan synthase 2 Mus musculus 52-56 28100484-12 2017 But, after treating with tunicamycin, the levels of Has2, Ptgs2, and Ptgfr increased relatively, whereas Igfbp4 expression decreased. Tunicamycin 25-36 prostaglandin-endoperoxide synthase 2 Mus musculus 58-63 28100484-12 2017 But, after treating with tunicamycin, the levels of Has2, Ptgs2, and Ptgfr increased relatively, whereas Igfbp4 expression decreased. Tunicamycin 25-36 prostaglandin F receptor Mus musculus 69-74 28100484-12 2017 But, after treating with tunicamycin, the levels of Has2, Ptgs2, and Ptgfr increased relatively, whereas Igfbp4 expression decreased. Tunicamycin 25-36 insulin-like growth factor binding protein 4 Mus musculus 105-111 28223691-5 2017 Maintenance of SKBR-3 cells in tunicamycin (an inhibitor of N-linked glycosylation) resulted in an increase in sensitivity to DXR (0.1 muM DXR P < 0.001) and a decrease in sensitivity to IGF-1 alone and to IGF-1 supplemented with EGF (P < 0.001). Tunicamycin 31-42 insulin like growth factor 1 Homo sapiens 190-195 27383524-0 2017 Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma. Tunicamycin 0-11 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 80-84 27383524-0 2017 Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma. Tunicamycin 0-11 activating transcription factor 4 Mus musculus 85-89 27383524-0 2017 Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma. Tunicamycin 0-11 DNA-damage inducible transcript 3 Mus musculus 90-94 27383524-4 2017 RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling. Tunicamycin 9-20 interleukin 6 Mus musculus 150-154 27383524-4 2017 RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling. Tunicamycin 9-20 chemokine (C-X-C motif) ligand 15 Mus musculus 156-160 27383524-4 2017 RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling. Tunicamycin 9-20 tumor necrosis factor Mus musculus 166-175 27383524-4 2017 RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling. Tunicamycin 9-20 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 180-184 27383524-4 2017 RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling. Tunicamycin 9-20 activating transcription factor 4 Mus musculus 185-189 27383524-4 2017 RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling. Tunicamycin 9-20 DNA-damage inducible transcript 3 Mus musculus 190-194 27383524-6 2017 Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVALPS-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma. Tunicamycin 14-25 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 204-208 27383524-6 2017 Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVALPS-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma. Tunicamycin 14-25 activating transcription factor 4 Mus musculus 209-213 27383524-6 2017 Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVALPS-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma. Tunicamycin 14-25 DNA-damage inducible transcript 3 Mus musculus 214-218 28303141-4 2017 FKBP13 expression was induced largely in the lumen of ER in response to treatment with an ER stressor tunicamycin or overexpression of an adaptive unfolded protein response (UPR) protein X-box binding protein 1 (XBP1). Tunicamycin 102-113 FK506 binding protein 2 Mus musculus 0-6 27915415-0 2017 Exendin-4 protects HUVECs from tunicamycin-induced apoptosis via inhibiting the IRE1a/JNK/caspase-3 pathway. Tunicamycin 31-42 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 80-85 27915415-0 2017 Exendin-4 protects HUVECs from tunicamycin-induced apoptosis via inhibiting the IRE1a/JNK/caspase-3 pathway. Tunicamycin 31-42 mitogen-activated protein kinase 8 Homo sapiens 86-89 27915415-0 2017 Exendin-4 protects HUVECs from tunicamycin-induced apoptosis via inhibiting the IRE1a/JNK/caspase-3 pathway. Tunicamycin 31-42 caspase 3 Homo sapiens 90-99 27915415-8 2017 Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4. Tunicamycin 109-120 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 26-35 27915415-8 2017 Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4. Tunicamycin 109-120 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 36-45 27915415-8 2017 Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4. Tunicamycin 109-120 mitogen-activated protein kinase 8 Homo sapiens 49-52 27915415-8 2017 Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4. Tunicamycin 109-120 mitogen-activated protein kinase 8 Homo sapiens 53-56 27915415-8 2017 Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4. Tunicamycin 109-120 caspase 3 Homo sapiens 68-77 27915415-8 2017 Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4. Tunicamycin 109-120 caspase 3 Homo sapiens 78-90 28298914-3 2017 Here, we report the tunicamycin (TM) -induced ER stress response in Arabidopsis roots by monitoring expression patterns of immunoglobulin-binding protein 3 (BiP3), a representative marker for the response. Tunicamycin 20-31 Heat shock protein 70 (Hsp 70) family protein Arabidopsis thaliana 123-155 28298914-3 2017 Here, we report the tunicamycin (TM) -induced ER stress response in Arabidopsis roots by monitoring expression patterns of immunoglobulin-binding protein 3 (BiP3), a representative marker for the response. Tunicamycin 20-31 Heat shock protein 70 (Hsp 70) family protein Arabidopsis thaliana 157-161 28298914-3 2017 Here, we report the tunicamycin (TM) -induced ER stress response in Arabidopsis roots by monitoring expression patterns of immunoglobulin-binding protein 3 (BiP3), a representative marker for the response. Tunicamycin 33-35 Heat shock protein 70 (Hsp 70) family protein Arabidopsis thaliana 123-155 28298914-3 2017 Here, we report the tunicamycin (TM) -induced ER stress response in Arabidopsis roots by monitoring expression patterns of immunoglobulin-binding protein 3 (BiP3), a representative marker for the response. Tunicamycin 33-35 Heat shock protein 70 (Hsp 70) family protein Arabidopsis thaliana 157-161 27488499-3 2017 In this study, we firstly treated fetal rat spinal cord neuron cells (SCN) and PC12 cells with ER stress activator thapsigargin (TG) or tunicamycin (TM) and then detected the expression pattern of SCIRR69 in response to ER stress at mRNA and protein levels using real-time PCR assay and immunoblotting. Tunicamycin 136-147 cAMP responsive element binding protein 3-like 2 Rattus norvegicus 197-204 28230089-3 2017 These studies aimed to determine whether the ET-1 system promotes renal ER stress development in response to tunicamycin. Tunicamycin 109-120 endothelin 1 Rattus norvegicus 45-49 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 28230089-6 2017 Pre-treatment of TG-con rats with the ETA blocker ABT-627 for 1 week prior to tunicamycin injection significantly reduced the ER stress response in cortex and medulla, and also inhibited renal apoptosis. Tunicamycin 78-89 endothelin receptor type A Rattus norvegicus 38-41 28230089-8 2017 In conclusion, the ET-1 system is important for the development of tunicamycin-induced renal ER stress and apoptosis. Tunicamycin 67-78 endothelin 1 Rattus norvegicus 19-23 26838680-6 2017 Moreover, Gstp1/p2-/- cells were significantly more sensitive to the cytotoxic effects of the ER-stress inducing drugs, thapsigargin (7-fold) and tunicamycin (2-fold). Tunicamycin 146-157 glutathione S-transferase, pi 1 Mus musculus 10-15 28223691-5 2017 Maintenance of SKBR-3 cells in tunicamycin (an inhibitor of N-linked glycosylation) resulted in an increase in sensitivity to DXR (0.1 muM DXR P < 0.001) and a decrease in sensitivity to IGF-1 alone and to IGF-1 supplemented with EGF (P < 0.001). Tunicamycin 31-42 insulin like growth factor 1 Homo sapiens 209-214 28007835-4 2017 Among mutants harboring a single native or chimeric RPL7 allele, expression from the RPL7A locus exceeded that from the RPL7B locus, and more Rpl7a was expressed from either locus than Rpl7b Phenotypic differences in tunicamycin sensitivity, ASH1 mRNA localization, and mobility of the Ty1 retrotransposon were strongly correlated with Rpl7 and ribosome levels, but not with the Rpl7 or snoRNA isoform expressed. Tunicamycin 217-228 Rlp7p Saccharomyces cerevisiae S288C 52-56 28181559-9 2017 Moreover, pharmacologic induction of ER stress with tunicamycin downregulated endothelial Cav1 and impaired endothelium-dependent vasorelaxation that was rescued by overexpressing Cav1. Tunicamycin 52-63 caveolin 1 Homo sapiens 90-94 28181559-9 2017 Moreover, pharmacologic induction of ER stress with tunicamycin downregulated endothelial Cav1 and impaired endothelium-dependent vasorelaxation that was rescued by overexpressing Cav1. Tunicamycin 52-63 caveolin 1 Homo sapiens 180-184 28246472-7 2017 Dramatically increased CCAAT-enhancer-binding protein homologous protein level, suppressed COX-2 and decreased Bcl-2/Bax ratio by melatonin or ATF-6 siRNA contributed the enhanced HepG2 cell apoptosis under tunicamycin (an ER stress inducer) stimulation. Tunicamycin 207-218 BCL2 apoptosis regulator Homo sapiens 111-116 28246472-7 2017 Dramatically increased CCAAT-enhancer-binding protein homologous protein level, suppressed COX-2 and decreased Bcl-2/Bax ratio by melatonin or ATF-6 siRNA contributed the enhanced HepG2 cell apoptosis under tunicamycin (an ER stress inducer) stimulation. Tunicamycin 207-218 activating transcription factor 6 Homo sapiens 143-148 28030827-8 2017 Furthermore, Sirt1 attenuated tunicamycin-induced cold intolerance and elevating thermogenesis by inhibiting ER stress and apoptosis in iBAT. Tunicamycin 30-41 sirtuin 1 Mus musculus 13-18 27993557-3 2017 In vitro, NRG-1 directly inhibited the upregulation of ER stress markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein and cleaved caspase-12 induced by the ER stress inducers tunicamycin or dithiothreitol in both neonatal and adult ventricular myocytes. Tunicamycin 218-229 neuregulin 1 Rattus norvegicus 10-15 28024901-6 2017 The ER stress inducer, tunicamycin, also up-regulated the kinase activity and protein expression of Cdk5 in podocytes accompanied with the increasing of GRP78. Tunicamycin 23-34 cyclin dependent kinase 5 Homo sapiens 100-104 28024901-6 2017 The ER stress inducer, tunicamycin, also up-regulated the kinase activity and protein expression of Cdk5 in podocytes accompanied with the increasing of GRP78. Tunicamycin 23-34 heat shock protein family A (Hsp70) member 5 Homo sapiens 153-158 28024901-7 2017 On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation. Tunicamycin 58-69 cyclin dependent kinase 5 Homo sapiens 19-23 28024901-7 2017 On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation. Tunicamycin 58-69 mitogen-activated protein kinase kinase kinase 1 Homo sapiens 39-44 28024901-7 2017 On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation. Tunicamycin 58-69 mitogen-activated protein kinase 8 Homo sapiens 121-124 27693501-7 2017 In cultured human chondrocytes Sesn1, 2 and 3 were expressed and increased by tunicamycin, an endoplasmic reticulum (ER) stress response inducer and 2-deoxyglucose (2DG), a metabolic stress inducer. Tunicamycin 78-89 sestrin 1 Homo sapiens 31-45 27993557-3 2017 In vitro, NRG-1 directly inhibited the upregulation of ER stress markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein and cleaved caspase-12 induced by the ER stress inducers tunicamycin or dithiothreitol in both neonatal and adult ventricular myocytes. Tunicamycin 218-229 caspase 12 Rattus norvegicus 173-183 27856453-4 2017 APPROACH AND RESULTS: In endothelial cells, we found that ER stress induced by tunicamycin activates the NADPH (nicotinamide adenine dinucleotide phosphate) oxidase Nox4 focally on the ER surface but not on the plasma membrane. Tunicamycin 79-90 NADPH oxidase 4 Homo sapiens 165-169 27909053-5 2017 In contrast, a significant reduction in the secreted form of PCSK9 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57BL/6 mice. Tunicamycin 129-140 proprotein convertase subtilisin/kexin type 9 Homo sapiens 61-66 27909053-5 2017 In contrast, a significant reduction in the secreted form of PCSK9 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57BL/6 mice. Tunicamycin 129-140 MIR7-3 host gene Homo sapiens 154-158 27909053-5 2017 In contrast, a significant reduction in the secreted form of PCSK9 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57BL/6 mice. Tunicamycin 142-144 proprotein convertase subtilisin/kexin type 9 Homo sapiens 61-66 27909053-5 2017 In contrast, a significant reduction in the secreted form of PCSK9 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57BL/6 mice. Tunicamycin 142-144 MIR7-3 host gene Homo sapiens 154-158 27717825-7 2017 Tunicamycin (TM) or thapsigargin (Tg) induced ER stress blunted leptin sensitivity and inhibited preadipocyte proliferation. Tunicamycin 0-11 leptin Mus musculus 64-70 27717825-7 2017 Tunicamycin (TM) or thapsigargin (Tg) induced ER stress blunted leptin sensitivity and inhibited preadipocyte proliferation. Tunicamycin 13-15 leptin Mus musculus 64-70 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 TNF superfamily member 10 Homo sapiens 49-54 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 mitogen-activated protein kinase 8 Homo sapiens 76-79 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 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 TNF receptor superfamily member 10b Homo sapiens 94-97 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 epidermal growth factor receptor Homo sapiens 137-141 27603596-2 2017 This paper reports that the combination of tunicamycin plus TRAIL produced a strong synergistic effect in TRAIL-sensitive human colon cancer HCT116 cells and TRAIL-resistant HT-29 cells. Tunicamycin 43-54 TNF superfamily member 10 Homo sapiens 106-111 27603596-2 2017 This paper reports that the combination of tunicamycin plus TRAIL produced a strong synergistic effect in TRAIL-sensitive human colon cancer HCT116 cells and TRAIL-resistant HT-29 cells. Tunicamycin 43-54 TNF superfamily member 10 Homo sapiens 106-111 27603596-3 2017 On a cellular mechanistic level, tunicamycin-enhanced TRAIL-induced apoptosis by death receptor (DR) 5 upregulation and DR4 deglycosylation. Tunicamycin 33-44 TNF superfamily member 10 Homo sapiens 54-59 27603596-3 2017 On a cellular mechanistic level, tunicamycin-enhanced TRAIL-induced apoptosis by death receptor (DR) 5 upregulation and DR4 deglycosylation. Tunicamycin 33-44 TNF receptor superfamily member 10a Homo sapiens 120-123 27603596-4 2017 Knockdown of DR5 but not DR4 expression by specific shRNAs or siRNAs significantly increased tunicamycin-mediated and TRAIL-mediated cell viability. Tunicamycin 93-104 TNF receptor superfamily member 10b Homo sapiens 13-16 27603596-6 2017 In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin. Tunicamycin 13-24 epidermal growth factor receptor Homo sapiens 35-67 27603596-6 2017 In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin. Tunicamycin 13-24 AKT serine/threonine kinase 1 Homo sapiens 121-124 27603596-6 2017 In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin. Tunicamycin 13-24 TNF superfamily member 10 Homo sapiens 213-218 27603596-6 2017 In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin. Tunicamycin 236-247 epidermal growth factor receptor Homo sapiens 35-67 27603596-6 2017 In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin. Tunicamycin 236-247 AKT serine/threonine kinase 1 Homo sapiens 121-124 27603596-6 2017 In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin. Tunicamycin 236-247 TNF superfamily member 10 Homo sapiens 213-218 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 TNF superfamily member 10 Homo sapiens 45-50 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 mitogen-activated protein kinase 8 Homo sapiens 83-86 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 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 TNF receptor superfamily member 10b Homo sapiens 101-104 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 epidermal growth factor receptor Homo sapiens 144-176 27803246-8 2017 Furthermore, the sensitivity of cells to tunicamycin without ER-PM contact was considerably elevated by the deletion of RIM21. Tunicamycin 41-52 Rim21p Saccharomyces cerevisiae S288C 120-125 28349059-11 2017 Pretreatment by IRE1 agonist tunicamycin or JNK agonist anisomycin attenuated the effect of psoralen on osteoporotic osteoblasts. Tunicamycin 29-40 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 16-20 27740623-7 2017 Some of the effects of TM7SF3 silencing are evident both under basal conditions, in otherwise untreated cells, as well as under different stress conditions induced by thapsigargin, tunicamycin or a mixture of pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin-1 beta and interferon gamma). Tunicamycin 181-192 transmembrane 7 superfamily member 3 Homo sapiens 23-29 27278863-3 2017 Here, we show that oxidative stress, induced by stimulation of the cells with the oxidant arsenite, strongly activated gene transcription via the stress-responsive element (StRE), while phorbol ester or tunicamycin, activators of AP-1/c-Jun or ATF4, respectively, activated AP-1 or nutrient-sensing response element-mediated transcription. Tunicamycin 203-214 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 230-234 27796797-10 2017 We also found that sublethal ER stress caused by tunicamycin treatment induced the synthesis of PYCR1 in murine fibroblasts. Tunicamycin 49-60 pyrroline-5-carboxylate reductase 1 Mus musculus 96-101 29130967-6 2017 The mutant p53 cell lines were treated with tunicamycin to induce ERS and rapamycin in order to inhibit mTOR. Tunicamycin 44-55 tumor protein p53 Homo sapiens 11-14 29130967-6 2017 The mutant p53 cell lines were treated with tunicamycin to induce ERS and rapamycin in order to inhibit mTOR. Tunicamycin 44-55 mechanistic target of rapamycin kinase Homo sapiens 104-108 27886513-7 2017 Furthermore, tunicamycin attenuated hCG-induced protein kinase A and extracellular signal-regulated kinase activation, as determined by Western blot analysis. Tunicamycin 13-24 chorionic gonadotropin subunit beta 5 Homo sapiens 36-39 27886513-8 2017 In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea. Tunicamycin 26-37 chorionic gonadotropin subunit beta 5 Homo sapiens 105-108 27886513-8 2017 In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea. Tunicamycin 26-37 chorionic gonadotropin subunit beta 5 Homo sapiens 133-136 27886513-8 2017 In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea. Tunicamycin 26-37 chorionic gonadotropin subunit beta 5 Homo sapiens 133-136 27886513-8 2017 In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea. Tunicamycin 26-37 steroidogenic acute regulatory protein Homo sapiens 216-220 27886513-8 2017 In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea. Tunicamycin 26-37 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 225-234 27886513-4 2017 Pretreatment with an ER stress inducer, tunicamycin or thapsigargin, inhibited human chorionic gonadotropin (hCG)-stimulated progesterone production in cultured human GLCs. Tunicamycin 40-51 chorionic gonadotropin subunit beta 5 Homo sapiens 109-112 27886513-5 2017 Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction. Tunicamycin 32-43 chorionic gonadotropin subunit beta 5 Homo sapiens 54-57 27886513-5 2017 Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction. Tunicamycin 32-43 steroidogenic acute regulatory protein Homo sapiens 83-121 27886513-5 2017 Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction. Tunicamycin 32-43 steroidogenic acute regulatory protein Homo sapiens 123-127 27886513-5 2017 Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction. Tunicamycin 32-43 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 133-167 27886513-5 2017 Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction. Tunicamycin 32-43 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 169-178 27886513-5 2017 Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction. Tunicamycin 32-43 cytochrome P450 family 11 subfamily A member 1 Homo sapiens 291-298 27886513-6 2017 Pretreatment with tunicamycin also inhibited hCG-stimulated expression of StAR protein and 3beta-HSD enzyme activity in cultured human GLCs, as determined by Western blot analysis and an enzyme immunoassay, respectively, but did not affect hCG-induced intracellular 3",5"-cyclic adenosine monophosphate accumulation. Tunicamycin 18-29 chorionic gonadotropin subunit beta 5 Homo sapiens 45-48 27886513-6 2017 Pretreatment with tunicamycin also inhibited hCG-stimulated expression of StAR protein and 3beta-HSD enzyme activity in cultured human GLCs, as determined by Western blot analysis and an enzyme immunoassay, respectively, but did not affect hCG-induced intracellular 3",5"-cyclic adenosine monophosphate accumulation. Tunicamycin 18-29 steroidogenic acute regulatory protein Homo sapiens 74-78 27886513-6 2017 Pretreatment with tunicamycin also inhibited hCG-stimulated expression of StAR protein and 3beta-HSD enzyme activity in cultured human GLCs, as determined by Western blot analysis and an enzyme immunoassay, respectively, but did not affect hCG-induced intracellular 3",5"-cyclic adenosine monophosphate accumulation. Tunicamycin 18-29 hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1 Homo sapiens 91-100 27886513-6 2017 Pretreatment with tunicamycin also inhibited hCG-stimulated expression of StAR protein and 3beta-HSD enzyme activity in cultured human GLCs, as determined by Western blot analysis and an enzyme immunoassay, respectively, but did not affect hCG-induced intracellular 3",5"-cyclic adenosine monophosphate accumulation. Tunicamycin 18-29 chorionic gonadotropin subunit beta 5 Homo sapiens 240-243 27278863-3 2017 Here, we show that oxidative stress, induced by stimulation of the cells with the oxidant arsenite, strongly activated gene transcription via the stress-responsive element (StRE), while phorbol ester or tunicamycin, activators of AP-1/c-Jun or ATF4, respectively, activated AP-1 or nutrient-sensing response element-mediated transcription. Tunicamycin 203-214 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 235-240 27278863-3 2017 Here, we show that oxidative stress, induced by stimulation of the cells with the oxidant arsenite, strongly activated gene transcription via the stress-responsive element (StRE), while phorbol ester or tunicamycin, activators of AP-1/c-Jun or ATF4, respectively, activated AP-1 or nutrient-sensing response element-mediated transcription. Tunicamycin 203-214 activating transcription factor 4 Homo sapiens 244-248 27278863-3 2017 Here, we show that oxidative stress, induced by stimulation of the cells with the oxidant arsenite, strongly activated gene transcription via the stress-responsive element (StRE), while phorbol ester or tunicamycin, activators of AP-1/c-Jun or ATF4, respectively, activated AP-1 or nutrient-sensing response element-mediated transcription. Tunicamycin 203-214 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 274-278 27616576-2 2016 In this study, we investigated whether treatment with tunicamycin, an endoplasmic reticulum (ER) stress inducer, led to the accumulation of alpha-syn in PC12 cells, and where alpha-syn protein was accumulated, and finally, whether bibenzyl compound 20c, a novel compound isolated from Gastrodia elata (Tian ma), could alleviate the accumulation of alpha-syn and ER stress activation in tunicamycin-treated PC12 cells. Tunicamycin 54-65 synuclein alpha Rattus norvegicus 140-149 27870947-5 2017 Receptor trafficking inhibitors; Tunicamycin and Brefeldin A induce ER retention of FLT3-ITD, resulting in a decrease in protein expression of NOX4 and its partner protein p22phox, thus demonstrating the critical importance of FLT3-ITD localization for the generation of pro-survival ROS. Tunicamycin 33-44 fms related receptor tyrosine kinase 3 Homo sapiens 84-88 27870947-5 2017 Receptor trafficking inhibitors; Tunicamycin and Brefeldin A induce ER retention of FLT3-ITD, resulting in a decrease in protein expression of NOX4 and its partner protein p22phox, thus demonstrating the critical importance of FLT3-ITD localization for the generation of pro-survival ROS. Tunicamycin 33-44 NADPH oxidase 4 Homo sapiens 143-147 27870947-5 2017 Receptor trafficking inhibitors; Tunicamycin and Brefeldin A induce ER retention of FLT3-ITD, resulting in a decrease in protein expression of NOX4 and its partner protein p22phox, thus demonstrating the critical importance of FLT3-ITD localization for the generation of pro-survival ROS. Tunicamycin 33-44 cytochrome b-245 alpha chain Homo sapiens 172-179 27870947-5 2017 Receptor trafficking inhibitors; Tunicamycin and Brefeldin A induce ER retention of FLT3-ITD, resulting in a decrease in protein expression of NOX4 and its partner protein p22phox, thus demonstrating the critical importance of FLT3-ITD localization for the generation of pro-survival ROS. Tunicamycin 33-44 fms related receptor tyrosine kinase 3 Homo sapiens 227-231 27616576-10 2016 CONCLUSION: Tunicamycin treatment caused accumulation of alpha-syn monomer and oligomer in PC12 cells. Tunicamycin 12-23 synuclein alpha Rattus norvegicus 57-66 27996033-3 2016 XBP1 induction accompanied both culture-based HSC activation and ER stress induced by tunicamycin. Tunicamycin 86-97 X-box binding protein 1 Homo sapiens 0-4 27616576-7 2016 RESULTS: Treatment of PC12 cells with tunicamycin (0.5-10 mug/mL) dose-dependently increased the accumulation of alpha-syn monomer (19 kDa) and oligomer (55 kDa), and decreased the cell viability. Tunicamycin 38-49 synuclein alpha Rattus norvegicus 113-122 27882945-3 2016 In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue. Tunicamycin 29-40 heat shock protein 5 Mus musculus 157-162 27612916-6 2016 This amino acid change was predicted to create a putative N-glycosylation motif NX(S/T) subsequently validated upon endoglycosidase H treatment of microsomal fractions and inhibition of N-glycosylation of endogenously produced UGT2B7 with tunicamycin in human embryonic kidney (HEK293) cells. Tunicamycin 239-250 UDP glucuronosyltransferase family 2 member B7 Homo sapiens 227-233 27980366-0 2016 Tunicamycin-induced Endoplasmic Reticulum Stress Upregulates the Expression of Pentraxin 3 in Human Retinal Pigment Epithelial Cells. Tunicamycin 0-11 pentraxin 3 Homo sapiens 79-90 27980366-1 2016 PURPOSE: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19. Tunicamycin 81-92 pentraxin 3 Homo sapiens 47-58 27980366-1 2016 PURPOSE: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19. Tunicamycin 81-92 pentraxin 3 Homo sapiens 60-64 27980366-1 2016 PURPOSE: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19. Tunicamycin 81-92 pentraxin 3 Homo sapiens 184-188 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 27980366-5 2016 RESULTS: The protein and mRNA levels of PTX3 were found to be significantly increased by tunicamycin treatment. Tunicamycin 89-100 pentraxin 3 Homo sapiens 40-44 27980366-7 2016 Furthermore, pretreatment with the NF-kappaB inhibitor abolished tunicamycin-induced PTX3 production. Tunicamycin 65-76 pentraxin 3 Homo sapiens 85-89 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 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 pentraxin 3 Homo sapiens 128-132 27980366-9 2016 CONCLUSIONS: These results suggest that PTX3 production increased in the presence of tunicamycin-induced ER stress. Tunicamycin 85-96 pentraxin 3 Homo sapiens 40-44 27882945-3 2016 In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue. Tunicamycin 29-40 DNA-damage inducible transcript 3 Mus musculus 164-168 27882945-3 2016 In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue. Tunicamycin 29-40 activating transcription factor 2 Mus musculus 170-174 27882945-3 2016 In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue. Tunicamycin 29-40 caspase 3 Mus musculus 179-188 27882945-3 2016 In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue. Tunicamycin 29-40 adiponectin, C1Q and collagen domain containing Mus musculus 202-213 27599897-8 2016 Furthermore, the SiHa cells were exposed to tunicamycin (TM), an endoplasmic reticulum (ER) stress inducer that inactivates STAT3, with or without TRAIL. Tunicamycin 44-55 signal transducer and activator of transcription 3 Homo sapiens 124-129 27496643-8 2016 The functional consequences of ER stress- GR signaling crosstalk were assessed and demonstrated that long time exposure (24-48 h) of A549 cells to dexamethasone (10(-6) M) reversed the Tunicamycin-induced cell death, a phenomenon associated with parallel increases in GR protein content, increases in cell survival parameters and decreases in cell apoptosis-related parameters. Tunicamycin 185-196 nuclear receptor subfamily 3 group C member 1 Homo sapiens 42-44 27496643-8 2016 The functional consequences of ER stress- GR signaling crosstalk were assessed and demonstrated that long time exposure (24-48 h) of A549 cells to dexamethasone (10(-6) M) reversed the Tunicamycin-induced cell death, a phenomenon associated with parallel increases in GR protein content, increases in cell survival parameters and decreases in cell apoptosis-related parameters. Tunicamycin 185-196 nuclear receptor subfamily 3 group C member 1 Homo sapiens 268-270 27582391-5 2016 Removing N-glycosylation from the CD16 protein core by tunicamycin also increases the ligand binding affinity. Tunicamycin 55-66 Fc gamma receptor IIIa Homo sapiens 34-38 27808250-4 2016 Here we observed that rapamycin, which inhibits the nutrient-sensing complex mTORC1, increased ER-mitochondria coupling in HeLa cells to a similar extent as did tunicamycin. Tunicamycin 161-172 CREB regulated transcription coactivator 1 Mus musculus 77-83 27654581-7 2016 Moreover, overexpression of Hax1 protected from apoptotic events triggered by Tunicamycin-induced ER stress. Tunicamycin 78-89 HCLS1 associated protein X-1 Homo sapiens 28-32 27654581-8 2016 Upon treatment with Tunicamycin, Hax1 protected from mitochondrial fission, downregulation of mitofusins 1 and 2 (MFN1 and MFN2), loss of mitochondrial membrane potential ( Psim), production of reactive oxygen species (ROS) and apoptotic cell death. Tunicamycin 20-31 HCLS1 associated protein X-1 Homo sapiens 33-37 27654581-8 2016 Upon treatment with Tunicamycin, Hax1 protected from mitochondrial fission, downregulation of mitofusins 1 and 2 (MFN1 and MFN2), loss of mitochondrial membrane potential ( Psim), production of reactive oxygen species (ROS) and apoptotic cell death. Tunicamycin 20-31 mitofusin 1 Homo sapiens 94-112 27654581-8 2016 Upon treatment with Tunicamycin, Hax1 protected from mitochondrial fission, downregulation of mitofusins 1 and 2 (MFN1 and MFN2), loss of mitochondrial membrane potential ( Psim), production of reactive oxygen species (ROS) and apoptotic cell death. Tunicamycin 20-31 mitofusin 1 Homo sapiens 114-118 27654581-8 2016 Upon treatment with Tunicamycin, Hax1 protected from mitochondrial fission, downregulation of mitofusins 1 and 2 (MFN1 and MFN2), loss of mitochondrial membrane potential ( Psim), production of reactive oxygen species (ROS) and apoptotic cell death. Tunicamycin 20-31 mitofusin 2 Homo sapiens 123-127 27599897-8 2016 Furthermore, the SiHa cells were exposed to tunicamycin (TM), an endoplasmic reticulum (ER) stress inducer that inactivates STAT3, with or without TRAIL. Tunicamycin 57-59 signal transducer and activator of transcription 3 Homo sapiens 124-129 27678294-6 2016 The level of SLC30A3 mRNA was significantly increased by tunicamycin treatment in human neuroblastoma cell line (SH-SY5Y) and human embryonic kidney cell line (HEK293). Tunicamycin 57-68 solute carrier family 30 member 3 Homo sapiens 13-20 27678294-7 2016 Cell viability under tunicamycin treatment was significantly decreased in SLC30A3 knockdown cells by siRNA in comparison with negative control (NC) cells. Tunicamycin 21-32 solute carrier family 30 (zinc transporter), member 3 Mus musculus 74-81 27678294-11 2016 The level of ERK1/2 phosphorylation was significantly increased by tunicamycin treatment in NC cells, not in SLC30A3 knockdown cells. Tunicamycin 67-78 mitogen-activated protein kinase 3 Mus musculus 13-19 27486236-7 2016 Enhanced Fgf21 expression attenuated tunicamycin-induced endoplasmic reticulum stress, as demonstrated by using a neutralizing antibody against FGF21. Tunicamycin 37-48 fibroblast growth factor 21 Mus musculus 9-14 27611865-9 2016 This expression was distinct from the UPR induced by well-studied ER stress inducer, tunicamycin, which robustly activated CHOP, PDIA4 and Dnajb9. Tunicamycin 85-96 DNA damage-inducible transcript 3 protein Oryzias latipes 123-127 27611865-9 2016 This expression was distinct from the UPR induced by well-studied ER stress inducer, tunicamycin, which robustly activated CHOP, PDIA4 and Dnajb9. Tunicamycin 85-96 protein disulfide-isomerase A4 Oryzias latipes 129-134 27611865-9 2016 This expression was distinct from the UPR induced by well-studied ER stress inducer, tunicamycin, which robustly activated CHOP, PDIA4 and Dnajb9. Tunicamycin 85-96 dnaJ homolog subfamily B member 9 Oryzias latipes 139-145 27565667-5 2016 Inhibition of N-glycosylation by tunicamycin indicated that N-glycosylation of S2-expressed hFIX had occurred to a similar extent as in the CHO-produced hFIX. Tunicamycin 33-44 coagulation factor IX Homo sapiens 92-96 27486236-7 2016 Enhanced Fgf21 expression attenuated tunicamycin-induced endoplasmic reticulum stress, as demonstrated by using a neutralizing antibody against FGF21. Tunicamycin 37-48 fibroblast growth factor 21 Mus musculus 144-149 27489309-7 2016 In contrast, SERCA2 activation with a small molecule allosteric activator increased ER Ca(2+) storage and rescued tunicamycin-induced beta-cell death. Tunicamycin 114-125 ATPase, Ca++ transporting, cardiac muscle, slow twitch 2 Mus musculus 13-19 27763330-0 2016 The expression of P-gp in leukemia cells is associated with cross-resistance to protein N-glycosylation inhibitor tunicamycin. Tunicamycin 114-125 phosphoglycolate phosphatase Homo sapiens 18-22 27763330-1 2016 In P-gp-positive cell variants obtained from L1210 cells either by selection with vincristine (L1210/R) or by transfection with the human gene encoding P-gp (L1210/T), we have previously described cross-resistance to tunicamycin (TNM), a protein N-glycosylation inhibitor. Tunicamycin 217-228 phosphoglycolate phosphatase Mus musculus 3-7 27763330-1 2016 In P-gp-positive cell variants obtained from L1210 cells either by selection with vincristine (L1210/R) or by transfection with the human gene encoding P-gp (L1210/T), we have previously described cross-resistance to tunicamycin (TNM), a protein N-glycosylation inhibitor. Tunicamycin 217-228 phosphoglycolate phosphatase Homo sapiens 152-156 27667108-8 2016 The in vitro experiment of tunicamycin-induced hepatocyte apoptosis showed that inhibition of GSK3beta activity increased the cell survival rate. Tunicamycin 27-38 glycogen synthase kinase 3 beta Mus musculus 94-102 27416758-4 2016 Whereas the glucocorticoid, dexamethasone, protects from tunicamycin-induced cell death, silencing endogeneous GILZ in dexamethasone-treated cancer cells alter the capacity of glucocorticoids to protect from tunicamycin-mediated apoptosis. Tunicamycin 208-219 TSC22 domain family member 3 Homo sapiens 111-115 27328454-7 2016 Mutagenesis of the putative ATF4-response element prevented the induction of luciferase activity in response to ATF4 overproduction, as well as in response to mitochondrial electron transfer chain inhibition by piericidin A and ER stress induction by tunicamycin and brefeldin A. Tunicamycin 251-262 activating transcription factor 4 Homo sapiens 28-32 28011957-11 2016 Tunicamycin treatment, as expected, increased the expression of Grp94, PDI, CHOP and inactivated PARP. Tunicamycin 0-11 heat shock protein 90 beta family member 1 Homo sapiens 64-69 28011957-11 2016 Tunicamycin treatment, as expected, increased the expression of Grp94, PDI, CHOP and inactivated PARP. Tunicamycin 0-11 peptidyl arginine deiminase 1 Homo sapiens 71-74 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 28011957-11 2016 Tunicamycin treatment, as expected, increased the expression of Grp94, PDI, CHOP and inactivated PARP. Tunicamycin 0-11 poly(ADP-ribose) polymerase 1 Homo sapiens 97-101 27449753-7 2016 Elevated ER stress markers, oxidative stress and reduction of NO bioavailability induced by tunicamycin in HUVECs, C57BJ/6J and PPARdelta WT mouse aortas were reversed by paeonol treatment. Tunicamycin 92-103 peroxisome proliferator activator receptor delta Mus musculus 128-137 27449753-10 2016 The present study delineates that paeonol protects against tunicamycin-induced vascular endothelial dysfunction by inhibition of ER stress and oxidative stress, thus elevating NO bioavailability via the AMPK/PPARdelta signaling pathway. Tunicamycin 59-70 peroxisome proliferator activator receptor delta Mus musculus 208-217 27667109-1 2016 Objective: To profile the gene expression changes associated with endoplasmic reticulum stress in INS-1-3 cells induced by thapsigargin (TG) and tunicamycin (TM). Tunicamycin 145-156 forkhead box M1 Homo sapiens 98-103 27667109-1 2016 Objective: To profile the gene expression changes associated with endoplasmic reticulum stress in INS-1-3 cells induced by thapsigargin (TG) and tunicamycin (TM). Tunicamycin 158-160 forkhead box M1 Homo sapiens 98-103 26957214-8 2016 Whereas autophagy induced by rapamycin or low serum levels caused a preferential loss of the mature p80 proteolytic cleavage product, infection with herpes simplex virus-1 and induction of cell stress with tunicamycin caused preferential loss of full-length Toll-like receptor-9, which is localized to the endoplasmic reticulum. Tunicamycin 206-217 toll like receptor 9 Homo sapiens 258-278 27321910-4 2016 We show that the EP2 receptor agonist butaprost protects TM cell death mediated by the ER stress inducer tunicamycin through a cyclic AMP (cAMP)-dependent mechanism, but independent of the classical cAMP sensors, protein kinase A and exchange proteins activated by cAMP. Tunicamycin 105-116 prostaglandin E receptor 2 Homo sapiens 17-20 27562249-6 2016 Furthermore, AICAR inhibited macrophage ER stress responses triggered by ER-stressors thapsigargin or tunicamycin. Tunicamycin 102-113 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 13-18 27322083-4 2016 Biochemical assays demonstrated that sphere-forming cells were shifted to pro-survival signaling through the inactivation of IRE1 (XBP-1 splicing) and activation of PERK (elF2alpha phosphorylation) branches under tunicamycin-induced ER stress conditions. Tunicamycin 213-224 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 125-129 27322083-4 2016 Biochemical assays demonstrated that sphere-forming cells were shifted to pro-survival signaling through the inactivation of IRE1 (XBP-1 splicing) and activation of PERK (elF2alpha phosphorylation) branches under tunicamycin-induced ER stress conditions. Tunicamycin 213-224 X-box binding protein 1 Homo sapiens 131-136 27322083-4 2016 Biochemical assays demonstrated that sphere-forming cells were shifted to pro-survival signaling through the inactivation of IRE1 (XBP-1 splicing) and activation of PERK (elF2alpha phosphorylation) branches under tunicamycin-induced ER stress conditions. Tunicamycin 213-224 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 165-169 27322083-5 2016 The proportion of apoptotic cells among sphere-forming cells was markedly increased by the tunicamycin+PERK inhibitor (PERKi) treatment, indicating that PERKi sensitized sphere-forming cells to tunicamycin-induced apoptosis. Tunicamycin 194-205 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 103-107 25966993-8 2016 Treatment of mice with tunicamycin (Tm) (an ER stress inducer) increased PHLDA3 expression in the liver. Tunicamycin 23-34 pleckstrin homology like domain, family A, member 3 Mus musculus 73-79 27350212-0 2016 Tunicamycin-induced endoplasmic reticulum stress reduces in vitro subpopulation and invasion of CD44+/CD24- phenotype breast cancer stem cells. Tunicamycin 0-11 CD44 molecule (Indian blood group) Homo sapiens 96-100 27350212-0 2016 Tunicamycin-induced endoplasmic reticulum stress reduces in vitro subpopulation and invasion of CD44+/CD24- phenotype breast cancer stem cells. Tunicamycin 0-11 CD24 molecule Homo sapiens 102-106 27350212-4 2016 In this study we show effect of tunicamycin on subpopulation and invasion of CD44+/CD24- MCF7 breast cancer stem cells. Tunicamycin 32-43 CD44 molecule (Indian blood group) Homo sapiens 77-81 27350212-4 2016 In this study we show effect of tunicamycin on subpopulation and invasion of CD44+/CD24- MCF7 breast cancer stem cells. Tunicamycin 32-43 CD24 molecule Homo sapiens 83-87 27350212-5 2016 CD44+/CD24- cells were isolated from MCF7 cell line by fluorescence activated cell sorting (FACS) and treated with tunicamycin. Tunicamycin 115-126 CD44 molecule (Indian blood group) Homo sapiens 0-4 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 X-box binding protein 1 Homo sapiens 27-32 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 activating transcription factor 6 Homo sapiens 34-38 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 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 CD44 molecule (Indian blood group) Homo sapiens 106-110 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 CD24 molecule Homo sapiens 112-116 27350212-10 2016 Also, a significant decline in CD44+/CD24- cell subpopulation was determined in the cells treated with tunicamycin. Tunicamycin 103-114 CD44 molecule (Indian blood group) Homo sapiens 31-35 27350212-10 2016 Also, a significant decline in CD44+/CD24- cell subpopulation was determined in the cells treated with tunicamycin. Tunicamycin 103-114 CD24 molecule Homo sapiens 37-41 27350212-11 2016 The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin. Tunicamycin 188-199 CD44 molecule (Indian blood group) Homo sapiens 120-124 27350212-11 2016 The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin. Tunicamycin 188-199 CD24 molecule Homo sapiens 126-130 27350212-11 2016 The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin. Tunicamycin 188-199 CD44 molecule (Indian blood group) Homo sapiens 136-140 27350212-11 2016 The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin. Tunicamycin 188-199 CD24 molecule Homo sapiens 142-146 27350212-12 2016 Our results indicate that CD44+/CD24- phenotype MCF7 cells are susceptible to tunicamycin. Tunicamycin 78-89 CD44 molecule (Indian blood group) Homo sapiens 26-30 27350212-12 2016 Our results indicate that CD44+/CD24- phenotype MCF7 cells are susceptible to tunicamycin. Tunicamycin 78-89 CD24 molecule Homo sapiens 32-36 27350212-13 2016 The results showed that tunicamycin-induced ER stress suppresses CD44+/CD24- phenotype cell subpopulation and in vitro invasion and accelerates tumorosphore formation. Tunicamycin 24-35 CD44 molecule (Indian blood group) Homo sapiens 65-69 27350212-13 2016 The results showed that tunicamycin-induced ER stress suppresses CD44+/CD24- phenotype cell subpopulation and in vitro invasion and accelerates tumorosphore formation. Tunicamycin 24-35 CD24 molecule Homo sapiens 71-75 27350212-14 2016 These results suggest that tunicamycin-induced ER stress inhibits CD44+/CD24- phenotype MCF7 breast cancer stem cells. Tunicamycin 27-38 CD44 molecule (Indian blood group) Homo sapiens 66-70 27350212-14 2016 These results suggest that tunicamycin-induced ER stress inhibits CD44+/CD24- phenotype MCF7 breast cancer stem cells. Tunicamycin 27-38 CD24 molecule Homo sapiens 72-76 25966993-8 2016 Treatment of mice with tunicamycin (Tm) (an ER stress inducer) increased PHLDA3 expression in the liver. Tunicamycin 36-38 pleckstrin homology like domain, family A, member 3 Mus musculus 73-79 27032713-4 2016 The ER stress inducer tunicamycin increased human chorionic gonadotropin-induced VEGFA production in human granulosa cells through the induction of XBP1(S), and pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) abrogated the effect of tunicamycin. Tunicamycin 22-33 vascular endothelial growth factor A Homo sapiens 81-86 27468698-4 2016 In vitro, like ERS inhibitor 4-phenylbutyric acid (PBA), HDL inhibited ox-LDL- or tunicamycin (TM, an ERS inducer)-induced increase in visfatin and resistin secretion. Tunicamycin 82-93 nicotinamide phosphoribosyltransferase Homo sapiens 135-143 27468698-4 2016 In vitro, like ERS inhibitor 4-phenylbutyric acid (PBA), HDL inhibited ox-LDL- or tunicamycin (TM, an ERS inducer)-induced increase in visfatin and resistin secretion. Tunicamycin 82-93 resistin Homo sapiens 148-156 27468698-4 2016 In vitro, like ERS inhibitor 4-phenylbutyric acid (PBA), HDL inhibited ox-LDL- or tunicamycin (TM, an ERS inducer)-induced increase in visfatin and resistin secretion. Tunicamycin 95-97 nicotinamide phosphoribosyltransferase Homo sapiens 135-143 27468698-4 2016 In vitro, like ERS inhibitor 4-phenylbutyric acid (PBA), HDL inhibited ox-LDL- or tunicamycin (TM, an ERS inducer)-induced increase in visfatin and resistin secretion. Tunicamycin 95-97 resistin Homo sapiens 148-156 27344174-7 2016 Pharmacological inhibition of LAT1 increased the growth inhibitory effects and the inactivation of the mTOR pathway resulting from glycosylation defects, an effect further emphasized during the regrowth period post-treatment with tunicamycin. Tunicamycin 230-241 solute carrier family 7 member 5 Homo sapiens 30-34 27344174-7 2016 Pharmacological inhibition of LAT1 increased the growth inhibitory effects and the inactivation of the mTOR pathway resulting from glycosylation defects, an effect further emphasized during the regrowth period post-treatment with tunicamycin. Tunicamycin 230-241 mechanistic target of rapamycin kinase Homo sapiens 103-107 27119230-7 2016 Overexpression of Sox2 obviously abrogates the reduction in glioma-initiating cell self-renewal induced by tunicamycin. Tunicamycin 107-118 SRY-box transcription factor 2 Homo sapiens 18-22 27119230-8 2016 Taken together, tunicamycin suppresses the self-renewal and tumorigenic potential of glioma-initiating cell partly through reducing Sox2 translation. Tunicamycin 16-27 SRY-box transcription factor 2 Homo sapiens 132-136 27779479-4 2016 Moreover, since diabetes induces endoplasmic reticulum (ER) stress, we compared the role of TRPA1 in diabetes and ER stress by assessing whether tunicamycin-induced ER stress, without diabetes, produces TRPA1-mediated pain hypersensitivity and by assessing whether ER stress and diabetes have similar modulatory effects on MG-induced hypersensitivity. Tunicamycin 145-156 transient receptor potential cation channel subfamily A member 1 Homo sapiens 203-208 27779479-5 2016 In vitro patch clamp recording was performed to assess whether tunicamycin is a TRPA1 agonist. Tunicamycin 63-74 transient receptor potential cation channel subfamily A member 1 Homo sapiens 80-85 27779479-9 2016 In vitro patch clamp recording indicated that tunicamycin itself (30 muM) is not a TRPA1 agonist. Tunicamycin 46-57 latexin Homo sapiens 69-72 27321923-3 2016 ER stress, induced by tunicamycin or SOD1(G93A), activates HIPK2 by phosphorylating highly conserved serine and threonine residues (S359/T360) within the activation loop of the HIPK2 kinase domain. Tunicamycin 22-33 homeodomain interacting protein kinase 2 Mus musculus 59-64 27321923-3 2016 ER stress, induced by tunicamycin or SOD1(G93A), activates HIPK2 by phosphorylating highly conserved serine and threonine residues (S359/T360) within the activation loop of the HIPK2 kinase domain. Tunicamycin 22-33 homeodomain interacting protein kinase 2 Mus musculus 177-182 27119230-0 2016 ER stress inducer tunicamycin suppresses the self-renewal of glioma-initiating cell partly through inhibiting Sox2 translation. Tunicamycin 18-29 SRY-box transcription factor 2 Homo sapiens 110-114 27119230-6 2016 Indeed, tunicamycin reduces the expression of self-renewal regulator Sox2 at translation level. Tunicamycin 8-19 SRY-box transcription factor 2 Homo sapiens 69-73 27281343-6 2016 When the N-linked glycosylation in ABCC11-expressing cells was chemically inhibited by tunicamycin treatment, the maturation of ABCC11 was suppressed and its protein level was significantly decreased. Tunicamycin 87-98 ATP binding cassette subfamily C member 11 Homo sapiens 35-41 27281343-6 2016 When the N-linked glycosylation in ABCC11-expressing cells was chemically inhibited by tunicamycin treatment, the maturation of ABCC11 was suppressed and its protein level was significantly decreased. Tunicamycin 87-98 ATP binding cassette subfamily C member 11 Homo sapiens 128-134 27169842-3 2016 Furthermore, it successfully demonstrated that the ER membrane is rapidly reorganized in the perinuclear region by an ER stress inducer, tunicamycin. Tunicamycin 137-148 ETS transcription factor ELK3 Homo sapiens 51-53 27169842-3 2016 Furthermore, it successfully demonstrated that the ER membrane is rapidly reorganized in the perinuclear region by an ER stress inducer, tunicamycin. Tunicamycin 137-148 ETS transcription factor ELK3 Homo sapiens 118-120 27032713-4 2016 The ER stress inducer tunicamycin increased human chorionic gonadotropin-induced VEGFA production in human granulosa cells through the induction of XBP1(S), and pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) abrogated the effect of tunicamycin. Tunicamycin 22-33 X-box binding protein 1 Homo sapiens 148-152 26740123-5 2016 In accordance with these findings in vivo, osteocalcin treatment also displayed a protective impact on adipocytes and myocytes against tunicamycin- or palmitate-induced ER stress and autophagy dysfunction in an XBP-1-independent manner, with these effects of osteocalcin being reversed by inhibition of mammalian target of rapamycin (mTOR) or nuclear factor-kappaB (NF-kappaB). Tunicamycin 135-146 bone gamma-carboxyglutamate protein Homo sapiens 43-54 27151646-3 2016 METHODS: Gene and protein expression of ICAM-1 in primary BRECs cultured in medium containing increasing concentrations of mannose or glucose in the presence or absence of tunicamycin were studied with reverse transcription-polymerase chain reaction and Western blot analysis, and the expression level of ICAM-1 at the surface of BRECs was examined with an immunofluorescence analysis. Tunicamycin 172-183 intercellular adhesion molecule 1 Bos taurus 40-46 27151646-6 2016 Consistent with these results, a dramatic increase in the N-glycosylation of ICAM-1 in BRECs cultured with a high concentration of glucose was observed, which could be partially attenuated by tunicamycin treatment. Tunicamycin 192-203 intercellular adhesion molecule 1 Bos taurus 77-83 27109260-7 2016 From this, paclitaxel (PTX) was identified to efficiently inhibit the promoter activity of the SelS gene, and further results revealed that PTX significantly inhibited the tunicamycin-induced upregulation of SelS at the mRNA and protein levels in HepG2 and HEK293T cells. Tunicamycin 172-183 selenoprotein S Homo sapiens 95-99 27109260-7 2016 From this, paclitaxel (PTX) was identified to efficiently inhibit the promoter activity of the SelS gene, and further results revealed that PTX significantly inhibited the tunicamycin-induced upregulation of SelS at the mRNA and protein levels in HepG2 and HEK293T cells. Tunicamycin 172-183 selenoprotein S Homo sapiens 208-212 26586570-3 2016 We show here that SK2 channels are present in ER membranes of neuronal HT-22 cells, and that positive pharmacological modulation of SK2 channels with CyPPA protects against cell death induced by the ER stressors brefeldin A and tunicamycin. Tunicamycin 228-239 skin antigen 2 Mus musculus 18-21 26586570-3 2016 We show here that SK2 channels are present in ER membranes of neuronal HT-22 cells, and that positive pharmacological modulation of SK2 channels with CyPPA protects against cell death induced by the ER stressors brefeldin A and tunicamycin. Tunicamycin 228-239 skin antigen 2 Mus musculus 132-135 27214655-8 2016 DIO suppressed uroguanylin through ER stress, an effect mimicked by tunicamycin and blocked by TUDCA. Tunicamycin 68-79 guanylate cyclase activator 2b (retina) Mus musculus 15-26 27177927-5 2016 Furthermore, mutant CALR protein stability and secretion were examined using brefeldin A, MG132, spautin-1, and tunicamycin treatment. Tunicamycin 112-123 calreticulin Mus musculus 20-24 26966233-7 2016 Consistent with these findings, the induction of UPR by tunicamycin treatment increases phosphorylation of Syt1p, resulting in Arl1p activation. Tunicamycin 56-67 Arf family guanine nucleotide exchange factor SYT1 Saccharomyces cerevisiae S288C 107-112 27330716-0 2016 Endoplasmic reticulum stress induced by tunicamycin increases resistin messenger ribonucleic acid through the pancreatic endoplasmic reticulum eukaryotic initiation factor 2alpha kinase-activating transcription factor 4-CAAT/enhancer binding protein-alpha homologous protein pathway in THP-1 human monocytes. Tunicamycin 40-51 resistin Homo sapiens 62-70 27330716-0 2016 Endoplasmic reticulum stress induced by tunicamycin increases resistin messenger ribonucleic acid through the pancreatic endoplasmic reticulum eukaryotic initiation factor 2alpha kinase-activating transcription factor 4-CAAT/enhancer binding protein-alpha homologous protein pathway in THP-1 human monocytes. Tunicamycin 40-51 activating transcription factor 4 Homo sapiens 186-219 27330716-3 2016 Tunicamycin is known to induce endoplasmic reticulum (ER) stress, and reduce resistin gene expression in 3T3-L1 mouse adipocytes. Tunicamycin 0-11 resistin Mus musculus 77-85 27330716-6 2016 The effect of endotoxin/lipopolysaccharides or tunicamycin on resistin gene expression was analyzed in THP-1 human monocytes. Tunicamycin 47-58 resistin Homo sapiens 62-70 27330716-10 2016 Tunicamycin also increased resistin mRNA. Tunicamycin 0-11 resistin Mus musculus 27-35 27330716-12 2016 Tunicamycin-induced resistin mRNA was inhibited by chemical chaperone, 4-phenylbutyric acid. Tunicamycin 0-11 resistin Mus musculus 20-28 27330716-13 2016 The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA. Tunicamycin 87-98 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 24-28 27330716-13 2016 The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA. Tunicamycin 87-98 activating transcription factor 4 Homo sapiens 30-63 27330716-13 2016 The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA. Tunicamycin 87-98 activating transcription factor 4 Homo sapiens 65-69 26828122-4 2016 Using several approaches including inhibiting de novo N-glycosylation in human colonic epithelial NCM460 cells with tunicamycin as well as enzymatic de-glycosylation, we show that the hTPPT protein is, indeed, a glycoprotein. Tunicamycin 116-127 solute carrier family 44 member 4 Homo sapiens 184-189 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 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 236-240 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 27011164-8 2016 Additionally, ER stress inducer tunicamycin significantly increased the expression level of C/EBP beta in hPDLCs. Tunicamycin 32-43 CCAAT enhancer binding protein beta Homo sapiens 92-102 27011164-9 2016 Blocking of C/EBP beta by siRNA resulted in a significant decrease in the secretion of IL-6 and IL-8 and expression of MMP-8 and MMP-9 induced by tunicamycin treatment in hPDLCs. Tunicamycin 146-157 CCAAT enhancer binding protein beta Homo sapiens 12-22 27011164-9 2016 Blocking of C/EBP beta by siRNA resulted in a significant decrease in the secretion of IL-6 and IL-8 and expression of MMP-8 and MMP-9 induced by tunicamycin treatment in hPDLCs. Tunicamycin 146-157 matrix metallopeptidase 8 Homo sapiens 119-124 27011164-9 2016 Blocking of C/EBP beta by siRNA resulted in a significant decrease in the secretion of IL-6 and IL-8 and expression of MMP-8 and MMP-9 induced by tunicamycin treatment in hPDLCs. Tunicamycin 146-157 matrix metallopeptidase 9 Homo sapiens 129-134 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 27330716-13 2016 The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA. Tunicamycin 87-98 resistin Mus musculus 107-115 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 resistin Mus musculus 75-83 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 101-105 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 activating transcription factor 4 Homo sapiens 106-110 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 27123103-5 2016 Furthermore, treatment of wild-type (wt) RSPO1-overexpressing HT1080 cells with tunicamycin (TM), which inhibits N-glycosylation, resulted in a significant reduction in the molecular weight of RSPO1. Tunicamycin 80-91 R-spondin 1 Homo sapiens 41-46 27123103-5 2016 Furthermore, treatment of wild-type (wt) RSPO1-overexpressing HT1080 cells with tunicamycin (TM), which inhibits N-glycosylation, resulted in a significant reduction in the molecular weight of RSPO1. Tunicamycin 80-91 R-spondin 1 Homo sapiens 193-198 27123103-5 2016 Furthermore, treatment of wild-type (wt) RSPO1-overexpressing HT1080 cells with tunicamycin (TM), which inhibits N-glycosylation, resulted in a significant reduction in the molecular weight of RSPO1. Tunicamycin 93-95 R-spondin 1 Homo sapiens 41-46 27123103-5 2016 Furthermore, treatment of wild-type (wt) RSPO1-overexpressing HT1080 cells with tunicamycin (TM), which inhibits N-glycosylation, resulted in a significant reduction in the molecular weight of RSPO1. Tunicamycin 93-95 R-spondin 1 Homo sapiens 193-198 26521941-4 2016 Cardiomyocyte ERS-triggered apoptosis induced by 100 ng/ml tunicamycin (TM) or 1 muM thapsigargin (TG), ERS inducers, was significantly reduced by miR-185 overexpression. Tunicamycin 59-70 microRNA 185 Homo sapiens 147-154 26796921-4 2016 Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM. Tunicamycin 0-11 mitogen-activated protein kinase 1 Homo sapiens 103-107 26796921-4 2016 Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM. Tunicamycin 0-11 mitogen-activated protein kinase 1 Homo sapiens 148-151 26796921-4 2016 Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM. Tunicamycin 0-11 mitogen-activated protein kinase kinase 7 Homo sapiens 159-162 26796921-4 2016 Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM. Tunicamycin 0-11 mitogen-activated protein kinase 1 Homo sapiens 164-167 26796921-4 2016 Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 214-219 26796921-4 2016 Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM. Tunicamycin 0-11 mitogen-activated protein kinase kinase 7 Homo sapiens 255-258 26796921-4 2016 Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 290-295 26796921-5 2016 Inhibition of the MEK/ERK pathway by U0126 sensitizes breast cancer cells to TM-induced apoptosis. Tunicamycin 77-79 mitogen-activated protein kinase kinase 7 Homo sapiens 18-21 26796921-5 2016 Inhibition of the MEK/ERK pathway by U0126 sensitizes breast cancer cells to TM-induced apoptosis. Tunicamycin 77-79 mitogen-activated protein kinase 1 Homo sapiens 22-25 26796921-7 2016 This sensitization of breast cancer cells to TM-induced apoptosis by inhibition of MEK/ERK and GRP78 is caspase-dependent, at least in part, by activation of caspase-4. Tunicamycin 45-47 mitogen-activated protein kinase kinase 7 Homo sapiens 83-86 26796921-7 2016 This sensitization of breast cancer cells to TM-induced apoptosis by inhibition of MEK/ERK and GRP78 is caspase-dependent, at least in part, by activation of caspase-4. Tunicamycin 45-47 mitogen-activated protein kinase 1 Homo sapiens 87-90 26796921-7 2016 This sensitization of breast cancer cells to TM-induced apoptosis by inhibition of MEK/ERK and GRP78 is caspase-dependent, at least in part, by activation of caspase-4. Tunicamycin 45-47 heat shock protein family A (Hsp70) member 5 Homo sapiens 95-100 26796921-7 2016 This sensitization of breast cancer cells to TM-induced apoptosis by inhibition of MEK/ERK and GRP78 is caspase-dependent, at least in part, by activation of caspase-4. Tunicamycin 45-47 caspase 4 Homo sapiens 158-167 26966233-7 2016 Consistent with these findings, the induction of UPR by tunicamycin treatment increases phosphorylation of Syt1p, resulting in Arl1p activation. Tunicamycin 56-67 Arf family GTPase ARL1 Saccharomyces cerevisiae S288C 127-132 26747710-12 2016 This protection was stimulus-independent as nCDase(-/-) cells were also protected from endoplasmic reticulum (ER) stressors [tunicamycin (TN) or thapsigargin (TG)]. Tunicamycin 125-136 N-acylsphingosine amidohydrolase 2 Mus musculus 44-50 27073326-3 2016 In this study, we have demonstrated for the first time that the expression level of miR-663 was significantly upregulated in HCC cells co-incubated with tunicamycin, an ER stress inducer, as measured by a microRNA-chromatin immunoprecipitation microarray and quantitative real-time polymerase chain reaction; however, the effect of miR-663 on HCC cell apoptosis remains unknown. Tunicamycin 153-164 microRNA 663a Homo sapiens 84-91 27073326-3 2016 In this study, we have demonstrated for the first time that the expression level of miR-663 was significantly upregulated in HCC cells co-incubated with tunicamycin, an ER stress inducer, as measured by a microRNA-chromatin immunoprecipitation microarray and quantitative real-time polymerase chain reaction; however, the effect of miR-663 on HCC cell apoptosis remains unknown. Tunicamycin 153-164 microRNA 663a Homo sapiens 332-339 26939760-3 2016 The ER stress inductor tunicamycin (TM) significantly decreased the expression of FAM3A at both mRNA and protein levels, which was shown to be dependent on the induction of reactive oxygen species (ROS). Tunicamycin 23-34 FAM3 metabolism regulating signaling molecule A Mus musculus 82-87 26750440-6 2016 Inhibition of miR-29a expression using sequence-specific antagomirs or the overexpression of Mcl-1 decreased cell death following tunicamycin treatment, while gene silencing of Mcl-1 increased cell death. Tunicamycin 130-141 microRNA 29a Homo sapiens 14-21 26750440-6 2016 Inhibition of miR-29a expression using sequence-specific antagomirs or the overexpression of Mcl-1 decreased cell death following tunicamycin treatment, while gene silencing of Mcl-1 increased cell death. Tunicamycin 130-141 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 93-98 26718307-7 2016 PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes. Tunicamycin 84-95 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 Homo sapiens 0-6 26718307-7 2016 PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes. Tunicamycin 84-95 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 41-45 26718307-7 2016 PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes. Tunicamycin 84-95 activating transcription factor 3 Homo sapiens 47-51 26718307-7 2016 PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes. Tunicamycin 84-95 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 53-57 26718307-7 2016 PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes. Tunicamycin 84-95 eukaryotic translation initiation factor 2A Homo sapiens 61-70 26718307-7 2016 PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes. Tunicamycin 84-95 matrix metallopeptidase 13 Homo sapiens 75-80 26939760-3 2016 The ER stress inductor tunicamycin (TM) significantly decreased the expression of FAM3A at both mRNA and protein levels, which was shown to be dependent on the induction of reactive oxygen species (ROS). Tunicamycin 36-38 FAM3 metabolism regulating signaling molecule A Mus musculus 82-87 26616221-4 2016 In this work, ApoE(-/-) mice underwent perivascular carotid collar placement surgeries or sham operations were given higher (3.0mg/kg) and lower (0.3mg/kg) doses of tunicamycin (TM), and plaque stability was evaluated. Tunicamycin 165-176 apolipoprotein E Mus musculus 14-18 25160872-5 2016 Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress. Tunicamycin 56-67 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 105-114 25160872-5 2016 Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress. Tunicamycin 56-67 activating transcription factor 6 Homo sapiens 116-120 25160872-5 2016 Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress. Tunicamycin 56-67 eukaryotic translation initiation factor 2A Homo sapiens 125-134 25160872-5 2016 Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress. Tunicamycin 69-71 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 105-114 25160872-5 2016 Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress. Tunicamycin 69-71 activating transcription factor 6 Homo sapiens 116-120 25160872-5 2016 Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress. Tunicamycin 69-71 eukaryotic translation initiation factor 2A Homo sapiens 125-134 26893680-6 2016 Treatment of A549 cells with tunicamycin followed by cisplatin resulted in elevated BAG1 levels. Tunicamycin 29-40 BAG cochaperone 1 Homo sapiens 84-88 26888485-9 2016 NGR1 inhibits Tunicamycin-induced cell death and cardiac dysfunction. Tunicamycin 14-25 reticulon 4 receptor Rattus norvegicus 0-4 26851027-3 2016 Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene. Tunicamycin 109-120 ATM serine/threonine kinase Homo sapiens 358-387 26851027-3 2016 Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene. Tunicamycin 109-120 ATM serine/threonine kinase Homo sapiens 389-392 26851027-3 2016 Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene. Tunicamycin 109-120 mitogen-activated protein kinase 8 Homo sapiens 403-426 26851027-3 2016 Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene. Tunicamycin 109-120 mitogen-activated protein kinase 8 Homo sapiens 428-431 26472337-4 2016 Further, blocking RBM3 expression in human embryonic kidney HEK293 cells by specific small interfering RNAs increased phosphorylation of PERK and eIF2alpha, whereas overexpression of RBM3 prevented PERK-eIF2alpha-CHOP signaling during ER stress induced by thapsigargin or tunicamycin. Tunicamycin 272-283 RNA binding motif protein 3 Homo sapiens 18-22 26472337-4 2016 Further, blocking RBM3 expression in human embryonic kidney HEK293 cells by specific small interfering RNAs increased phosphorylation of PERK and eIF2alpha, whereas overexpression of RBM3 prevented PERK-eIF2alpha-CHOP signaling during ER stress induced by thapsigargin or tunicamycin. Tunicamycin 272-283 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 137-141 26472337-4 2016 Further, blocking RBM3 expression in human embryonic kidney HEK293 cells by specific small interfering RNAs increased phosphorylation of PERK and eIF2alpha, whereas overexpression of RBM3 prevented PERK-eIF2alpha-CHOP signaling during ER stress induced by thapsigargin or tunicamycin. Tunicamycin 272-283 RNA binding motif protein 3 Homo sapiens 183-187 26472337-4 2016 Further, blocking RBM3 expression in human embryonic kidney HEK293 cells by specific small interfering RNAs increased phosphorylation of PERK and eIF2alpha, whereas overexpression of RBM3 prevented PERK-eIF2alpha-CHOP signaling during ER stress induced by thapsigargin or tunicamycin. Tunicamycin 272-283 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 198-202 26567221-5 2016 Inhibition of N-glycosylation with tunicamycin resulted in a molecular shift of HMGB1 as assessed by gel electrophoresis. Tunicamycin 35-46 high mobility group box 1 Homo sapiens 80-85 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 26058460-6 2016 SelS gene silence by small interference RNA (siRNA) rendered VSMCs more sensitive to hydrogen peroxide- or tunicamycin- induced injury and apoptosis, as determined by MTT assay, Hoechst staining, and annexin V/propidium iodide staining. Tunicamycin 107-118 selenoprotein S Homo sapiens 0-4 26740650-5 2016 We evoked mild endoplasmic reticulum (ER) stress with tunicamycin (Tu), producing modest increases in the level of nuclear ATF6, phosphorylated eukaryotic initiation factor 2alpha, nuclear XBP1, and the downstream proapoptotic effector nuclear C/EBP homologous protein. Tunicamycin 54-65 activating transcription factor 6 Mus musculus 123-127 26740650-5 2016 We evoked mild endoplasmic reticulum (ER) stress with tunicamycin (Tu), producing modest increases in the level of nuclear ATF6, phosphorylated eukaryotic initiation factor 2alpha, nuclear XBP1, and the downstream proapoptotic effector nuclear C/EBP homologous protein. Tunicamycin 67-69 activating transcription factor 6 Mus musculus 123-127 26740650-5 2016 We evoked mild endoplasmic reticulum (ER) stress with tunicamycin (Tu), producing modest increases in the level of nuclear ATF6, phosphorylated eukaryotic initiation factor 2alpha, nuclear XBP1, and the downstream proapoptotic effector nuclear C/EBP homologous protein. Tunicamycin 67-69 X-box binding protein 1 Mus musculus 189-193 26021843-7 2016 Cardiac cell pretreatment with tunicamycin, an inducer of trib3, also protected them against H2O2-induced cell death. Tunicamycin 31-42 tribbles pseudokinase 3 Rattus norvegicus 58-63 26058460-8 2016 Furthermore, SelS silence enhanced endoplasmic reticulum (ER) stress induced by hydrogen peroxide or tunicamycin, as showed by the increased protein levels of ER chaperone 78 kDa glucose-regulated protein (GRP78), ER stress transducer phosphorylated protein kinase RNA like ER kinase (PERK), and the proapoptotic transcription factor C/EBP homologous protein (CHOP). Tunicamycin 101-112 selenoprotein S Homo sapiens 13-17 26577412-6 2015 Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation. Tunicamycin 25-36 X-box binding protein 1 Homo sapiens 90-94 26548430-3 2016 The INS-1 islet cell line was treated with various concentrations of tunicamycin to establish the ERS model. Tunicamycin 69-80 insulin 1 Rattus norvegicus 4-9 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 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 endoplasmic reticulum protein 29 Rattus norvegicus 206-211 26551463-8 2015 Pre-incubation with ER stress inducer tunicamycin before leucine stimulation increased S6K1 phosphorylation beyond the level reached by leucine alone. Tunicamycin 38-49 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 87-91 26577412-6 2015 Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation. Tunicamycin 25-36 activating transcription factor 4 Homo sapiens 96-100 26709511-7 2015 In addition, Ang 1-7 decreased the levels of ER stress markers and augmented NO production in HUVECs treated with ER stress inducer, tunicamycin. Tunicamycin 133-144 angiogenin, ribonuclease, RNase A family, 5 Mus musculus 13-18 26577412-6 2015 Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation. Tunicamycin 25-36 activating transcription factor 6 Homo sapiens 102-106 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 26782403-6 2015 The reverse transcription quantitative polymerase chain reaction results showed that knockdown Herp inhibited the expression of ER stress-related genes during exposure to tunicamycin or thapsigargin. Tunicamycin 171-182 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 95-99 28955827-4 2016 Moreover, in cultured brown adipocytes exposed to tunicamycin and hydrogen peroxide, at concentrations not affecting cellular viability, GDF1 expression was significantly downregulated. Tunicamycin 50-61 growth differentiation factor 1 Mus musculus 137-141 26782403-7 2015 In RAW 264.7 macrophages, knockdown Herp markedly attenuated the expression of inflammatory cytokines when exposed to tunicamycin; however, it strongly enhanced the expression of inflammatory cytokines when exposed to thapsigargin. Tunicamycin 118-129 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 36-40 26782403-8 2015 We concluded that Herp lentiviral shRNA vectors had been successfully constructed; knockdown Herp inhibited ER stress and had a different effect on inflammatory responses in RAW 264.7 macrophages depending on whether they were exposed to tunicamycin or thapsigargin. Tunicamycin 238-249 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 18-22 26782403-8 2015 We concluded that Herp lentiviral shRNA vectors had been successfully constructed; knockdown Herp inhibited ER stress and had a different effect on inflammatory responses in RAW 264.7 macrophages depending on whether they were exposed to tunicamycin or thapsigargin. Tunicamycin 238-249 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 93-97 26680341-7 2015 The most remarkable effect was that of tunicamycin, an inhibitor of the first step of N-glycosylation, which resulted in significantly reduced KIR3DL1-Fc binding despite sustained expression of HLA-B*57:01 on 721.221 cells. Tunicamycin 39-50 killer cell immunoglobulin like receptor, three Ig domains and long cytoplasmic tail 1 Homo sapiens 143-150 26603934-5 2015 Biochemical characterisation of transiently expressed human CPX-1 revealed that CPX-1 was secreted in an N-glycosylation-dependent manner as treatment with the N-glycosylation inhibitor tunicamycin inhibited secretion concomitant with a reduction in CPX-1 mobility on Western blot. Tunicamycin 186-197 carboxypeptidase X, M14 family member 1 Homo sapiens 60-65 26603934-5 2015 Biochemical characterisation of transiently expressed human CPX-1 revealed that CPX-1 was secreted in an N-glycosylation-dependent manner as treatment with the N-glycosylation inhibitor tunicamycin inhibited secretion concomitant with a reduction in CPX-1 mobility on Western blot. Tunicamycin 186-197 carboxypeptidase X, M14 family member 1 Homo sapiens 80-85 26603934-5 2015 Biochemical characterisation of transiently expressed human CPX-1 revealed that CPX-1 was secreted in an N-glycosylation-dependent manner as treatment with the N-glycosylation inhibitor tunicamycin inhibited secretion concomitant with a reduction in CPX-1 mobility on Western blot. Tunicamycin 186-197 carboxypeptidase X, M14 family member 1 Homo sapiens 80-85 26680341-7 2015 The most remarkable effect was that of tunicamycin, an inhibitor of the first step of N-glycosylation, which resulted in significantly reduced KIR3DL1-Fc binding despite sustained expression of HLA-B*57:01 on 721.221 cells. Tunicamycin 39-50 major histocompatibility complex, class I, B Homo sapiens 194-199 26680341-8 2015 This effect was paralleled by decreased activation of KIR3DL1zeta+ Jurkat reporter cells, as well as increased degranulation of primary human KIR3DL1+ NK cell clones when encountering HLA-B*57:01-expressing 721.221 cells that were pre-treated with tunicamycin. Tunicamycin 248-259 major histocompatibility complex, class I, B Homo sapiens 184-189 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 C1q and TNF related 9 Homo sapiens 13-18 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 eukaryotic translation initiation factor 2A Homo sapiens 90-99 26419929-4 2015 Treating HepG2 cells with human recombinant CTRP9 significantly ameliorated palmitate- or tunicamycin-induced dysregulation of lipid metabolism, caspase 3 activity and chromatin condensation, which lead to reduction of hepatic triglyceride (TG) accumulation. Tunicamycin 90-101 C1q and TNF related 9 Homo sapiens 44-49 26419929-4 2015 Treating HepG2 cells with human recombinant CTRP9 significantly ameliorated palmitate- or tunicamycin-induced dysregulation of lipid metabolism, caspase 3 activity and chromatin condensation, which lead to reduction of hepatic triglyceride (TG) accumulation. Tunicamycin 90-101 caspase 3 Homo sapiens 145-154 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 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 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 110-115 26531105-0 2015 Knockdown of 15-kDa selenoprotein (Sep15) increases hLE cells" susceptibility to tunicamycin-induced apoptosis. Tunicamycin 81-92 selenoprotein F Homo sapiens 13-33 26531105-0 2015 Knockdown of 15-kDa selenoprotein (Sep15) increases hLE cells" susceptibility to tunicamycin-induced apoptosis. Tunicamycin 81-92 selenoprotein F Homo sapiens 35-40 26531105-2 2015 The results showed that sole knockdown of Sep15 by RNA interference did not result in apoptosis; however, reduction of Sep15 expression aggravated tunicamycin (Tm)-induced cell apoptosis and caspases activation. Tunicamycin 147-158 selenoprotein F Homo sapiens 119-124 26531105-2 2015 The results showed that sole knockdown of Sep15 by RNA interference did not result in apoptosis; however, reduction of Sep15 expression aggravated tunicamycin (Tm)-induced cell apoptosis and caspases activation. Tunicamycin 160-162 selenoprotein F Homo sapiens 119-124 26373796-6 2015 In addition, PGRN-deficient adipocytes were more refractory to tunicamycin- or dexamethasone-induced insulin resistance, indicating the causative role of the TNFR1 pathway in the action of PGRN. Tunicamycin 63-74 granulin Mus musculus 13-17 26610463-8 2015 Treatment with UP resulted in reduced increment of ATF6 and CHOP, and recovered the decrease of phosphorylation of Akt/mTOR by tunicamycin and the increment of autophagy. Tunicamycin 127-138 thymoma viral proto-oncogene 1 Mus musculus 115-118 26497741-9 2015 The apoptotic rate and the loss of mitochondrial membrane potential (DeltaPsim) of the TM-stimulated chondrocytes treated with BZD was markedly decreased compared with those of chondrocytes not treated with BZD, as shown by 4",6-diamidino-2-phenylindole (DAPI) staining, Annexin V-FITC binding assay and JC-1 assay. Tunicamycin 87-89 annexin A5 Rattus norvegicus 271-280 26610463-8 2015 Treatment with UP resulted in reduced increment of ATF6 and CHOP, and recovered the decrease of phosphorylation of Akt/mTOR by tunicamycin and the increment of autophagy. Tunicamycin 127-138 mechanistic target of rapamycin kinase Mus musculus 119-123 26449458-5 2015 Treatment of C2C12 myotubes with palmitate or tunicamycin significantly increased the expression of musclin as well as ER stress-related genes, but treatment with oleate did not. Tunicamycin 46-57 osteocrin Homo sapiens 100-107 26599396-11 2015 In contrast, inhibition of glycosylation by treatment with tunicamycin dramatically reduced membrane translocation of intracellular hNIS, resulting in reduced radioiodine uptake. Tunicamycin 59-70 solute carrier family 5 member 5 Homo sapiens 132-136 26599511-6 2015 TGF-beta and tunicamycin promoted MUC5AC induction after 72 h in human bronchial airway epithelial BEAS-2B cells, which was dampened by 20 muM kaempferol. Tunicamycin 13-24 mucin 5AC, oligomeric mucus/gel-forming Homo sapiens 34-40 26599511-7 2015 Kaempferol inhibited tunicamycin-induced ER stress of airway epithelial cells through disturbing the activation of the ER transmembrane sensor ATF6 and IRE1alpha. Tunicamycin 21-32 activating transcription factor 6 Mus musculus 143-147 26599511-7 2015 Kaempferol inhibited tunicamycin-induced ER stress of airway epithelial cells through disturbing the activation of the ER transmembrane sensor ATF6 and IRE1alpha. Tunicamycin 21-32 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 152-161 26599511-8 2015 Additionally, this compound demoted the induction of ER chaperones such as GRP78 and HSP70 and the splicing of XBP-1 mRNA by tunicamycin. Tunicamycin 125-136 X-box binding protein 1 Mus musculus 111-116 26599511-10 2015 TGF-beta and tunicamycin induced TRAF2 with JNK activation and such induction was deterred by kaempferol. Tunicamycin 13-24 TNF receptor-associated factor 2 Mus musculus 33-38 26599511-10 2015 TGF-beta and tunicamycin induced TRAF2 with JNK activation and such induction was deterred by kaempferol. Tunicamycin 13-24 mitogen-activated protein kinase 8 Mus musculus 44-47 26599511-11 2015 The inhibition of JNK activation encumbered the XBP-1 mRNA splicing and MUC5AC induction by tunicamycin and TGF-beta. Tunicamycin 92-103 mitogen-activated protein kinase 8 Mus musculus 18-21 26599511-11 2015 The inhibition of JNK activation encumbered the XBP-1 mRNA splicing and MUC5AC induction by tunicamycin and TGF-beta. Tunicamycin 92-103 mucin 5, subtypes A and C, tracheobronchial/gastric Mus musculus 72-78 26449458-6 2015 Pre-treatment of C2C12 myotubes with 4-phenyl butyrate suppressed the expression of ER stress-related genes, simultaneously, resulting in decreased expression of the musclin gene induced by palmitate or tunicamycin. Tunicamycin 203-214 osteocrin Homo sapiens 166-173 26419589-11 2015 FADD-DN also attenuated tunicamycin-induced UPR and ER stress. Tunicamycin 24-35 Fas associated via death domain Homo sapiens 0-4 28955811-4 2016 Partial or non-glycosylated forms of a secreted form of hCES2 have been obtained by three approaches: (i) enzymatic deglycosylation with peptide N-glycosidase F; (ii) incubation with the inhibitor tunicamycin; ii) site directed mutagenesis of each or both N-glycosylation sites. Tunicamycin 197-208 carboxylesterase 2 Homo sapiens 56-61 28955811-6 2016 On the other hand, tunicamycin led to decreased levels of secreted hCES2 but the enzyme was still active. Tunicamycin 19-30 carboxylesterase 2 Homo sapiens 67-72 26498681-2 2015 In this study, results showed that tunicamycin, an inhibitor of N-glycosylation, synergistically enhanced the antitumor activity of trastuzumab against HER2-overexpressing breast cancer cells through induction of cell cycle arrest and apoptosis. Tunicamycin 35-46 erb-b2 receptor tyrosine kinase 2 Homo sapiens 152-156 26498681-3 2015 Combined treatment of tunicamycin with trastuzumab dramatically decreased the expression of EGFR family and its down signaling pathway in SKBR3 and MCF-7/HER2 cells. Tunicamycin 22-33 epidermal growth factor receptor Homo sapiens 92-96 26498681-3 2015 Combined treatment of tunicamycin with trastuzumab dramatically decreased the expression of EGFR family and its down signaling pathway in SKBR3 and MCF-7/HER2 cells. Tunicamycin 22-33 erb-b2 receptor tyrosine kinase 2 Homo sapiens 154-158 26498681-4 2015 Tunicamycin dose-dependently inhibited tumor growth in both of SKBR3 xenografts and MCF-7/HER2 xenografts. Tunicamycin 0-11 erb-b2 receptor tyrosine kinase 2 Homo sapiens 90-94 26498681-5 2015 Optimal tunicamycin without inducing ER stress in liver tissue significantly increased the antitumor effect of trastuzumab in MCF-7/HER2 xenografts. Tunicamycin 8-19 erb-b2 receptor tyrosine kinase 2 Homo sapiens 132-136 26329269-0 2015 Duhuo Jisheng decoction inhibits endoplasmic reticulum stress in chondrocytes induced by tunicamycin through the downregulation of miR-34a. Tunicamycin 89-100 microRNA 34a Homo sapiens 131-138 26540043-4 2015 MEAO inhibited the tunicamycin-induced increase in luciferase activity of ER stress-reporter constructs containing ER stress response element and ATF6 response element. Tunicamycin 19-30 activating transcription factor 6 Homo sapiens 146-150 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 87-92 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 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 X-box binding protein 1 Homo sapiens 104-109 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 113-124 X-box binding protein 1 Homo sapiens 104-109 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 113-124 X-box binding protein 1 Homo sapiens 104-109 26540043-10 2015 Alismol, a guaiane-type sesquiterpenes in Alisma orientale, inhibited GRP78 expression in tunicamycin-treated HepG2 cells. Tunicamycin 90-101 heat shock protein family A (Hsp70) member 5 Homo sapiens 70-75 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 26361146-8 2015 Tunicamycin-exposed islets from NLRP3 KO mice exhibited similar levels of ER stress and apoptosis induction as islets from WT (Ins2(+/+); NLRP3(+/+)) mice. Tunicamycin 0-11 NLR family, pyrin domain containing 3 Mus musculus 32-37 26254015-3 2015 The expression of ANGPTL8 was significantly increased in HepG2 cells exposed to palmitic acid, tunicamycin, or T0901317, and was reversed in cells treated with AICAR. Tunicamycin 95-106 angiopoietin like 8 Homo sapiens 18-25 26254015-3 2015 The expression of ANGPTL8 was significantly increased in HepG2 cells exposed to palmitic acid, tunicamycin, or T0901317, and was reversed in cells treated with AICAR. Tunicamycin 95-106 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase Homo sapiens 160-165 26254015-4 2015 Palmitic acid, tunicamycin, and T0901317 increased LXRalpha and SREBP-1c mRNA expression. Tunicamycin 15-26 nuclear receptor subfamily 1 group H member 3 Homo sapiens 51-59 26254015-4 2015 Palmitic acid, tunicamycin, and T0901317 increased LXRalpha and SREBP-1c mRNA expression. Tunicamycin 15-26 sterol regulatory element binding transcription factor 1 Homo sapiens 64-72 26444017-2 2015 We demonstrate that the ER stress inducer tunicamycin triggers an unfolded protein response, upregulates ER chaperone Grp78, and activates the autophagy pathway in renal tubular epithelial cells in culture. Tunicamycin 42-53 heat shock protein 5 Mus musculus 118-123 26444017-7 2015 In mouse kidney, similarly to renal epithelial cells in culture, tunicamycin triggered ER stress, markedly upregulated Grp78, and activated autophagy without impairing the autophagic flux. Tunicamycin 65-76 heat shock protein 5 Mus musculus 119-124 26192086-4 2015 ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression. Tunicamycin 20-31 SMAD family member 2 Homo sapiens 77-84 26192086-4 2015 ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression. Tunicamycin 20-31 catenin beta 1 Homo sapiens 140-152 26192086-4 2015 ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression. Tunicamycin 20-31 snail family transcriptional repressor 1 Homo sapiens 157-162 26192086-4 2015 ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression. Tunicamycin 33-35 SMAD family member 2 Homo sapiens 77-84 26192086-4 2015 ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression. Tunicamycin 33-35 catenin beta 1 Homo sapiens 140-152 26192086-4 2015 ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression. Tunicamycin 33-35 snail family transcriptional repressor 1 Homo sapiens 157-162 26448323-7 2015 Inhibition of endoplasmic reticulum (ER) stress with chemical chaperones partially blocked ischemic injury-induced CXCL10 upregulation, whereas induction of ER stress with tunicamycin enhanced CXCL10 expression in retina and primary retinal ganglion cells. Tunicamycin 172-183 chemokine (C-X-C motif) ligand 10 Mus musculus 193-199 25968954-6 2015 Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity. Tunicamycin 10-21 BCL2-associated X protein Mus musculus 105-108 25968954-6 2015 Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity. Tunicamycin 10-21 caspase 9 Mus musculus 110-119 25968954-6 2015 Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity. Tunicamycin 10-21 caspase 12 Mus musculus 125-135 25968954-6 2015 Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity. Tunicamycin 10-21 caspase 3 Mus musculus 172-181 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 26355342-8 2015 In livers from obese mice, administration of LPS or tunicamycin results in IRE1alpha and PERK activation, leading to the overexpression of CHOP. Tunicamycin 52-63 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 75-84 26429299-7 2015 Tunicamycin greatly increased both mRNA and protein levels of GRP78. Tunicamycin 0-11 heat shock protein 5 Mus musculus 62-67 26355342-8 2015 In livers from obese mice, administration of LPS or tunicamycin results in IRE1alpha and PERK activation, leading to the overexpression of CHOP. Tunicamycin 52-63 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 89-93 26355342-8 2015 In livers from obese mice, administration of LPS or tunicamycin results in IRE1alpha and PERK activation, leading to the overexpression of CHOP. Tunicamycin 52-63 DNA-damage inducible transcript 3 Mus musculus 139-143 26049021-3 2015 Here we investigated gene expression profiles under ER stress in melanoma cells and found that IDH1 was dramatically increased with ER stress induced by tunicamycin. Tunicamycin 153-164 isocitrate dehydrogenase (NADP(+)) 1 Homo sapiens 95-99 26100023-8 2015 Thus, the spatiotemporal regulation of Rab7 activity during tunicamycin-induced autophagy is regulated by LRRK1. Tunicamycin 60-71 RAB7, member RAS oncogene family Mus musculus 39-43 26172539-6 2015 Moreover, the transcription factor ATF4 is found to mediate both the apoptosis induced by 2-DG and the glycosylation inhibitor tunicamycin, as well as the necrosis provoked by glucose withdrawal. Tunicamycin 127-138 activating transcription factor 4 Homo sapiens 35-39 25801913-5 2015 HDAC4 knockdown showed modest cell growth inhibition; however, it markedly enhanced cytotoxicity induced by either tunicamycin or carfilzomib (CFZ), associated with upregulating ATF4 and CHOP. Tunicamycin 115-126 histone deacetylase 4 Homo sapiens 0-5 26100023-8 2015 Thus, the spatiotemporal regulation of Rab7 activity during tunicamycin-induced autophagy is regulated by LRRK1. Tunicamycin 60-71 leucine-rich repeat kinase 1 Mus musculus 106-111 25972450-8 2015 This in vivo finding is corroborated by the in vitro study showing that cultured cardiac fibroblasts treated with recombinant sFRP2 protein exhibited progressive increase in the expression and activity of TNAP, which was completely abrogated by cycloheximide or tunicamycin. Tunicamycin 262-273 secreted frizzled-related protein 2 Mus musculus 126-131 26080997-7 2015 Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta. Tunicamycin 177-188 sterol regulatory element binding transcription factor 1 Mus musculus 97-140 26080997-7 2015 Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta. Tunicamycin 177-188 sterol regulatory element binding transcription factor 1 Mus musculus 142-149 26080997-7 2015 Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta. Tunicamycin 177-188 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 155-164 26080997-7 2015 Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta. Tunicamycin 177-188 sterol regulatory element binding transcription factor 1 Mus musculus 260-267 26080997-7 2015 Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta. Tunicamycin 177-188 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 272-281 26317416-5 2015 Block of core glycosylation with tunicamycin demonstrated that changes in plasma membrane CaSR levels were due to differences in exocytic rate. Tunicamycin 33-44 calcium sensing receptor Homo sapiens 90-94 26288094-6 2015 Here we demonstrate that guanabenz is protective in fibroblasts expressing G93A mutant SOD1 when they are exposed to tunicamycin mediated ER stress. Tunicamycin 117-128 superoxide dismutase 1, soluble Mus musculus 87-91 26079879-4 2015 In this study, the results showed that tunicamycin decreased insulin-stimulated Akt phosphorylation, but promoted the phosphorylation of protein kinase R-like ER protein kinase (PERK) time-dependently in C2C12 cells. Tunicamycin 39-50 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 137-176 26079879-4 2015 In this study, the results showed that tunicamycin decreased insulin-stimulated Akt phosphorylation, but promoted the phosphorylation of protein kinase R-like ER protein kinase (PERK) time-dependently in C2C12 cells. Tunicamycin 39-50 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 178-182 26079879-5 2015 Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently. Tunicamycin 198-209 heat shock protein 5 Mus musculus 42-72 26079879-5 2015 Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently. Tunicamycin 198-209 heat shock protein 5 Mus musculus 74-77 26079879-5 2015 Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently. Tunicamycin 198-209 heat shock protein 5 Mus musculus 109-114 26079879-5 2015 Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently. Tunicamycin 198-209 X-box binding protein 1 Mus musculus 147-170 26079879-5 2015 Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently. Tunicamycin 198-209 X-box binding protein 1 Mus musculus 172-177 26022098-6 2015 We hypothesized that TN-induced activation of p38 MAPK signaling pathway is responsible for cell death. Tunicamycin 21-23 mitogen-activated protein kinase 14 Homo sapiens 46-49 26137860-7 2015 However, when Hrd1 was knocked down, thapsigargin and tunicamycin dramatically decreased ERAD, while increasing maladaptive ER stress proteins and cell death. Tunicamycin 54-65 synovial apoptosis inhibitor 1, synoviolin Mus musculus 14-18 26079879-8 2015 A strong phosphorylation of inositol-requiring enzyme 1 (IRE-1), c-JUN NH2-terminal kinase (JNK), and insulin receptor substrate 1 (IRS-1) serine, and simultaneously, a dramatic decrease of IRS-1 tyrosine phosphorylation were observed in the presence of tunicamycin, leading to a blockade of insulin signaling, which was reversed by melatonin pretreatment. Tunicamycin 254-265 insulin receptor substrate 1 Mus musculus 132-137 26079879-8 2015 A strong phosphorylation of inositol-requiring enzyme 1 (IRE-1), c-JUN NH2-terminal kinase (JNK), and insulin receptor substrate 1 (IRS-1) serine, and simultaneously, a dramatic decrease of IRS-1 tyrosine phosphorylation were observed in the presence of tunicamycin, leading to a blockade of insulin signaling, which was reversed by melatonin pretreatment. Tunicamycin 254-265 insulin receptor substrate 1 Mus musculus 190-195 26079879-10 2015 Therefore, these results demonstrated that melatonin pretreatment inhibited the activated role of tunicamycin on ERS and insulin resistance through melatonin receptor-mediated IRE-1/JNK/IRS-1 insulin signaling in skeletal muscle cells. Tunicamycin 98-109 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 176-181 26079879-10 2015 Therefore, these results demonstrated that melatonin pretreatment inhibited the activated role of tunicamycin on ERS and insulin resistance through melatonin receptor-mediated IRE-1/JNK/IRS-1 insulin signaling in skeletal muscle cells. Tunicamycin 98-109 mitogen-activated protein kinase 8 Mus musculus 182-185 26079879-10 2015 Therefore, these results demonstrated that melatonin pretreatment inhibited the activated role of tunicamycin on ERS and insulin resistance through melatonin receptor-mediated IRE-1/JNK/IRS-1 insulin signaling in skeletal muscle cells. Tunicamycin 98-109 insulin receptor substrate 1 Mus musculus 186-191 26349962-3 2015 Tunicamycin blocks the first step of P-gp (glycoprotein P) and BCRP (breast cancer resistance protein) N-glycosylation, which is a very important modification for the activity and cellular localisation of these proteins. Tunicamycin 0-11 phosphoglycolate phosphatase Homo sapiens 37-41 26349962-3 2015 Tunicamycin blocks the first step of P-gp (glycoprotein P) and BCRP (breast cancer resistance protein) N-glycosylation, which is a very important modification for the activity and cellular localisation of these proteins. Tunicamycin 0-11 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 63-67 26349962-3 2015 Tunicamycin blocks the first step of P-gp (glycoprotein P) and BCRP (breast cancer resistance protein) N-glycosylation, which is a very important modification for the activity and cellular localisation of these proteins. Tunicamycin 0-11 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 69-101 26349962-11 2015 Western blot analysis showed that, in LoVo/Dx and W1PR cells, tunicamycin treatment resulted in the expression of a 70kDa P-gp protein instead of the mature 170kDa P-gp. Tunicamycin 62-73 phosphoglycolate phosphatase Homo sapiens 122-126 26349962-11 2015 Western blot analysis showed that, in LoVo/Dx and W1PR cells, tunicamycin treatment resulted in the expression of a 70kDa P-gp protein instead of the mature 170kDa P-gp. Tunicamycin 62-73 phosphoglycolate phosphatase Homo sapiens 164-168 26349962-13 2015 In tunicamycin-treated W1TR cells, the size of the BCRP protein did not differ from that of its native unglycosylated form. Tunicamycin 3-14 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 51-55 26349962-14 2015 In tunicamycin-treated A2780T1 cells, BCRP expression was completely inhibited, but pre-treatment with MG132 or BMA suppressed the effect of tunicamycin. Tunicamycin 3-14 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 38-42 26349962-15 2015 Immunocytochemistry analysis indicated that tunicamycin only affected the translocation of P-gp but not that of BCRP. Tunicamycin 44-55 phosphoglycolate phosphatase Homo sapiens 91-95 26065400-7 2015 Then we explored the role of IRE1-XBP1-snail pathway in transforming growth factor (TGF)-beta1/tunicamycin (TM)-induced EMT. Tunicamycin 95-106 X-box binding protein 1 Rattus norvegicus 34-38 25713411-11 2015 The potent ER stress inducers (thapsigargin and tunicamycin) directly decreased precursor and mature forms of integrin-beta1 and led appearance of unglycosylated core protein of integrin-beta1. Tunicamycin 48-59 integrin subunit beta 1 Rattus norvegicus 110-124 25713411-11 2015 The potent ER stress inducers (thapsigargin and tunicamycin) directly decreased precursor and mature forms of integrin-beta1 and led appearance of unglycosylated core protein of integrin-beta1. Tunicamycin 48-59 integrin subunit beta 1 Rattus norvegicus 178-192 25824433-8 2015 Tunicamycin treatment of oocytes expressing Cav1.2/WT mimicked the effects of the quadruple mutations. Tunicamycin 0-11 calcium channel, voltage-dependent, L type, alpha 1C subunit S homeolog Xenopus laevis 44-50 26447625-6 2015 Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). Tunicamycin 0-11 tumor necrosis factor Mus musculus 68-72 26447625-6 2015 Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). Tunicamycin 0-11 interleukin 6 Mus musculus 74-78 26227493-4 2015 RTN1 overexpression in renal cells induces ER stress and apoptosis, whereas RTN1 knockdown attenuates tunicamycin-induced and hyperglycaemia-induced ER stress and apoptosis. Tunicamycin 102-113 reticulon 1 Mus musculus 76-80 26447625-6 2015 Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). Tunicamycin 0-11 interleukin 1 beta Mus musculus 83-88 26447625-6 2015 Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). Tunicamycin 0-11 tumor necrosis factor Mus musculus 101-105 26447625-6 2015 Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). Tunicamycin 0-11 interleukin 1 beta Mus musculus 138-143 26447625-6 2015 Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). Tunicamycin 0-11 interleukin 6 Mus musculus 176-180 26140985-0 2015 Nuclear versus cytosolic activity of the yeast Hog1 MAP kinase in response to osmotic and tunicamycin-induced ER stress. Tunicamycin 90-101 mitogen-activated protein kinase HOG1 Saccharomyces cerevisiae S288C 47-51 25881988-7 2015 Tunicamycin treatment increased (P < 0.01) and TUDCA treatment decreased (P < 0.01) the expression level of ER chaperones, GRP78 and GRP94. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 129-134 25881988-7 2015 Tunicamycin treatment increased (P < 0.01) and TUDCA treatment decreased (P < 0.01) the expression level of ER chaperones, GRP78 and GRP94. Tunicamycin 0-11 heat shock protein 90 beta family member 1 Homo sapiens 139-144 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 26100877-7 2015 Endogenous PAR1 rendered deficient in glycosylation using tunicamycin, a glycoprotein synthesis inhibitor, also exhibited increased PI signaling and diminished RhoA activation opposite to native receptor. Tunicamycin 58-69 coagulation factor II thrombin receptor Homo sapiens 11-15 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 17-28 activating transcription factor 4 Homo sapiens 100-104 25808625-4 2015 Sphk2, a major isotype of sphingosine kinase in the liver, was transcriptionally up-regulated by tunicamycin and lipopolysaccharides. Tunicamycin 97-108 sphingosine kinase 2 Mus musculus 0-5 25737469-3 2015 We studied the role of GADD34 on the induction of autophagy and/or apoptosis by NaF- or tunicamycin-induced ER-stress in HepG2 cells transfected with GADD34 siRNA. Tunicamycin 88-99 protein phosphatase 1 regulatory subunit 15A Homo sapiens 23-29 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 17-28 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 42-46 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 17-28 eukaryotic translation initiation factor 2A Homo sapiens 70-79 25737469-6 2015 After 4 h, GADD34 mRNA expression was also increased by NaF and tunicamycin. Tunicamycin 64-75 protein phosphatase 1 regulatory subunit 15A Homo sapiens 11-17 25737469-7 2015 Suppression of GADD34 by GADD34 siRNA increased ATF4 expression in both NaF- and tunicamycin-treated cells. Tunicamycin 81-92 protein phosphatase 1 regulatory subunit 15A Homo sapiens 15-21 25737469-7 2015 Suppression of GADD34 by GADD34 siRNA increased ATF4 expression in both NaF- and tunicamycin-treated cells. Tunicamycin 81-92 protein phosphatase 1 regulatory subunit 15A Homo sapiens 25-31 25737469-7 2015 Suppression of GADD34 by GADD34 siRNA increased ATF4 expression in both NaF- and tunicamycin-treated cells. Tunicamycin 81-92 activating transcription factor 4 Homo sapiens 48-52 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 protein phosphatase 1 regulatory subunit 15A Homo sapiens 4-10 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 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 activating transcription factor 4 Homo sapiens 76-80 25896661-5 2015 MATERIALS AND METHODS: Treatment of endoplasmic stress inducers, thapsigargin and tunicamycin, inhibited adipocyte differentiation, stimulated Smile mRNA expression, and repressed the expression of adiponectin (Adipoq) in 3T3-L1 pre-adipocyte. Tunicamycin 82-93 CREB/ATF bZIP transcription factor Mus musculus 143-148 25241896-6 2015 UDP-GlcNAc is essential for N-linked glycosylation occurring in the endoplasmic reticulum (ER) and high UAP1 expression associates with resistance against inhibitors of N-linked glycosylation (tunicamycin and 2-deoxyglucose) but not with a general ER stress-inducing agent, the calcium ionophore A23187. Tunicamycin 193-204 UDP-N-acetylglucosamine pyrophosphorylase 1 Homo sapiens 104-108 25926156-8 2015 Finally, we investigated the levels of TMEM132A mRNA and protein after exposure to five different neurotoxic stimuli, including thapsigargin, tunicamycin, serum starvation, homocysteine, and hydrogen peroxide. Tunicamycin 142-153 transmembrane protein 132A Mus musculus 39-47 25896661-5 2015 MATERIALS AND METHODS: Treatment of endoplasmic stress inducers, thapsigargin and tunicamycin, inhibited adipocyte differentiation, stimulated Smile mRNA expression, and repressed the expression of adiponectin (Adipoq) in 3T3-L1 pre-adipocyte. Tunicamycin 82-93 adiponectin, C1Q and collagen domain containing Mus musculus 198-209 25896661-5 2015 MATERIALS AND METHODS: Treatment of endoplasmic stress inducers, thapsigargin and tunicamycin, inhibited adipocyte differentiation, stimulated Smile mRNA expression, and repressed the expression of adiponectin (Adipoq) in 3T3-L1 pre-adipocyte. Tunicamycin 82-93 adiponectin, C1Q and collagen domain containing Mus musculus 211-217 26194078-7 2015 Exendin-4 also reduced the expression of SEPP1 and fetuin-A in cells treated with tunicamycin, an ER stress inducer. Tunicamycin 82-93 selenoprotein P Homo sapiens 41-46 26109405-6 2015 The expression of iRhom1 was increased by endoplasmic reticulum (ER) stressors, such as thapsigargin and tunicamycin, leading to the enhancement of proteasome activity, especially in ER-containing microsomes. Tunicamycin 105-116 rhomboid 5 homolog 1 Homo sapiens 18-24 25855079-7 2015 Inhibition of glycosylation by tunicamycin significantly decreased ASBT activity and shifted ASBT bands to ~30 kDa, representing a deglycosylated protein. Tunicamycin 31-42 solute carrier family 10 member 2 Homo sapiens 67-71 25855079-7 2015 Inhibition of glycosylation by tunicamycin significantly decreased ASBT activity and shifted ASBT bands to ~30 kDa, representing a deglycosylated protein. Tunicamycin 31-42 solute carrier family 10 member 2 Homo sapiens 93-97 26194078-7 2015 Exendin-4 also reduced the expression of SEPP1 and fetuin-A in cells treated with tunicamycin, an ER stress inducer. Tunicamycin 82-93 alpha 2-HS glycoprotein Homo sapiens 51-59 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 25827060-4 2015 Here, we demonstrate that thapsigargin (TG) and tunicamycin (TM), two ERS inducers activated macrophages were able to increase TRAIL mRNA and protein expression in RAW264.7 macrophages, the culture supernatant of THP-1 cells, and mouse peritoneal macrophages, indicating that ERS as a potent inducer of TRAIL transcription and expression in macrophages. Tunicamycin 48-59 TNF superfamily member 10 Homo sapiens 127-132 25827060-4 2015 Here, we demonstrate that thapsigargin (TG) and tunicamycin (TM), two ERS inducers activated macrophages were able to increase TRAIL mRNA and protein expression in RAW264.7 macrophages, the culture supernatant of THP-1 cells, and mouse peritoneal macrophages, indicating that ERS as a potent inducer of TRAIL transcription and expression in macrophages. Tunicamycin 48-59 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 303-308 25827060-4 2015 Here, we demonstrate that thapsigargin (TG) and tunicamycin (TM), two ERS inducers activated macrophages were able to increase TRAIL mRNA and protein expression in RAW264.7 macrophages, the culture supernatant of THP-1 cells, and mouse peritoneal macrophages, indicating that ERS as a potent inducer of TRAIL transcription and expression in macrophages. Tunicamycin 61-63 TNF superfamily member 10 Homo sapiens 127-132 25827060-4 2015 Here, we demonstrate that thapsigargin (TG) and tunicamycin (TM), two ERS inducers activated macrophages were able to increase TRAIL mRNA and protein expression in RAW264.7 macrophages, the culture supernatant of THP-1 cells, and mouse peritoneal macrophages, indicating that ERS as a potent inducer of TRAIL transcription and expression in macrophages. Tunicamycin 61-63 tumor necrosis factor (ligand) superfamily, member 10 Mus musculus 303-308 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 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 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 X-box binding protein 1 Rattus norvegicus 266-271 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 X-box binding protein 1 Rattus norvegicus 288-293 25889874-4 2015 AtBiP3 promoter activity clearly reflected the effects of inducers of ER stress, such as tunicamycin, dithiothreitol, and salicylic acid. Tunicamycin 89-100 Heat shock protein 70 (Hsp 70) family protein Arabidopsis thaliana 0-6 25923692-3 2015 We aimed to investigate the impact on LOX-1 expression by tunicamycin (TM)-induced ER stress and to determine the effect of HDL on TM-affected LOX-1 expression in hepatic L02 cells. Tunicamycin 58-69 oxidized low density lipoprotein receptor 1 Homo sapiens 38-43 25923692-9 2015 Knock down of IRE1 or XBP-1 effectively restored LOX-1 expression and improved lipid uptake in TM-treated cells. Tunicamycin 95-97 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 14-18 25923692-9 2015 Knock down of IRE1 or XBP-1 effectively restored LOX-1 expression and improved lipid uptake in TM-treated cells. Tunicamycin 95-97 X-box binding protein 1 Homo sapiens 22-27 25620058-9 2015 Tunicamycin-induced caspase-3 activation was also shown on PD12 but to a much lesser degree and mainly located in the dentate gyrus of the hippocampus, deep cerebellar nuclei and pons. Tunicamycin 0-11 caspase 3 Mus musculus 20-29 25537833-8 2015 Fgf21-null mice exhibited increased expression of ER stress marker genes and augmented hepatic lipid accumulation after tunicamycin treatment. Tunicamycin 120-131 fibroblast growth factor 21 Mus musculus 0-5 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 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 151-156 25417142-0 2015 Wogonin protects rat dorsal root ganglion neurons against tunicamycin-induced ER stress through the PERK-eIF2alpha-ATF4 signaling pathway. Tunicamycin 58-69 eukaryotic translation initiation factor 2A Rattus norvegicus 105-114 25417142-0 2015 Wogonin protects rat dorsal root ganglion neurons against tunicamycin-induced ER stress through the PERK-eIF2alpha-ATF4 signaling pathway. Tunicamycin 58-69 activating transcription factor 4 Rattus norvegicus 115-119 25711465-0 2015 Melatonin-mediated Bim up-regulation and cyclooxygenase-2 (COX-2) down-regulation enhances tunicamycin-induced apoptosis in MDA-MB-231 cells. Tunicamycin 91-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 41-57 25711465-0 2015 Melatonin-mediated Bim up-regulation and cyclooxygenase-2 (COX-2) down-regulation enhances tunicamycin-induced apoptosis in MDA-MB-231 cells. Tunicamycin 91-102 prostaglandin-endoperoxide synthase 2 Homo sapiens 59-64 25711465-4 2015 Melatonin up-regulates pro-apoptotic protein Bim expression at the transcriptional levels in the presence of tunicamycin. Tunicamycin 109-120 BCL2 like 11 Homo sapiens 45-48 25711465-5 2015 Melatonin inhibits tunicamycin-induced COX-2 expression in MDA-MB-231 cells. Tunicamycin 19-30 prostaglandin-endoperoxide synthase 2 Homo sapiens 39-44 25711465-6 2015 Furthermore, inhibition of COX-2 activity using the COX-2 inhibitor, NS398, increases tunicamycin-induced apoptosis. Tunicamycin 86-97 prostaglandin-endoperoxide synthase 2 Homo sapiens 27-32 25711465-6 2015 Furthermore, inhibition of COX-2 activity using the COX-2 inhibitor, NS398, increases tunicamycin-induced apoptosis. Tunicamycin 86-97 prostaglandin-endoperoxide synthase 2 Homo sapiens 52-57 25711465-9 2015 In addition, melatonin blocked tunicamycin-induced NF-kappaB transcriptional activity, p65 nuclear translocation, and p38 MAPK activation. Tunicamycin 31-42 RELA proto-oncogene, NF-kB subunit Homo sapiens 87-90 25711465-9 2015 In addition, melatonin blocked tunicamycin-induced NF-kappaB transcriptional activity, p65 nuclear translocation, and p38 MAPK activation. Tunicamycin 31-42 mitogen-activated protein kinase 14 Homo sapiens 118-121 25711465-11 2015 Taken together, our results suggest that melatonin enhances antitumor function through up-regulation of Bim expression and down-regulation of COX-2 expression in tunicamycin-treated MDA-MB-231 cells. Tunicamycin 162-173 prostaglandin-endoperoxide synthase 2 Homo sapiens 142-147 25727012-5 2015 In vivo study indicates that administration of the ER stressor tunicamycin in mice led to increased expression of beta-klotho in the liver. Tunicamycin 63-74 klotho beta Mus musculus 114-125 25620058-6 2015 Tunicamycin caused UPR in the cerebral cortex, hippocampus and cerebellum of mice of PD4 and PD12, which was evident by the upregulation of ATF6, XBP1s, p-eIF2alpha, GRP78, GRP94 and MANF, but failed to induce UPR in the brain of PD25 mice. Tunicamycin 0-11 activating transcription factor 6 Mus musculus 140-144 25620058-6 2015 Tunicamycin caused UPR in the cerebral cortex, hippocampus and cerebellum of mice of PD4 and PD12, which was evident by the upregulation of ATF6, XBP1s, p-eIF2alpha, GRP78, GRP94 and MANF, but failed to induce UPR in the brain of PD25 mice. Tunicamycin 0-11 heat shock protein 5 Mus musculus 166-171 25620058-6 2015 Tunicamycin caused UPR in the cerebral cortex, hippocampus and cerebellum of mice of PD4 and PD12, which was evident by the upregulation of ATF6, XBP1s, p-eIF2alpha, GRP78, GRP94 and MANF, but failed to induce UPR in the brain of PD25 mice. Tunicamycin 0-11 heat shock protein 90, beta (Grp94), member 1 Mus musculus 173-178 25620058-6 2015 Tunicamycin caused UPR in the cerebral cortex, hippocampus and cerebellum of mice of PD4 and PD12, which was evident by the upregulation of ATF6, XBP1s, p-eIF2alpha, GRP78, GRP94 and MANF, but failed to induce UPR in the brain of PD25 mice. Tunicamycin 0-11 mesencephalic astrocyte-derived neurotrophic factor Mus musculus 183-187 25620058-8 2015 In PD4 mice, tunicamycin-induced caspase-3 activation was observed in layer II of the parietal and optical cortex, CA1-CA3 and the subiculum of the hippocampus, the cerebellar external germinal layer and the superior/inferior colliculus. Tunicamycin 13-24 caspase 3 Mus musculus 33-42 25620058-8 2015 In PD4 mice, tunicamycin-induced caspase-3 activation was observed in layer II of the parietal and optical cortex, CA1-CA3 and the subiculum of the hippocampus, the cerebellar external germinal layer and the superior/inferior colliculus. Tunicamycin 13-24 carbonic anhydrase 1 Mus musculus 115-122 25660451-6 2015 GLP-1 (7-36) prevented H2O2-, l-glutamate-, tunicamycin-, thapsigargin-, and amyloid beta1-42-induced neuronal cell death in a concentration-dependent manner. Tunicamycin 44-55 glucagon Mus musculus 0-5 25660457-7 2015 We also demonstrated that expression of miR-23a stimulated with tunicamycin was rescued by melatonin treatment, resulting in reduced ER stress in primary hepatocytes. Tunicamycin 64-75 microRNA 23a Homo sapiens 40-47 24691093-3 2015 Fibroblasts from the skin of two such mutants (Snell dwarf and PAPP-A knockout) were found to have higher levels of ATF4 protein and expression of several ATF4 target genes in responses to amino acid withdrawal, cadmium, hydrogen peroxide, and tunicamycin. Tunicamycin 244-255 pregnancy-associated plasma protein A Mus musculus 63-69 25667230-5 2015 We also show that CIA2-deficient cells display an increased resistance to tunicamycin-induced endoplasmic reticulum (ER) stress, as evidenced by the upregulated splicing of the mRNA of HAC1, which encodes a functional transcription factor that regulates the transcription of unfolded protein response (UPR) target genes, suggesting enhanced intracellular UPR activity. Tunicamycin 74-85 transcription factor HAC1 Saccharomyces cerevisiae S288C 185-189 25573487-8 2015 On the other hand inhibition of elongation of N-glycosylation by tunicamycin (TM) resulted in inhibition of Phaseolus vulgaris-L (L-PHA) lectin-binding activity and inhibited cell adhesion to galectin-8, laminin and fibronectin. Tunicamycin 65-76 galectin 8 Homo sapiens 192-202 25573487-8 2015 On the other hand inhibition of elongation of N-glycosylation by tunicamycin (TM) resulted in inhibition of Phaseolus vulgaris-L (L-PHA) lectin-binding activity and inhibited cell adhesion to galectin-8, laminin and fibronectin. Tunicamycin 65-76 fibronectin 1 Homo sapiens 216-227 25249581-8 2015 ASK1 knockdown in C17.2 neural stem cells diminished high glucose- or tunicamycin-induced IRE1alpha activation, which further supports our hypothesis that ASK1 plays a causal role in diabetes-induced ER stress and apoptosis. Tunicamycin 70-81 mitogen-activated protein kinase kinase kinase 5 Mus musculus 0-4 25249581-8 2015 ASK1 knockdown in C17.2 neural stem cells diminished high glucose- or tunicamycin-induced IRE1alpha activation, which further supports our hypothesis that ASK1 plays a causal role in diabetes-induced ER stress and apoptosis. Tunicamycin 70-81 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 90-99 25249581-8 2015 ASK1 knockdown in C17.2 neural stem cells diminished high glucose- or tunicamycin-induced IRE1alpha activation, which further supports our hypothesis that ASK1 plays a causal role in diabetes-induced ER stress and apoptosis. Tunicamycin 70-81 mitogen-activated protein kinase kinase kinase 5 Mus musculus 155-159 24691093-3 2015 Fibroblasts from the skin of two such mutants (Snell dwarf and PAPP-A knockout) were found to have higher levels of ATF4 protein and expression of several ATF4 target genes in responses to amino acid withdrawal, cadmium, hydrogen peroxide, and tunicamycin. Tunicamycin 244-255 activating transcription factor 4 Mus musculus 155-159 25539857-7 2015 The Cox-2 response to PFF was fourfold decreased in cells from old bones (p < 0.001), while tunicamycin decreased PFF-induced Cox-2 expression by threefold in cells from adult bones (p < 0.01). Tunicamycin 95-106 prostaglandin-endoperoxide synthase 2 Mus musculus 129-134 25405329-7 2015 Furthermore, pretreatment with tunicamycin significantly attenuated the induction of proinflammatory cytokines and CD40, by LDL. Tunicamycin 31-42 CD40 molecule Homo sapiens 115-119 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 58-62 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 eukaryotic translation initiation factor 2A Homo sapiens 67-76 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 136-141 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 25428129-6 2015 Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K. Tunicamycin 49-60 mechanistic target of rapamycin kinase Homo sapiens 15-19 25428129-6 2015 Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K. Tunicamycin 49-60 mechanistic target of rapamycin kinase Homo sapiens 112-116 25428129-6 2015 Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K. Tunicamycin 49-60 ribosomal protein S6 kinase B1 Homo sapiens 121-127 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 mechanistic target of rapamycin kinase Homo sapiens 14-18 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 78-82 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 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 123-128 24356728-0 2015 Unfolded protein response inducers tunicamycin and dithiothreitol promote myeloma cell differentiation mediated by XBP-1. Tunicamycin 35-46 X-box binding protein 1 Homo sapiens 115-120 24356728-4 2015 Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity. Tunicamycin 62-73 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 132-136 24356728-4 2015 Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity. Tunicamycin 62-73 X-box binding protein 1 Homo sapiens 137-142 24356728-4 2015 Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity. Tunicamycin 62-73 X-box binding protein 1 Homo sapiens 232-237 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 patatin-like phospholipase domain containing 8 Rattus norvegicus 56-66 24356728-4 2015 Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity. Tunicamycin 75-77 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 132-136 24356728-4 2015 Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity. Tunicamycin 75-77 X-box binding protein 1 Homo sapiens 137-142 24356728-4 2015 Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity. Tunicamycin 75-77 X-box binding protein 1 Homo sapiens 232-237 25389134-6 2015 Tunicamycin treatment selectively reduced R345W F3 secretion by 87% (vs. WT F3). Tunicamycin 0-11 EGF containing fibulin extracellular matrix protein 1 Homo sapiens 48-50 25389134-6 2015 Tunicamycin treatment selectively reduced R345W F3 secretion by 87% (vs. WT F3). Tunicamycin 0-11 EGF containing fibulin extracellular matrix protein 1 Homo sapiens 76-78 25736111-0 2015 [Role of KA1 receptor in excitotoxic neurodegeneration in mouse hippocampus triggered by kainic acid- or tunicamycin-induced endoplasmic reticulum stress]. Tunicamycin 105-116 glutamate receptor, ionotropic, kainate 4 Mus musculus 9-12 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 activating transcription factor 6 Rattus norvegicus 177-210 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 activating transcription factor 6 Rattus norvegicus 212-216 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 90 beta family member 1 Rattus norvegicus 254-282 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 90 beta family member 1 Rattus norvegicus 284-289 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 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 25492867-6 2015 Tunicamycin-induced cytotoxicity was reduced in GECs expressing iPLA2gamma, and the cytoprotection was reversed by dominant-negative ATF6. Tunicamycin 0-11 patatin-like phospholipase domain containing 8 Rattus norvegicus 64-74 25492867-6 2015 Tunicamycin-induced cytotoxicity was reduced in GECs expressing iPLA2gamma, and the cytoprotection was reversed by dominant-negative ATF6. Tunicamycin 0-11 activating transcription factor 6 Rattus norvegicus 133-137 25492867-7 2015 GECs from iPLA2gamma knock-out mice showed blunted ATF6 activation and chaperone up-regulation in response to tunicamycin. Tunicamycin 110-121 patatin-like phospholipase domain containing 8 Mus musculus 10-20 26018731-2 2015 Here we report that RIPK1 functions as an important prosurvival mechanism in melanoma cells undergoing pharmacological ER stress induced by tunicamycin (TM) or thapsigargin (TG) through activation of autophagy. Tunicamycin 140-151 receptor interacting serine/threonine kinase 1 Homo sapiens 20-25 26018731-2 2015 Here we report that RIPK1 functions as an important prosurvival mechanism in melanoma cells undergoing pharmacological ER stress induced by tunicamycin (TM) or thapsigargin (TG) through activation of autophagy. Tunicamycin 153-155 receptor interacting serine/threonine kinase 1 Homo sapiens 20-25 24865476-15 2015 Imatinib-induced cell survival of tunicamycin-treated cells was partially mediated by ERK activation. Tunicamycin 34-45 Eph receptor B1 Rattus norvegicus 86-89 26237103-6 2015 An isolated homozygous mutant of AGB1, agb1-3, was more sensitive to the tunicamycin-induced ER stress compared to the wild type and the other loss-of-function mutants of G protein subunits. Tunicamycin 73-84 GTP binding protein beta 1 Arabidopsis thaliana 33-37 25823847-4 2015 METHODS: THP-1 and HT-29 IECs were stimulated with 2 microg/ml tunicamycin (TNM) for the indicated periods of time. Tunicamycin 63-74 GLI family zinc finger 2 Homo sapiens 9-14 25630719-10 2015 In vitro, ER stress induced by tunicamycin synergistically increased LPS-triggered pro-inflammatory cytokine induction and promoted the activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) pathway in bone marrow-derived macrophages; moreover, tunicamycin also cooperated with TNF-alpha to increase hepatocyte apoptosis. Tunicamycin 31-42 tumor necrosis factor Mus musculus 315-324 26237103-6 2015 An isolated homozygous mutant of AGB1, agb1-3, was more sensitive to the tunicamycin-induced ER stress compared to the wild type and the other loss-of-function mutants of G protein subunits. Tunicamycin 73-84 GTP binding protein beta 1 Arabidopsis thaliana 39-43 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 45-50 25494629-4 2014 RESULTS: We provide first evidence that SND1 promoter activity is increased in human liver cancer cells upon exposure to thapsigargin or tunicamycin or by ectopic expression of ATF6, a crucial transcription factor in the unfolded protein response triggered by ER stress. Tunicamycin 137-148 staphylococcal nuclease and tudor domain containing 1 Homo sapiens 40-44 25494629-6 2014 Quantitative real-time PCR revealed a near 3 fold increase in SND1 mRNA expression by either of the stress-inducers; whereas SND1 protein was maximally upregulated (3.4-fold) in cells exposed to tunicamycin, a protein glycosylation inhibitor. Tunicamycin 195-206 staphylococcal nuclease and tudor domain containing 1 Homo sapiens 62-66 25494629-6 2014 Quantitative real-time PCR revealed a near 3 fold increase in SND1 mRNA expression by either of the stress-inducers; whereas SND1 protein was maximally upregulated (3.4-fold) in cells exposed to tunicamycin, a protein glycosylation inhibitor. Tunicamycin 195-206 staphylococcal nuclease and tudor domain containing 1 Homo sapiens 125-129 25231320-0 2014 Tunicamycin-induced ER stress regulates chemokine CCL5 expression and secretion via STAT3 followed by decreased transmigration of MCF-7 breast cancer cells. Tunicamycin 0-11 C-C motif chemokine ligand 5 Homo sapiens 50-54 25231320-0 2014 Tunicamycin-induced ER stress regulates chemokine CCL5 expression and secretion via STAT3 followed by decreased transmigration of MCF-7 breast cancer cells. Tunicamycin 0-11 signal transducer and activator of transcription 3 Homo sapiens 84-89 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 C-C motif chemokine ligand 5 Homo sapiens 96-100 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 signal transducer and activator of transcription 3 Homo sapiens 102-107 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 25231320-7 2014 Moreover, tunicamycin-induced CCL5 expression was positively related to upregulation of unphosphorylated STAT3 (U-STAT3) but negatively related to STAT3 phosphorylation at the Tyr705 site. Tunicamycin 10-21 C-C motif chemokine ligand 5 Homo sapiens 30-34 25231320-7 2014 Moreover, tunicamycin-induced CCL5 expression was positively related to upregulation of unphosphorylated STAT3 (U-STAT3) but negatively related to STAT3 phosphorylation at the Tyr705 site. Tunicamycin 10-21 signal transducer and activator of transcription 3 Homo sapiens 105-110 25231320-7 2014 Moreover, tunicamycin-induced CCL5 expression was positively related to upregulation of unphosphorylated STAT3 (U-STAT3) but negatively related to STAT3 phosphorylation at the Tyr705 site. Tunicamycin 10-21 signal transducer and activator of transcription 3 Homo sapiens 114-119 25231320-7 2014 Moreover, tunicamycin-induced CCL5 expression was positively related to upregulation of unphosphorylated STAT3 (U-STAT3) but negatively related to STAT3 phosphorylation at the Tyr705 site. Tunicamycin 10-21 signal transducer and activator of transcription 3 Homo sapiens 114-119 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 25360516-4 2014 The blocking of cell surface GRP78 by anti-GRP78 antibody prevented apoptosis, suggesting that induction of cell surface GRP78 by doxorubicin and tunicamycin is required for apoptosis. Tunicamycin 146-157 heat shock protein family A (Hsp70) member 5 Homo sapiens 29-34 25360516-4 2014 The blocking of cell surface GRP78 by anti-GRP78 antibody prevented apoptosis, suggesting that induction of cell surface GRP78 by doxorubicin and tunicamycin is required for apoptosis. Tunicamycin 146-157 heat shock protein family A (Hsp70) member 5 Homo sapiens 43-48 25360516-4 2014 The blocking of cell surface GRP78 by anti-GRP78 antibody prevented apoptosis, suggesting that induction of cell surface GRP78 by doxorubicin and tunicamycin is required for apoptosis. Tunicamycin 146-157 heat shock protein family A (Hsp70) member 5 Homo sapiens 43-48 25112878-5 2014 Of these mutants, pro3 was the most sensitive to tunicamycin and was rescued by anaerobic growth conditions or reduced thiol reagents. Tunicamycin 49-60 pyrroline-5-carboxylate reductase Saccharomyces cerevisiae S288C 18-22 25816608-7 2014 At the same time, the induction of endoplasmic reticulum stress by tunicamycin in glioma cells with suppressed activity of ERN1 endoribonuclease decreases the expression level of PRPS1 and PRPS2 genes only. Tunicamycin 67-78 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 123-127 25816608-7 2014 At the same time, the induction of endoplasmic reticulum stress by tunicamycin in glioma cells with suppressed activity of ERN1 endoribonuclease decreases the expression level of PRPS1 and PRPS2 genes only. Tunicamycin 67-78 phosphoribosyl pyrophosphate synthetase 1 Homo sapiens 179-184 25816608-7 2014 At the same time, the induction of endoplasmic reticulum stress by tunicamycin in glioma cells with suppressed activity of ERN1 endoribonuclease decreases the expression level of PRPS1 and PRPS2 genes only. Tunicamycin 67-78 phosphoribosyl pyrophosphate synthetase 2 Homo sapiens 189-194 25170079-5 2014 Intraperitoneal administration of the ER stressor tunicamycin in mice resulted in hepatic steatosis, accompanied by activation of the three canonical UPR branches and increased the expression of FGF21. Tunicamycin 50-61 fibroblast growth factor 21 Mus musculus 195-200 25170079-7 2014 Administration of recombinant FGF21 in mice alleviated tunicamycin-induced liver steatosis, in parallel with reduced eIF2alpha-ATF4-CHOP signaling. Tunicamycin 55-66 fibroblast growth factor 21 Mus musculus 30-35 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 microRNA 615 Homo sapiens 16-23 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 25457612-8 2014 This mechanism is potentially involved in mTORC1 regulation by amino acids, rotenone, and tunicamycin, connecting stress response with mTORC1 inhibition. Tunicamycin 90-101 CREB regulated transcription coactivator 1 Mus musculus 42-48 25457612-8 2014 This mechanism is potentially involved in mTORC1 regulation by amino acids, rotenone, and tunicamycin, connecting stress response with mTORC1 inhibition. Tunicamycin 90-101 CREB regulated transcription coactivator 1 Mus musculus 135-141 24983772-0 2014 Histone H3K4 methyltransferase Mll1 regulates protein glycosylation and tunicamycin-induced apoptosis through transcriptional regulation. Tunicamycin 72-83 lysine methyltransferase 2A Homo sapiens 31-35 24983772-4 2014 Here, we find that Mll1 deficiency enhances UPR and apoptosis induced by the glycosylation inhibitor TM (tunicamycin). Tunicamycin 105-116 lysine methyltransferase 2A Homo sapiens 19-23 25340554-3 2014 In this study, we examined the biological significance of gp130 glycosylation using tunicamycin (Tm), an inhibitor of enzyme involved in N-linked glycosylation. Tunicamycin 84-95 interleukin 6 cytokine family signal transducer Homo sapiens 58-63 25340554-3 2014 In this study, we examined the biological significance of gp130 glycosylation using tunicamycin (Tm), an inhibitor of enzyme involved in N-linked glycosylation. Tunicamycin 97-99 interleukin 6 cytokine family signal transducer Homo sapiens 58-63 25106896-7 2014 Tunicamycin-induced ER stress altered reactive oxygen species (ROS) (6.34-fold ), membrane potential (4.1-fold ), mitochondrial biogenesis (2.4-fold ), and adiponectin secretion (3.5-fold ). Tunicamycin 0-11 adiponectin, C1Q and collagen domain containing Homo sapiens 156-167 25011082-6 2014 In comparison to NSCLC cells with functional LKB1, treatment of NSCLC cells lacking LKB1 with the ER stress activators (ERSA), tunicamycin, brefeldin A or 2DG, resulted in aggravation of ER stress, increased cytotoxicity, and evidence of ER stress-mediated cell death. Tunicamycin 127-138 serine/threonine kinase 11 Homo sapiens 84-88 25063273-5 2014 PPARbeta/delta activation also prevented thapsigargin- and tunicamycin-induced ER stress in human and murine skeletal muscle cells. Tunicamycin 59-70 peroxisome proliferator activated receptor delta Homo sapiens 0-8 25126734-0 2014 Endoplasmic reticulum stress induced by tunicamycin and thapsigargin protects against transient ischemic brain injury: Involvement of PARK2-dependent mitophagy. Tunicamycin 40-51 parkin RBR E3 ubiquitin protein ligase Mus musculus 134-139 25228093-6 2014 The protein and mRNA expression levels of MICA/B in SMMC7721 and HepG2 cells treated by tunicamycin were evaluated by flow cytometry, Western Blot and RT-PCR. Tunicamycin 88-99 MHC class I polypeptide-related sequence A Homo sapiens 42-46 25092289-6 2014 Also, the addition of the TGF-beta inhibitor SB431542 and the Wnt/beta-catenin antagonist IWP-2 negated the endodermal differentiation of ESCs mediated by thapsigargin and tunicamycin. Tunicamycin 172-183 catenin (cadherin associated protein), beta 1 Mus musculus 66-78 25108065-8 2014 Additionally, although progesterone secretion and levels of steroidogenic enzymes decreased following intra-peritoneal injection of Tunicamycin, an ER stress inducer, the expression of Grp78/Bip, p50ATF6, and CHOP dramatically increased. Tunicamycin 132-143 heat shock protein 5 Mus musculus 185-190 25108065-8 2014 Additionally, although progesterone secretion and levels of steroidogenic enzymes decreased following intra-peritoneal injection of Tunicamycin, an ER stress inducer, the expression of Grp78/Bip, p50ATF6, and CHOP dramatically increased. Tunicamycin 132-143 heat shock protein 5 Mus musculus 191-194 25108065-8 2014 Additionally, although progesterone secretion and levels of steroidogenic enzymes decreased following intra-peritoneal injection of Tunicamycin, an ER stress inducer, the expression of Grp78/Bip, p50ATF6, and CHOP dramatically increased. Tunicamycin 132-143 DNA-damage inducible transcript 3 Mus musculus 209-213 25232251-3 2014 The N-/O-glycosylation inhibitors (tunicamycin and benzyl-N-acetyl-alpha-galactosaminide) were then used to interfere with KL-6/MUC1 glycosylation in two pancreatic carcinoma cell lines, and the effects on KL-6/MUC1 expression, and cell adhesion and invasion were determined. Tunicamycin 35-46 mucin 1, cell surface associated Homo sapiens 123-127 25232251-3 2014 The N-/O-glycosylation inhibitors (tunicamycin and benzyl-N-acetyl-alpha-galactosaminide) were then used to interfere with KL-6/MUC1 glycosylation in two pancreatic carcinoma cell lines, and the effects on KL-6/MUC1 expression, and cell adhesion and invasion were determined. Tunicamycin 35-46 mucin 1, cell surface associated Homo sapiens 128-132 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 24723324-5 2014 We evaluated whether neuronal differentiation and dendrite outgrowth were regulated by HRD1, a ubiquitin ligase that was induced under mild conditions of tunicamycin-induced ER stress. Tunicamycin 154-165 synovial apoptosis inhibitor 1, synoviolin Mus musculus 87-91 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 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 growth differentiation factor 10 Homo sapiens 21-24 24962313-8 2014 We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6. Tunicamycin 31-42 X-box binding protein 1 Homo sapiens 81-85 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 24962313-10 2014 Knockdown endogenous BiP with siRNA abolished the suppression of propofol on tunicamycin-mediated activation of CHOP and caspase-3. Tunicamycin 77-88 caspase 3 Homo sapiens 121-130 24962313-11 2014 Meanwhile, knockdown BiP attenuated the protective effects of propofol on the neural cells exposed to tunicamycin. Tunicamycin 102-113 growth differentiation factor 10 Homo sapiens 21-24 24962313-8 2014 We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6. Tunicamycin 31-42 X-box binding protein 1 Homo sapiens 87-92 24962313-8 2014 We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6. Tunicamycin 31-42 activating transcription factor 6 Homo sapiens 106-139 24962313-8 2014 We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6. Tunicamycin 31-42 activating transcription factor 6 Homo sapiens 141-145 24962313-8 2014 We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6. Tunicamycin 31-42 activating transcription factor 6 Homo sapiens 166-170 24970053-9 2014 Hence, various concentrations of tunicamycin were used to treat the cells in order to study its influence on CD147 N-glycosylation and MMP-2 expression. Tunicamycin 33-44 basigin (Ok blood group) Homo sapiens 109-114 24838315-9 2014 Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction. Tunicamycin 78-89 mucin 1, cell surface associated Homo sapiens 28-32 24838315-9 2014 Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction. Tunicamycin 78-89 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 154-157 24838315-9 2014 Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction. Tunicamycin 78-89 mucin 1, cell surface associated Homo sapiens 158-162 24838315-9 2014 Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction. Tunicamycin 78-89 galectin 3 Homo sapiens 165-175 24838315-9 2014 Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction. Tunicamycin 78-89 mucin 1, cell surface associated Homo sapiens 158-162 24838315-9 2014 Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction. Tunicamycin 78-89 mucin 1, cell surface associated Homo sapiens 158-162 24970053-9 2014 Hence, various concentrations of tunicamycin were used to treat the cells in order to study its influence on CD147 N-glycosylation and MMP-2 expression. Tunicamycin 33-44 matrix metallopeptidase 2 Homo sapiens 135-140 25035425-4 2014 We report here that Lmf1 expression is induced by ER stress in various cell lines and in tunicamycin (TM)-injected mice. Tunicamycin 89-100 lipase maturation factor 1 Mus musculus 20-24 25064675-6 2014 Treatment of larvae or adult fish with tunicamycin induces ER stress and upregulates the expression of several key components of the gp78 ERAD complex in the liver. Tunicamycin 39-50 autocrine motility factor receptor a Danio rerio 133-137 25035425-4 2014 We report here that Lmf1 expression is induced by ER stress in various cell lines and in tunicamycin (TM)-injected mice. Tunicamycin 102-104 lipase maturation factor 1 Mus musculus 20-24 25023286-5 2014 However, these changes were countered by Bcl-xL induction, which is necessary to protect differentiating cells both from ER stress-induced death by tunicamycin and from the death signals inherent in differentiation. Tunicamycin 148-159 BCL2-like 1 Mus musculus 41-47 24357007-6 2014 Tunicamycin and thapsigargin, compounds known to induce ER stress, also decreased the SCD protein. Tunicamycin 0-11 stearoyl-CoA desaturase Homo sapiens 86-89 24973711-7 2014 We show that chemical ER stress inducers, such as tunicamycin or thapsigargin, enhanced IR-induced caspase 3 activation and DNA fragmentation in intestinal epithelial cells. Tunicamycin 50-61 caspase 3 Rattus norvegicus 99-108 25064675-7 2014 Moreover, liver-specific overexpression of the dominant-negative form of gp78 (gp78-R2M) renders liver more sensitive to tunicamycin-induced ER stress and enhances the expression of sterol response element binding protein (Srebp)-target genes, which was largely suppressed in fish overexpressing wild-type gp78. Tunicamycin 121-132 autocrine motility factor receptor a Danio rerio 73-77 25064675-7 2014 Moreover, liver-specific overexpression of the dominant-negative form of gp78 (gp78-R2M) renders liver more sensitive to tunicamycin-induced ER stress and enhances the expression of sterol response element binding protein (Srebp)-target genes, which was largely suppressed in fish overexpressing wild-type gp78. Tunicamycin 121-132 autocrine motility factor receptor a Danio rerio 79-83 25064675-7 2014 Moreover, liver-specific overexpression of the dominant-negative form of gp78 (gp78-R2M) renders liver more sensitive to tunicamycin-induced ER stress and enhances the expression of sterol response element binding protein (Srebp)-target genes, which was largely suppressed in fish overexpressing wild-type gp78. Tunicamycin 121-132 autocrine motility factor receptor a Danio rerio 79-83 24982359-4 2014 MATERIALS AND METHODS: GRP78 was over-expressed in A549 cells with 2-deoxyglucose (2-dG) or tunicamycin (TM) treatments for 48 h and subsequently exposed to cisplatin for 2 h. Viability of these cells was determined at 0, 12, 24, 36 and 48 h afterwards. Tunicamycin 105-107 heat shock protein family A (Hsp70) member 5 Homo sapiens 23-28 25026174-5 2014 Tunicamycin or brefeldin A, two ER stress inducers, increased APE1 and GRP78, an ER stress marker, expression in HepG2 and Huh-7 cells. Tunicamycin 0-11 apurinic/apyrimidinic endodeoxyribonuclease 1 Homo sapiens 62-66 25026174-5 2014 Tunicamycin or brefeldin A, two ER stress inducers, increased APE1 and GRP78, an ER stress marker, expression in HepG2 and Huh-7 cells. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 71-76 24982359-4 2014 MATERIALS AND METHODS: GRP78 was over-expressed in A549 cells with 2-deoxyglucose (2-dG) or tunicamycin (TM) treatments for 48 h and subsequently exposed to cisplatin for 2 h. Viability of these cells was determined at 0, 12, 24, 36 and 48 h afterwards. Tunicamycin 92-103 heat shock protein family A (Hsp70) member 5 Homo sapiens 23-28 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 24813659-3 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 24813659-3 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 mitogen activated protein kinase 14 Rattus norvegicus 343-346 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 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 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 AKT serine/threonine kinase 1 Rattus norvegicus 129-132 24963635-9 2014 The endoplasmic reticulum (ER) stress-inducing reagent tunicamycin induced OPN mRNA expression in A549, MLE12 and HPAEpiC, and OPN mRNA expression was induced via activation of the ERK-dependent signaling pathway in A549 and MLE12. Tunicamycin 55-66 secreted phosphoprotein 1 Homo sapiens 75-78 24722832-0 2014 Overexpression of CREB protein protects from tunicamycin-induced apoptosis in various rat cell types. Tunicamycin 45-56 cAMP responsive element binding protein 1 Rattus norvegicus 18-22 24722832-4 2014 The significance of the ubiquitously expressed transcription factor CREB is demonstrated in prolonged, tunicamycin (TM)-induced ER stress in this study. Tunicamycin 103-114 cAMP responsive element binding protein 1 Rattus norvegicus 68-72 24722832-4 2014 The significance of the ubiquitously expressed transcription factor CREB is demonstrated in prolonged, tunicamycin (TM)-induced ER stress in this study. Tunicamycin 116-118 cAMP responsive element binding protein 1 Rattus norvegicus 68-72 25050111-0 2014 IRE1alpha knockdown rescues tunicamycin-induced developmental defects and apoptosis in Xenopus laevis. Tunicamycin 28-39 endoplasmic reticulum to nucleus signaling 1 S homeolog Xenopus laevis 0-9 24807724-5 2014 CRT was also found to be of high importance for proper oligomerization of the viral structural proteins VP26 and VP28, and when CRT glycosylation was blocked with tunicamycin, a significant decrease in both viral replication and assembly was detected. Tunicamycin 163-174 calreticulin Homo sapiens 0-3 24807724-5 2014 CRT was also found to be of high importance for proper oligomerization of the viral structural proteins VP26 and VP28, and when CRT glycosylation was blocked with tunicamycin, a significant decrease in both viral replication and assembly was detected. Tunicamycin 163-174 calreticulin Homo sapiens 128-131 24604564-5 2014 GRP78 protein levels were similar in the tunicamycin (Tm), salubrinal, and SP600125 groups, but were lower in cells treated with SN50. Tunicamycin 41-52 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 24963635-9 2014 The endoplasmic reticulum (ER) stress-inducing reagent tunicamycin induced OPN mRNA expression in A549, MLE12 and HPAEpiC, and OPN mRNA expression was induced via activation of the ERK-dependent signaling pathway in A549 and MLE12. Tunicamycin 55-66 secreted phosphoprotein 1 Homo sapiens 127-130 24963635-9 2014 The endoplasmic reticulum (ER) stress-inducing reagent tunicamycin induced OPN mRNA expression in A549, MLE12 and HPAEpiC, and OPN mRNA expression was induced via activation of the ERK-dependent signaling pathway in A549 and MLE12. Tunicamycin 55-66 mitogen-activated protein kinase 1 Homo sapiens 181-184 24576409-6 2014 Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expressions enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation. Tunicamycin 95-106 mitogen-activated protein kinase 14 Mus musculus 33-36 24945938-6 2014 Treatment of ECs with tunicamycin, an N-glycosylation inhibitor, suppressed CD62P (P-selectin) expression on the cell surface as well as the 140 kDa form in the cytoplasm. Tunicamycin 22-33 selectin, platelet Mus musculus 76-81 24945938-6 2014 Treatment of ECs with tunicamycin, an N-glycosylation inhibitor, suppressed CD62P (P-selectin) expression on the cell surface as well as the 140 kDa form in the cytoplasm. Tunicamycin 22-33 selectin, platelet Mus musculus 83-93 24945938-8 2014 Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression. Tunicamycin 94-105 thymoma viral proto-oncogene 1 Mus musculus 116-119 24945938-8 2014 Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression. Tunicamycin 94-105 thymoma viral proto-oncogene 1 Mus musculus 116-119 24945938-8 2014 Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression. Tunicamycin 186-197 coagulation factor II Mus musculus 0-8 24945938-8 2014 Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression. Tunicamycin 186-197 selectin, platelet Mus musculus 27-37 24945938-8 2014 Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression. Tunicamycin 186-197 selectin, platelet Mus musculus 221-231 24944523-3 2014 METHODS: Cancer cells were treated with tunicamycin (TM) for 8 and 24 h. The expression of Derlin-1 and autophagy-related genes was determined by western blot. Tunicamycin 40-51 derlin 1 Homo sapiens 91-99 24944523-3 2014 METHODS: Cancer cells were treated with tunicamycin (TM) for 8 and 24 h. The expression of Derlin-1 and autophagy-related genes was determined by western blot. Tunicamycin 53-55 derlin 1 Homo sapiens 91-99 24784707-8 2014 This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. Tunicamycin 68-79 mitogen-activated protein kinase 8 Homo sapiens 88-111 24784707-8 2014 This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. Tunicamycin 68-79 mitogen-activated protein kinase 8 Homo sapiens 113-116 24892553-5 2014 (i) Tunicamycin induced ER stress as measured by increased mRNA and protein levels of glucose-regulated protein 78 kDa, P-eIF2alpha, activating transcription factor 4, C/EBP homologous protein, and cell death. Tunicamycin 4-15 eukaryotic translation initiation factor 2A Rattus norvegicus 122-131 24892553-5 2014 (i) Tunicamycin induced ER stress as measured by increased mRNA and protein levels of glucose-regulated protein 78 kDa, P-eIF2alpha, activating transcription factor 4, C/EBP homologous protein, and cell death. Tunicamycin 4-15 activating transcription factor 4 Rattus norvegicus 133-166 24892553-5 2014 (i) Tunicamycin induced ER stress as measured by increased mRNA and protein levels of glucose-regulated protein 78 kDa, P-eIF2alpha, activating transcription factor 4, C/EBP homologous protein, and cell death. Tunicamycin 4-15 CCAAT/enhancer binding protein gamma Rattus norvegicus 168-173 24576409-6 2014 Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expressions enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation. Tunicamycin 95-106 DNA-damage inducible transcript 3 Mus musculus 58-62 24576409-6 2014 Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expressions enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation. Tunicamycin 95-106 heat shock protein 5 Mus musculus 67-70 25033633-8 2014 Under stress conditions, the FCM assay showed that cell percentage of S phases increased, whereas that of G1 phases decreased in the IRE1alpha group (P < 0.05) compared with the control group of tunicamycin (TM) treatment. Tunicamycin 198-209 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 133-142 24888588-4 2014 In addition, we found that experimental induction of ER stress by tunicamycin injections in mice results in a block of pro-B-cell to pre-B-cell differentiation specifically in Mzb1(-/-) mice. Tunicamycin 66-77 marginal zone B and B1 cell-specific protein 1 Mus musculus 176-180 24714921-3 2014 Following treatment of the cells with the ER stress inducers, thapsigargin (TG) or tunicamycin (TM), the lentiviral short hairpin RNA (shRNA)-mediated knockdown of Ufm1 increased the apoptosis of Raw264.7 cells. Tunicamycin 83-94 ubiquitin-fold modifier 1 Mus musculus 164-168 24714921-3 2014 Following treatment of the cells with the ER stress inducers, thapsigargin (TG) or tunicamycin (TM), the lentiviral short hairpin RNA (shRNA)-mediated knockdown of Ufm1 increased the apoptosis of Raw264.7 cells. Tunicamycin 96-98 ubiquitin-fold modifier 1 Mus musculus 164-168 24714921-5 2014 The overexpression of Ufm1 induced by lentiviral infection in the Raw264.7 cells treated with the ER stress inducers, TG or TM, resulted in the opposite effect. Tunicamycin 124-126 ubiquitin-fold modifier 1 Mus musculus 22-26 25033633-8 2014 Under stress conditions, the FCM assay showed that cell percentage of S phases increased, whereas that of G1 phases decreased in the IRE1alpha group (P < 0.05) compared with the control group of tunicamycin (TM) treatment. Tunicamycin 211-213 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 133-142 24652289-7 2014 Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1). Tunicamycin 57-68 insulin Homo sapiens 122-129 24666819-8 2014 The induction of the UPR by tunicamycin was accompanied by activation of NF-kappaB in NSC34 cells and motor neurons. Tunicamycin 28-39 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 73-82 24412219-6 2014 Tunicamycin to inhibit glycosylation reduced SGLT1 activity comparable to that seen with L-NAME treatment. Tunicamycin 0-11 solute carrier family 5 member 1 Rattus norvegicus 45-50 24412219-8 2014 Immunoblots of luminal membranes from tunicamycin treated or L-NAME treated IEC-18 cells showed a decrease in the apparent molecular size of SGLT1 protein to 62 and 67 kD, respectively suggesting an alteration in protein glycosylation. Tunicamycin 38-49 solute carrier family 5 member 1 Rattus norvegicus 141-146 24652289-7 2014 Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1). Tunicamycin 57-68 insulin receptor substrate 1 Homo sapiens 157-161 24652289-7 2014 Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1). Tunicamycin 57-68 insulin receptor substrate 1 Homo sapiens 175-179 24652289-7 2014 Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1). Tunicamycin 57-68 insulin receptor substrate 1 Homo sapiens 175-179 24468888-11 2014 In addition, induction of ER stress by tunicamycin resulted in significantly increased expression of pro-inflammatory molecules such as IL-1beta and TNF-alpha in cultured inflammatory FLS. Tunicamycin 39-50 interleukin 1 beta Rattus norvegicus 136-144 24589479-5 2014 Upon induction of autophagy, by using amino acid deprivation as well as tunicamycin, we found that GD3 ganglioside, considered as a paradigmatic raft constituent, actively contributed to the biogenesis and maturation of autophagic vacuoles. Tunicamycin 72-83 GRDX Homo sapiens 99-102 24370996-6 2014 As a result of impaired ATF6 activation, dermal fibroblasts and adult thyrocytes from ERp29(-/-) mice display significantly lower apoptosis sensitivities when treated with tunicamycin and hydrogen peroxide. Tunicamycin 172-183 endoplasmic reticulum protein 29 Mus musculus 86-91 24468888-11 2014 In addition, induction of ER stress by tunicamycin resulted in significantly increased expression of pro-inflammatory molecules such as IL-1beta and TNF-alpha in cultured inflammatory FLS. Tunicamycin 39-50 tumor necrosis factor Rattus norvegicus 149-158 24743137-6 2014 Time-lapse confocal microscopy indicated that A1AT co-localized with Golgi in the endothelium whilst inhibition of the classical secretory pathway with tunicamycin significantly increased intracellular retention of A1AT. Tunicamycin 152-163 serpin family A member 1 Homo sapiens 215-219 24699413-0 2014 The Batten disease gene CLN3 confers resistance to endoplasmic reticulum stress induced by tunicamycin. Tunicamycin 91-102 CLN3 lysosomal/endosomal transmembrane protein, battenin Homo sapiens 24-28 24576488-0 2014 Inhibition of inducible nitric oxide synthase and interleukin-1beta expression by tunicamycin in cultured glial cells exposed to lipopolysaccharide. Tunicamycin 82-93 nitric oxide synthase 2 Homo sapiens 14-45 24576488-0 2014 Inhibition of inducible nitric oxide synthase and interleukin-1beta expression by tunicamycin in cultured glial cells exposed to lipopolysaccharide. Tunicamycin 82-93 interleukin 1 beta Homo sapiens 50-67 24389415-4 2014 Tunicamycin, an inducer of endoplasmic reticulum stress, stimulated SMILE expression. Tunicamycin 0-11 CREB/ATF bZIP transcription factor Mus musculus 68-73 24663680-6 2014 Experiments using tunicamycin, an inhibitor of N-glycosylation, indicated that the N-glycosylation of hKv1.5 is more effective at 28 C than at 37 C. Finally, the hypothermic treatment also rescued the protein expression and currents of trafficking-defective hKv1.5 mutants. Tunicamycin 18-29 potassium voltage-gated channel subfamily A member 5 Homo sapiens 102-108 24482374-9 2014 Metformin and PPARdelta agonist GW1516 reversed tunicamycin (ER stress inducer)-induced ER stress, oxidative stress, and impairment of endothelium-dependent relaxation in mouse aortae as well as NO production in mouse aortic endothelial cells. Tunicamycin 48-59 peroxisome proliferator activator receptor delta Mus musculus 14-23 24366244-0 2014 Inhibition of serine/threonine protein phosphatase PP1 protects cardiomyocytes from tunicamycin-induced apoptosis and I/R through the upregulation of p-eIF2alpha. Tunicamycin 84-95 neuropeptide Y receptor Y4 Rattus norvegicus 51-54 24583133-7 2014 In vitro, treatment of RAW264.7 macrophages with tunicamycin, and subsequently stimulation with lipopolysaccharide (LPS) and interferon (IFN)-gamma enhances MIP2 mRNA und protein expression compared to proinflammatory stimulation alone. Tunicamycin 49-60 chemokine (C-X-C motif) ligand 2 Mus musculus 157-161 24583133-8 2014 However, LPS/IFNgamma induced vascular endothelial growth factor (VEGF) production was blunted by tunicamycin induced-ER stress. Tunicamycin 98-109 interferon gamma Mus musculus 13-21 24583133-8 2014 However, LPS/IFNgamma induced vascular endothelial growth factor (VEGF) production was blunted by tunicamycin induced-ER stress. Tunicamycin 98-109 vascular endothelial growth factor A Mus musculus 30-64 24583133-8 2014 However, LPS/IFNgamma induced vascular endothelial growth factor (VEGF) production was blunted by tunicamycin induced-ER stress. Tunicamycin 98-109 vascular endothelial growth factor A Mus musculus 66-70 24667182-7 2014 In mProx24 renal proximal tubular cells, the treatment with ER-stress inducers, tunicamycin and thapsigargin, increased the expression of GRP78, which was reduced by transfection of a shRNA lentivirus for Pemt (shRNA-Pemt). Tunicamycin 80-91 heat shock protein 5 Mus musculus 138-143 24667182-7 2014 In mProx24 renal proximal tubular cells, the treatment with ER-stress inducers, tunicamycin and thapsigargin, increased the expression of GRP78, which was reduced by transfection of a shRNA lentivirus for Pemt (shRNA-Pemt). Tunicamycin 80-91 phosphatidylethanolamine N-methyltransferase Mus musculus 205-209 24667182-7 2014 In mProx24 renal proximal tubular cells, the treatment with ER-stress inducers, tunicamycin and thapsigargin, increased the expression of GRP78, which was reduced by transfection of a shRNA lentivirus for Pemt (shRNA-Pemt). Tunicamycin 80-91 phosphatidylethanolamine N-methyltransferase Mus musculus 211-221 24647338-7 2014 Expression of p85beta was significantly more decreased under treatment with melatonin and thapsigargin or tunicamycin plus the PI3K inhibitors LY294002 or wortmannin than under treatment with only melatonin or a PI3K inhibitor. Tunicamycin 106-117 phosphoinositide-3-kinase regulatory subunit 2 Mus musculus 14-21 24647338-8 2014 The PI3K downstream target p-Akt (Ser473, Thr308) showed significantly decreased expression under treatment with melatonin and thapsigargin or tunicamycin plus PI3K inhibitors than under treatment with melatonin or PI3K inhibitors only. Tunicamycin 143-154 thymoma viral proto-oncogene 1 Mus musculus 29-32 24366244-0 2014 Inhibition of serine/threonine protein phosphatase PP1 protects cardiomyocytes from tunicamycin-induced apoptosis and I/R through the upregulation of p-eIF2alpha. Tunicamycin 84-95 eukaryotic translation initiation factor 2A Rattus norvegicus 152-161 24605085-9 2014 To discriminate between these possibilities, HEK293 cells expressing TRPM4 WT were treated with tunicamycin, an inhibitor of glycosylation. Tunicamycin 96-107 transient receptor potential cation channel subfamily M member 4 Homo sapiens 69-74 24605085-10 2014 In contrast to N-glycosylation signal abolishment by mutagenesis, tunicamycin treatment led to an increase in the TRPM4-mediated current. Tunicamycin 66-77 transient receptor potential cation channel subfamily M member 4 Homo sapiens 114-119 24240056-4 2014 In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells. Tunicamycin 263-274 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 80-89 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 nitric oxide synthase 3 Rattus norvegicus 64-68 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 nitric oxide synthase 3 Rattus norvegicus 102-106 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 24240056-4 2014 In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells. Tunicamycin 263-274 activating transcription factor 6 Homo sapiens 94-98 24240056-4 2014 In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells. Tunicamycin 263-274 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 203-212 24240056-4 2014 In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells. Tunicamycin 263-274 activating transcription factor 6 Homo sapiens 217-221 24240056-4 2014 In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells. Tunicamycin 276-278 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 80-89 24240056-4 2014 In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells. Tunicamycin 276-278 activating transcription factor 6 Homo sapiens 94-98 24240056-4 2014 In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells. Tunicamycin 276-278 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 203-212 24240056-4 2014 In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells. Tunicamycin 276-278 activating transcription factor 6 Homo sapiens 217-221 24275540-8 2014 SelS protein expression was unaffected by enterocytic differentiation but increased in response to selenium supplementation and after treatment with the ER stress inducer tunicamycin. Tunicamycin 171-182 selenoprotein S Homo sapiens 0-4 24575364-9 2014 (3) Induction of ERSR stress by tunicamycin in H9C2 resulted in the upregulation of ERSR stress response genes along with downregulation of adiponectin, adiponectin receptors 1 and 2, and Serca2A. Tunicamycin 32-43 adiponectin, C1Q and collagen domain containing Mus musculus 140-151 23921951-6 2014 Similar to knockdown of glucose-regulated protein 78 (GRP78), inhibition of XBP1 decelerated melanoma cell proliferation and enhanced apoptosis induced by the pharmacological ER stress inducers tunicamycin and thapasigargin. Tunicamycin 194-205 X-box binding protein 1 Homo sapiens 76-80 24465394-9 2014 PST also inhibited the up-regulation of GRP78 expression during UPR activation (by tunicamycin) in hepatocytes. Tunicamycin 83-94 heat shock protein 5 Mus musculus 40-45 24315873-4 2014 Treatment with tunicamycin (TM), an ER stress inducer, increased ATF3 expression in the preosteoblast cell line, MC3T3-E1. Tunicamycin 15-26 activating transcription factor 3 Mus musculus 65-69 24315873-4 2014 Treatment with tunicamycin (TM), an ER stress inducer, increased ATF3 expression in the preosteoblast cell line, MC3T3-E1. Tunicamycin 28-30 activating transcription factor 3 Mus musculus 65-69 24125761-8 2014 The treatment of wild-type AADAC-expressing HuH-7 cells with tunicamycin, which produces unglycosylated protein, decreased AADAC enzyme activity. Tunicamycin 61-72 arylacetamide deacetylase Homo sapiens 27-32 24125761-8 2014 The treatment of wild-type AADAC-expressing HuH-7 cells with tunicamycin, which produces unglycosylated protein, decreased AADAC enzyme activity. Tunicamycin 61-72 arylacetamide deacetylase Homo sapiens 123-128 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 24575364-9 2014 (3) Induction of ERSR stress by tunicamycin in H9C2 resulted in the upregulation of ERSR stress response genes along with downregulation of adiponectin, adiponectin receptors 1 and 2, and Serca2A. Tunicamycin 32-43 adiponectin receptor 1 Mus musculus 153-182 24575364-9 2014 (3) Induction of ERSR stress by tunicamycin in H9C2 resulted in the upregulation of ERSR stress response genes along with downregulation of adiponectin, adiponectin receptors 1 and 2, and Serca2A. Tunicamycin 32-43 ATPase, Ca++ transporting, cardiac muscle, slow twitch 2 Mus musculus 188-195 24309597-6 2014 Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance. Tunicamycin 0-11 insulin Homo sapiens 80-87 24309597-7 2014 Moreover, disturbance of autophagy and insulin sensitivity induced by tunicamycin can be effectively corrected by the addition of osteocalcin in an NFkappaB-dependent manner in vitro. Tunicamycin 70-81 bone gamma-carboxyglutamate protein Homo sapiens 130-141 24418603-5 2014 Quantitative RT-PCR assays showed that the metabolic stressors histidinol and tunicamycin increased ATF4 levels and up-regulated ALT2 in HepG2 and Huh7 cells. Tunicamycin 78-89 activating transcription factor 4 Homo sapiens 100-104 24418603-5 2014 Quantitative RT-PCR assays showed that the metabolic stressors histidinol and tunicamycin increased ATF4 levels and up-regulated ALT2 in HepG2 and Huh7 cells. Tunicamycin 78-89 glutamic--pyruvic transaminase 2 Homo sapiens 129-133 24418603-7 2014 Moreover, ATF4 silencing prevented the activating effect of histidinol and tunicamycin on ATF4 and ALT2 expression. Tunicamycin 75-86 activating transcription factor 4 Homo sapiens 10-14 24418603-7 2014 Moreover, ATF4 silencing prevented the activating effect of histidinol and tunicamycin on ATF4 and ALT2 expression. Tunicamycin 75-86 activating transcription factor 4 Homo sapiens 90-94 24418603-7 2014 Moreover, ATF4 silencing prevented the activating effect of histidinol and tunicamycin on ATF4 and ALT2 expression. Tunicamycin 75-86 glutamic--pyruvic transaminase 2 Homo sapiens 99-103 25229868-6 2014 The interaction with Cne1p was abrogated by the addition of tunicamycin, an inhibitor of N-glycosylation, indicating that N-linked carbohydrates might be necessary for protein binding to Cne1p. Tunicamycin 60-71 calnexin Saccharomyces cerevisiae S288C 21-26 25229868-6 2014 The interaction with Cne1p was abrogated by the addition of tunicamycin, an inhibitor of N-glycosylation, indicating that N-linked carbohydrates might be necessary for protein binding to Cne1p. Tunicamycin 60-71 calnexin Saccharomyces cerevisiae S288C 187-192 24309597-6 2014 Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance. Tunicamycin 0-11 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 155-159 24309597-6 2014 Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance. Tunicamycin 0-11 mitogen-activated protein kinase 8 Homo sapiens 160-163 24309597-6 2014 Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance. Tunicamycin 0-11 insulin Homo sapiens 237-244 24309597-7 2014 Moreover, disturbance of autophagy and insulin sensitivity induced by tunicamycin can be effectively corrected by the addition of osteocalcin in an NFkappaB-dependent manner in vitro. Tunicamycin 70-81 insulin Homo sapiens 39-46 24787918-4 2014 As endoplasmic reticulum (ER) stress was reported in the early stage of AD, we injected tunicamycin, an ER stress inducer, into the lateral ventricular of rats and 48 hours later found in the other three brain regions but not cerebellum, increasing of binding immunoglobulin protein with the increased phosphorylation of pancreatic ER kinase, inositol-requiring enzyme 1, and activating transcription factor 6. Tunicamycin 88-99 activating transcription factor 6 Rattus norvegicus 343-409 25011668-7 2014 Most interestingly, GLUT4 gene expression induced by 4-PBA was not associated with ER stress even in the presence of tunicamycin, an ER stress inducer. Tunicamycin 117-128 solute carrier family 2 member 4 Homo sapiens 20-25 24787918-6 2014 The synapse-associated proteins, GluR2, PSD95, and synapsin1, were found decreased in the hippocampus after tunicamycin exposure. Tunicamycin 108-119 glutamate ionotropic receptor AMPA type subunit 2 Rattus norvegicus 33-38 24787918-6 2014 The synapse-associated proteins, GluR2, PSD95, and synapsin1, were found decreased in the hippocampus after tunicamycin exposure. Tunicamycin 108-119 discs large MAGUK scaffold protein 4 Rattus norvegicus 40-45 24787918-6 2014 The synapse-associated proteins, GluR2, PSD95, and synapsin1, were found decreased in the hippocampus after tunicamycin exposure. Tunicamycin 108-119 synapsin I Rattus norvegicus 51-60 24314051-4 2013 A complete deletion of L7 in Sec61p resulted in viable, cold- and tunicamycin-hypersensitive yeast cells with strong defects in posttranslational protein import of soluble proteins into the ER, and in ERAD of soluble substrates. Tunicamycin 66-77 translocon subunit SEC61 Saccharomyces cerevisiae S288C 29-35 24863135-8 2014 RESULTS: Chemical ER stress inducers such as tunicamycin (TM, 0.2 muM) and thapsigargin (TG, 0.2 muM) induced EMT, as shown by upregulation of alpha-smooth muscle actin and downregulation of E-cadherin. Tunicamycin 45-56 cadherin 1 Homo sapiens 191-201 24863135-8 2014 RESULTS: Chemical ER stress inducers such as tunicamycin (TM, 0.2 muM) and thapsigargin (TG, 0.2 muM) induced EMT, as shown by upregulation of alpha-smooth muscle actin and downregulation of E-cadherin. Tunicamycin 58-60 cadherin 1 Homo sapiens 191-201 24056124-0 2013 Tunicamycin inhibits Toll-like receptor-activated inflammation in RAW264.7 cells by suppression of NF-kappaB and c-Jun activity via a mechanism that is independent of ER-stress and N-glycosylation. Tunicamycin 0-11 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 99-108 24056124-0 2013 Tunicamycin inhibits Toll-like receptor-activated inflammation in RAW264.7 cells by suppression of NF-kappaB and c-Jun activity via a mechanism that is independent of ER-stress and N-glycosylation. Tunicamycin 0-11 jun proto-oncogene Mus musculus 113-118 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 nitric oxide synthase 2, inducible Mus musculus 93-114 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 nitric oxide synthase 2, inducible Mus musculus 116-120 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 prostaglandin-endoperoxide synthase 2 Mus musculus 123-139 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 prostaglandin-endoperoxide synthase 2 Mus musculus 141-146 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 interleukin 1 beta Mus musculus 149-167 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 interleukin 1 beta Mus musculus 169-177 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 tumor necrosis factor Mus musculus 183-210 24056124-2 2013 Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha). Tunicamycin 0-11 tumor necrosis factor Mus musculus 212-221 24056124-5 2013 Tunicamycin also inhibited the expression of inflammatory molecule mRNAs induced by stimulation of TLR2 (with lipoteichoic acid) or TLR3 (with polyinosinic:polycytidylic acid), which do not require myeloid differentiation protein-2 (MD2) for their activation. Tunicamycin 0-11 toll-like receptor 2 Mus musculus 99-103 24056124-5 2013 Tunicamycin also inhibited the expression of inflammatory molecule mRNAs induced by stimulation of TLR2 (with lipoteichoic acid) or TLR3 (with polyinosinic:polycytidylic acid), which do not require myeloid differentiation protein-2 (MD2) for their activation. Tunicamycin 0-11 toll-like receptor 3 Mus musculus 132-136 24056124-5 2013 Tunicamycin also inhibited the expression of inflammatory molecule mRNAs induced by stimulation of TLR2 (with lipoteichoic acid) or TLR3 (with polyinosinic:polycytidylic acid), which do not require myeloid differentiation protein-2 (MD2) for their activation. Tunicamycin 0-11 lymphocyte antigen 96 Mus musculus 233-236 24056124-6 2013 Moreover, inhibition of LPS-induced iNOS expression was not inhibited by castanospermine, another N-glycosylation inhibitor, suggesting that the inhibitory effect of tunicamycin on LPS-induced iNOS induction is likely independent of MD2 N-glycosylation. Tunicamycin 166-177 nitric oxide synthase 2, inducible Mus musculus 36-40 24056124-6 2013 Moreover, inhibition of LPS-induced iNOS expression was not inhibited by castanospermine, another N-glycosylation inhibitor, suggesting that the inhibitory effect of tunicamycin on LPS-induced iNOS induction is likely independent of MD2 N-glycosylation. Tunicamycin 166-177 nitric oxide synthase 2, inducible Mus musculus 193-197 24056124-7 2013 Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter. Tunicamycin 0-11 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 45-54 24056124-7 2013 Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter. Tunicamycin 0-11 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 117-120 24056124-7 2013 Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter. Tunicamycin 0-11 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 151-154 24056124-7 2013 Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter. Tunicamycin 0-11 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 159-162 24056124-7 2013 Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter. Tunicamycin 0-11 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 170-179 24056124-7 2013 Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter. Tunicamycin 0-11 nitric oxide synthase 2, inducible Mus musculus 192-196 24056124-8 2013 Tunicamycin also inhibited the transcriptional activity of a cAMP-response element (CRE) reporter, possibly by inhibiting c-Jun activation. Tunicamycin 0-11 jun proto-oncogene Mus musculus 122-127 24056124-9 2013 Therefore, we conclude that tunicamycin represses TLR-induced inflammation through suppression of NF-kappaB and CRE activity via a mechanism that is independent of ER-stress and N-glycosylation. Tunicamycin 28-39 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 98-107 24142515-5 2013 In A549 cells, inhibition of glycosylation by tunicamycin increased the electrophoretic mobility (Mr) and reduced the expression level of wild-type ABCA3 in a dose-dependent manner. Tunicamycin 46-57 ATP binding cassette subfamily A member 3 Homo sapiens 148-153 24130050-0 2013 Tunicamycin potentiates cisplatin anticancer efficacy through the DPAGT1/Akt/ABCG2 pathway in mouse Xenograft models of human hepatocellular carcinoma. Tunicamycin 0-11 dolichyl-phosphate (UDP-N-acetylglucosamine) acetylglucosaminephosphotransferase 1 (GlcNAc-1-P transferase) Mus musculus 66-72 24130050-0 2013 Tunicamycin potentiates cisplatin anticancer efficacy through the DPAGT1/Akt/ABCG2 pathway in mouse Xenograft models of human hepatocellular carcinoma. Tunicamycin 0-11 thymoma viral proto-oncogene 1 Mus musculus 73-76 24130050-10 2013 Finally, the CDDP treatment combined with UDP-GlcNAc-dolichol-phosphate N-acetylglucosamine-1 phosphate transferase (DPAGT1) knockdown recapitulated the effect observed when CDDP was used in combination with tunicamycin. Tunicamycin 208-219 dolichyl-phosphate (UDP-N-acetylglucosamine) acetylglucosaminephosphotransferase 1 (GlcNAc-1-P transferase) Mus musculus 117-123 24130050-11 2013 In summary, our results suggest that tunicamycin may reverse the drug resistance and improve the efficacy of combination treatments for hepatocellular carcinomas by targeting the DPAGT1/Akt/ABCG2 pathway. Tunicamycin 37-48 dolichyl-phosphate (UDP-N-acetylglucosamine) acetylglucosaminephosphotransferase 1 (GlcNAc-1-P transferase) Mus musculus 179-185 24130050-11 2013 In summary, our results suggest that tunicamycin may reverse the drug resistance and improve the efficacy of combination treatments for hepatocellular carcinomas by targeting the DPAGT1/Akt/ABCG2 pathway. Tunicamycin 37-48 thymoma viral proto-oncogene 1 Mus musculus 186-189 24130050-0 2013 Tunicamycin potentiates cisplatin anticancer efficacy through the DPAGT1/Akt/ABCG2 pathway in mouse Xenograft models of human hepatocellular carcinoma. Tunicamycin 0-11 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 77-82 24130050-11 2013 In summary, our results suggest that tunicamycin may reverse the drug resistance and improve the efficacy of combination treatments for hepatocellular carcinomas by targeting the DPAGT1/Akt/ABCG2 pathway. Tunicamycin 37-48 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 190-195 24130050-6 2013 The N-linked glycosylation (NLG) inhibitor tunicamycin dramatically reduced ABCG2 expression, altered its subcellular localization, and reversed its drug efflux effect in multiple hepatocellular carcinoma cell lines. Tunicamycin 43-54 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 76-81 24130050-7 2013 Furthermore, tunicamycin reduced the expression levels of several CSC markers and suppressed the tumorigenicity of CD133(+) CSCs. Tunicamycin 13-24 prominin 1 Mus musculus 115-120 24130050-8 2013 Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr. Tunicamycin 0-11 proliferating cell nuclear antigen Mus musculus 53-87 24130050-8 2013 Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr. Tunicamycin 0-11 proliferating cell nuclear antigen Mus musculus 89-93 24130050-8 2013 Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr. Tunicamycin 0-11 poly (ADP-ribose) polymerase family, member 1 Mus musculus 136-140 24130050-8 2013 Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr. Tunicamycin 0-11 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 201-206 24130050-8 2013 Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr. Tunicamycin 0-11 thymoma viral proto-oncogene 1 Mus musculus 210-213 24142703-6 2013 The pathogenic yeast Candida albicans carries only one homolog of Kch1/Kch2, and homozygous knock-out mutants were similarly deficient in the activation of HACS during the responses to tunicamycin. Tunicamycin 185-196 Kch1p Saccharomyces cerevisiae S288C 66-70 24142703-6 2013 The pathogenic yeast Candida albicans carries only one homolog of Kch1/Kch2, and homozygous knock-out mutants were similarly deficient in the activation of HACS during the responses to tunicamycin. Tunicamycin 185-196 pheromone-regulated K(+) transporter PRM6 Saccharomyces cerevisiae S288C 71-75 23537529-9 2013 Moreover, OLFP significantly attenuated the tunicamycin-induced expression of the ER stress marker BiP (immunoglobulin heavy chain-binding protein) in the cells. Tunicamycin 44-55 heat shock protein 5 Mus musculus 99-102 23537529-9 2013 Moreover, OLFP significantly attenuated the tunicamycin-induced expression of the ER stress marker BiP (immunoglobulin heavy chain-binding protein) in the cells. Tunicamycin 44-55 heat shock protein 5 Mus musculus 104-146 24045949-5 2013 Tunicamycin, which induces ER stress, significantly suppressed PAC1 gene expression, and salubrinal, a selective inhibitor of the protein kinase RNA-like endoplasmic reticulum kinase signaling pathway of ER stress, blocked the suppression. Tunicamycin 0-11 adenylate cyclase activating polypeptide 1 receptor 1 Mus musculus 63-67 24045949-6 2013 In luciferase reporter assay, we found that two Sp1 sites were involved in suppression of PAC1 gene expression due to tunicamycin or OGD. Tunicamycin 118-129 adenylate cyclase activating polypeptide 1 receptor 1 Mus musculus 90-94 24008518-9 2013 Protein levels of both p53 and glucosidase II were increased in response to UV irradiation but decreased in response to tunicamycin-induced ER stress. Tunicamycin 120-131 tumor protein p53 Homo sapiens 23-26 23958596-9 2013 The WT transfectants treated with tunicamycin markedly lost LPLA2 activity. Tunicamycin 34-45 phospholipase A2 group XV Homo sapiens 60-65 24204574-8 2013 In fact, peritoneal macrophages isolated from Herp-deficient mice and RAW264.7 macrophages in which Herp was eliminated with a siRNA expressed lower levels of mRNA for inflammatory cytokines when they were treated with tunicamycin. Tunicamycin 219-230 homocysteine-inducible, endoplasmic reticulum stress-inducible, ubiquitin-like domain member 1 Mus musculus 46-50 24204574-8 2013 In fact, peritoneal macrophages isolated from Herp-deficient mice and RAW264.7 macrophages in which Herp was eliminated with a siRNA expressed lower levels of mRNA for inflammatory cytokines when they were treated with tunicamycin. Tunicamycin 219-230 homocysteine-inducible, endoplasmic reticulum stress-inducible, ubiquitin-like domain member 1 Mus musculus 100-104 24146856-9 2013 The ER-stress inducer tunicamycin increased gp96-expression in a concentration- and time-dependent manner. Tunicamycin 22-33 heat shock protein 90 beta family member 1 Homo sapiens 44-48 24204775-9 2013 Treatment of C2C12 myotubes with the ER-stressor tunicamycin resulted in the accumulation of reactive oxygen species (ROS), leading to the activation of protein expression of PTP1B. Tunicamycin 49-60 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 175-180 24204775-10 2013 Furthermore, tunicamycin-induced ROS production activated nuclear translocation of NFkappaB p65 and was required for ER stress-mediated expression of PTP1B. Tunicamycin 13-24 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 83-91 24204775-10 2013 Furthermore, tunicamycin-induced ROS production activated nuclear translocation of NFkappaB p65 and was required for ER stress-mediated expression of PTP1B. Tunicamycin 13-24 v-rel reticuloendotheliosis viral oncogene homolog A (avian) Mus musculus 92-95 24204775-10 2013 Furthermore, tunicamycin-induced ROS production activated nuclear translocation of NFkappaB p65 and was required for ER stress-mediated expression of PTP1B. Tunicamycin 13-24 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 150-155 23911939-5 2013 The trafficking and glycosylation inhibitors brefeldin, monensin and tunicamycin substantially reduced cleavage and release of the N-terminal ectodomain of FLT1 and inhibited secretion of the isoforms of sFLT1. Tunicamycin 69-80 fms related receptor tyrosine kinase 1 Homo sapiens 156-160 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 24021650-2 2013 We show that the ER stress inducer tunicamycin stimulates selective degradation of Rad51 via the 26S proteasome, impairing DSB repair and enhancing radiosensitivity in human lung cancer A549 cells. Tunicamycin 35-46 RAD51 recombinase Homo sapiens 83-88 23318453-11 2013 Ectopic expression of RRBP1 alleviated apoptosis that was induced by the ER-stress agent tunicamycin, 2-deoxy-D-glucose (2DG) or doxorubicin via enhancing GRP78 protein expression. Tunicamycin 89-100 ribosome binding protein 1 Homo sapiens 22-27 23711292-0 2013 Inhibition of x-box binding protein 1 reduces tunicamycin-induced apoptosis in aged murine macrophages. Tunicamycin 46-57 X-box binding protein 1 Mus musculus 14-37 23711292-5 2013 Reduced gene expression of x-box binding protein 1 (XBP1), a downstream effector of IRE1alpha, enhanced p-IRE1alpha levels and reduced apoptosis in aged, but not young macrophages treated with tunicamycin. Tunicamycin 193-204 X-box binding protein 1 Mus musculus 27-50 23711292-5 2013 Reduced gene expression of x-box binding protein 1 (XBP1), a downstream effector of IRE1alpha, enhanced p-IRE1alpha levels and reduced apoptosis in aged, but not young macrophages treated with tunicamycin. Tunicamycin 193-204 X-box binding protein 1 Mus musculus 52-56 23711292-5 2013 Reduced gene expression of x-box binding protein 1 (XBP1), a downstream effector of IRE1alpha, enhanced p-IRE1alpha levels and reduced apoptosis in aged, but not young macrophages treated with tunicamycin. Tunicamycin 193-204 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 84-93 23711292-5 2013 Reduced gene expression of x-box binding protein 1 (XBP1), a downstream effector of IRE1alpha, enhanced p-IRE1alpha levels and reduced apoptosis in aged, but not young macrophages treated with tunicamycin. Tunicamycin 193-204 endoplasmic reticulum (ER) to nucleus signalling 1 Mus musculus 106-115 23707365-9 2013 Tunicamycin upregulated StARD1 expression and this outcome was abrogated by tauroursodeoxycholic acid. Tunicamycin 0-11 steroidogenic acute regulatory protein Mus musculus 24-30 24304569-5 2013 Similarly, inhibition of ET-1 receptors fully restored the impairment of acetylcholine-mediated relaxation induced by ER stress (maximal relaxation: control = 94+-2%, tunicamycin = 76+-5%, tunicamycin + tezosentan = 90+-3). Tunicamycin 167-178 endothelin 1 Rattus norvegicus 25-29 24304569-5 2013 Similarly, inhibition of ET-1 receptors fully restored the impairment of acetylcholine-mediated relaxation induced by ER stress (maximal relaxation: control = 94+-2%, tunicamycin = 76+-5%, tunicamycin + tezosentan = 90+-3). Tunicamycin 189-200 endothelin 1 Rattus norvegicus 25-29 23711089-8 2013 Simultaneously, the expression of phosphorylated AKT (p-AKT) was elevated in HepG2 and SMMC-7721 cells given tunicamycin but reduced in the presence of melatonin. Tunicamycin 109-120 AKT serine/threonine kinase 1 Homo sapiens 49-52 24012670-4 2013 Like other chaperones (e.g., GRP94 and GRP78), calumenin expression was highly upregulated during ERS induced by 10 mug/ml tunicamycin, but attenuated in the presence of 500 muM PBA, the chemical chaperone in neonatal rat ventricular cardiomyocytes (NRVCs). Tunicamycin 123-134 calumenin Rattus norvegicus 47-56 23811795-4 2013 This effect was reversed by glycosyltransferase inactive mutant Mgat5 L188R transfection, alpha-mannosidase II inhibitor swainsonine treatment and N-acetyl glucosamine (GlcNAc) phosphotransferase (GPT) inhibitor tunicamycin administration. Tunicamycin 212-223 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 64-69 23811795-4 2013 This effect was reversed by glycosyltransferase inactive mutant Mgat5 L188R transfection, alpha-mannosidase II inhibitor swainsonine treatment and N-acetyl glucosamine (GlcNAc) phosphotransferase (GPT) inhibitor tunicamycin administration. Tunicamycin 212-223 N-acetylglucosamine-1-phosphate transferase subunits alpha and beta Homo sapiens 147-195 23711089-8 2013 Simultaneously, the expression of phosphorylated AKT (p-AKT) was elevated in HepG2 and SMMC-7721 cells given tunicamycin but reduced in the presence of melatonin. Tunicamycin 109-120 AKT serine/threonine kinase 1 Homo sapiens 56-59 23711134-10 2013 In tunicamycin treatment, HuD and insulin proteins showed similar expression tendencies. Tunicamycin 3-14 insulin Homo sapiens 34-41 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 activating transcription factor 4 Homo sapiens 113-117 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 activating transcription factor 4 Homo sapiens 0-4 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 activating transcription factor 4 Homo sapiens 92-96 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 activating transcription factor 4 Homo sapiens 92-96 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 23615711-5 2013 Chac1 mRNA expression was also induced immediately following treatment with tunicamycin (Tm) and brefeldin A. Tunicamycin 76-87 ChaC, cation transport regulator 1 Mus musculus 0-5 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 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 23976981-4 2013 Tunicamycin-induced death of SH-SY5H cells was prevented by terminal aromatic substituted butyric or valeric acids, in association with a decrease in the mRNA expression of stress-related factors, and in the accumulation of the ATF4 protein. Tunicamycin 0-11 activating transcription factor 4 Homo sapiens 228-232 23774476-2 2013 The present study demonstrated that treatment with 1-10 mug/ml tunicamycin, a potent revulsant of ER stress, drastically induced TXNIP expression accompanied by the generation of cleaved caspase-3 as an indicator of apoptosis in SK-N-SH human neuroblastoma cells. Tunicamycin 63-74 thioredoxin interacting protein Homo sapiens 129-134 23774476-5 2013 Co-treatment of SK-N-SH cells with 100 muM nobiletin and 1 mug/ml tunicamycin for 24h strongly suppressed apoptosis and increased TXNIP expression induced by 1 mug/ml tunicamycin treatment alone. Tunicamycin 66-77 thioredoxin interacting protein Homo sapiens 130-135 23774476-5 2013 Co-treatment of SK-N-SH cells with 100 muM nobiletin and 1 mug/ml tunicamycin for 24h strongly suppressed apoptosis and increased TXNIP expression induced by 1 mug/ml tunicamycin treatment alone. Tunicamycin 167-178 thioredoxin interacting protein Homo sapiens 130-135 23319378-10 2013 Moreover, ERS inducer--thapsigargin and tunicamycin, decreased the expression of RESP18, which is different from the changes of BiP, GRP94, and CHOP. Tunicamycin 40-51 regulated endocrine-specific protein 18 Mus musculus 81-87 23319378-10 2013 Moreover, ERS inducer--thapsigargin and tunicamycin, decreased the expression of RESP18, which is different from the changes of BiP, GRP94, and CHOP. Tunicamycin 40-51 heat shock protein 5 Mus musculus 128-131 23319378-10 2013 Moreover, ERS inducer--thapsigargin and tunicamycin, decreased the expression of RESP18, which is different from the changes of BiP, GRP94, and CHOP. Tunicamycin 40-51 heat shock protein 90, beta (Grp94), member 1 Mus musculus 133-138 23319378-10 2013 Moreover, ERS inducer--thapsigargin and tunicamycin, decreased the expression of RESP18, which is different from the changes of BiP, GRP94, and CHOP. Tunicamycin 40-51 DNA-damage inducible transcript 3 Mus musculus 144-148 33209651-8 2013 The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252). Tunicamycin 20-31 cyclin D1 Mus musculus 93-102 33209651-8 2013 The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252). Tunicamycin 20-31 cyclin-dependent kinase 4 Mus musculus 107-111 33209651-8 2013 The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252). Tunicamycin 20-31 cyclin D1 Mus musculus 116-125 33209651-8 2013 The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252). Tunicamycin 20-31 cyclin-dependent kinase 4 Mus musculus 134-138 33209651-8 2013 The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252). Tunicamycin 20-31 RB transcriptional corepressor 1 Mus musculus 187-189 33209651-12 2013 Down regulated expression of caspase-9 and caspase-3 proposes a non-canonical pathway of cell death during "ER stress" induced by nano-formulated Tunicamycin. Tunicamycin 146-157 caspase 9 Mus musculus 29-38 33209651-12 2013 Down regulated expression of caspase-9 and caspase-3 proposes a non-canonical pathway of cell death during "ER stress" induced by nano-formulated Tunicamycin. Tunicamycin 146-157 caspase 3 Mus musculus 43-52 23434931-4 2013 In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis. Tunicamycin 93-104 transcription factor 7 like 2 Homo sapiens 128-134 23904594-4 2013 An endoplasmic reticulum stress inducer tunicamycin replicated the effect of NOC18 with regard to decrease of orexin-IR neurons and formation of aggregates. Tunicamycin 40-51 hypocretin Mus musculus 110-116 23894433-8 2013 Using cell lines, DNAJB3 protein was reduced following treatment with palmitate and tunicamycin which is suggestive of the link between the expression of DNAJB3 and the activation of the endoplasmic reticulum stress. Tunicamycin 84-95 DnaJ heat shock protein family (Hsp40) member B3 Homo sapiens 18-24 23894433-8 2013 Using cell lines, DNAJB3 protein was reduced following treatment with palmitate and tunicamycin which is suggestive of the link between the expression of DNAJB3 and the activation of the endoplasmic reticulum stress. Tunicamycin 84-95 DnaJ heat shock protein family (Hsp40) member B3 Homo sapiens 154-160 23737521-5 2013 Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor. Tunicamycin 13-24 prion protein Homo sapiens 83-87 23737521-5 2013 Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor. Tunicamycin 13-24 endoplasmic reticulum lectin 1 Homo sapiens 139-145 23737521-5 2013 Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor. Tunicamycin 13-24 growth arrest and DNA damage inducible beta Homo sapiens 147-154 23737521-5 2013 Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor. Tunicamycin 13-24 sestrin 2 Homo sapiens 156-161 23737521-5 2013 Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor. Tunicamycin 13-24 solute carrier family 38 member 5 Homo sapiens 167-174 23665163-9 2013 Interestingly, PADI4 was up-regulated by various stresses such as H2O2, acrylamide, and tunicamycin in neuroblastoma SK-N-SH cells but inhibited by RG. Tunicamycin 88-99 peptidyl arginine deiminase 4 Homo sapiens 15-20 23434931-4 2013 In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis. Tunicamycin 93-104 vascular endothelial growth factor A Homo sapiens 139-144 23434931-4 2013 In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis. Tunicamycin 93-104 transcription factor 7 like 2 Homo sapiens 234-240 23434931-4 2013 In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis. Tunicamycin 93-104 vascular endothelial growth factor A Homo sapiens 256-261 23434931-4 2013 In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis. Tunicamycin 93-104 PDR Homo sapiens 306-309 23580093-6 2013 Meanwhile, ER stress inhibitor salubrinal- or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin"s anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin"s actions on HuH-6 cells. Tunicamycin 186-197 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 46-73 23580093-6 2013 Meanwhile, ER stress inhibitor salubrinal- or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin"s anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin"s actions on HuH-6 cells. Tunicamycin 186-197 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 75-80 23580093-6 2013 Meanwhile, ER stress inhibitor salubrinal- or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin"s anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin"s actions on HuH-6 cells. Tunicamycin 199-201 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 46-73 23580093-6 2013 Meanwhile, ER stress inhibitor salubrinal- or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin"s anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin"s actions on HuH-6 cells. Tunicamycin 199-201 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 75-80 23826334-5 2013 Wild type levels of tunicamycin sensitivity were restored in iph1 null cells when the TORC1 complex was inhibited by rapamycin or by heat inactivation of the Tor2 kinase. Tunicamycin 20-31 CREB regulated transcription coactivator 1 Homo sapiens 86-91 23708521-5 2013 Consistent with these results in vivo, the addition of osteocalcin reversed autophagy and ER stress and restored defective insulin sensitivity in vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs) in the presence of tunicamycin or in knockout XBP-1 (a transcription factor which mediates ER stress response) cells or in Atg7(-/-) cells. Tunicamycin 240-251 bone gamma-carboxyglutamate protein 2 Mus musculus 55-66 23146721-7 2013 Simultaneous activation of WT KIT and treatment with endoplasmic reticulum (ER) inhibitors, tunicamycin or brefeldin A induced a complete inhibition of membrane expression of the 145 kDa form of KIT. Tunicamycin 92-103 KIT proto-oncogene, receptor tyrosine kinase Homo sapiens 195-198 23755268-6 2013 We show that VCD was highly cytotoxic only under hypoglycemic conditions, but not in the presence of normal glucose levels, and VCD blocked GRP78 expression only when glycolysis was impaired (due to hypoglycemia or the presence of the glycolysis inhibitor 2-deoxyglucose), but not when GRP78 was induced by other means (hypoxia, thapsigargin, tunicamycin). Tunicamycin 343-354 heat shock protein family A (Hsp70) member 5 Homo sapiens 140-145 23313043-9 2013 An insulin-resistant state was induced by exposing cells to 5mug/ml of tunicamycin as indicated by decreased insulin-mediated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and glucose uptake. Tunicamycin 71-82 insulin receptor substrate 1 Mus musculus 154-182 23313043-9 2013 An insulin-resistant state was induced by exposing cells to 5mug/ml of tunicamycin as indicated by decreased insulin-mediated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and glucose uptake. Tunicamycin 71-82 insulin receptor substrate 1 Mus musculus 184-189 23665024-7 2013 Tunicamycin, an established ER stress inducer, increased vascular cellular adhesion molecule (VCAM)-1 expression in endothelial cells. Tunicamycin 0-11 vascular cell adhesion molecule 1 Homo sapiens 57-101 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 23624196-6 2013 The secretion and mRNA expression levels of pro-inflammatory cytokines were increased by tunicamycin, and this stimulation was significantly suppressed by an overexpression of CDNF, demonstrating that CDNF plays an important role in astrocyte inflammation and functioning by resisting ER stress. Tunicamycin 89-100 cerebral dopamine neurotrophic factor Homo sapiens 201-205 23724116-6 2013 In addition, tunicamycin inhibited the androgen-induced expression of AR target genes KLK3 and CaMKK2 by 50%. Tunicamycin 13-24 kallikrein related peptidase 3 Homo sapiens 86-90 23724116-6 2013 In addition, tunicamycin inhibited the androgen-induced expression of AR target genes KLK3 and CaMKK2 by 50%. Tunicamycin 13-24 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 95-101 23724116-11 2013 Confocal imaging revealed that androgen induced plasma-membrane localization of IGF-1R was blocked by tunicamycin. Tunicamycin 102-113 insulin like growth factor 1 receptor Homo sapiens 80-86 23618865-0 2013 A sigma-1 receptor antagonist (NE-100) prevents tunicamycin-induced cell death via GRP78 induction in hippocampal cells. Tunicamycin 48-59 sigma non-opioid intracellular receptor 1 Mus musculus 2-18 23500541-4 2013 Here, we find that ER stress induced by 2-DG as well as tunicamycin activates AMPK via Ca2+-CaMKKbeta leading to stimulation of autophagy. Tunicamycin 56-67 calcium/calmodulin dependent protein kinase kinase 2 Homo sapiens 92-101 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 mitochondrially encoded cytochrome c oxidase II Homo sapiens 78-83 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 AKT serine/threonine kinase 1 Homo sapiens 112-115 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 23460517-4 2013 Hepatocyte-specific mutation of STAT3 prevented the induction of these secretory pathways during pneumonia, with similar results observed following pharmacological activation of ER stress by using tunicamycin. Tunicamycin 197-208 signal transducer and activator of transcription 3 Mus musculus 32-37 23385868-6 2013 Our results show that tunicamycin triggered ER stress in myoblasts and led to an increase in protein synthesis via a decorin-dependent pathway. Tunicamycin 22-33 decorin Homo sapiens 117-124 23884247-6 2014 From various stimuli tested, 12-O-tetradecanoylphorbol-13-acetate and tunicamycin affected SKI-1 expression. Tunicamycin 70-81 membrane bound transcription factor peptidase, site 1 Homo sapiens 91-96 23448571-3 2013 In the present study, we showed that pretreatment with FGF-2 decreased the inhibition of DNA synthesis and induction of apoptosis by two different ER stress inducers, TM (tunicamycin) and TG (thapsigargin), in both human hepatoblastoma HepG2 cells and breast cancer MCF-7 cells. Tunicamycin 167-169 fibroblast growth factor 2 Homo sapiens 55-60 23448571-3 2013 In the present study, we showed that pretreatment with FGF-2 decreased the inhibition of DNA synthesis and induction of apoptosis by two different ER stress inducers, TM (tunicamycin) and TG (thapsigargin), in both human hepatoblastoma HepG2 cells and breast cancer MCF-7 cells. Tunicamycin 171-182 fibroblast growth factor 2 Homo sapiens 55-60 23373714-1 2013 BACKGROUND AND PURPOSE: Endoplasmic reticulum (ER) stress has been implicated in the pathogeneses of insulin resistance and type 2 diabetes, and extracellular signal-regulated kinase (ERK) antagonist is an insulin sensitizer that can restore muscle insulin responsiveness in both tunicamycin-treated muscle cells and type 2 diabetic mice. Tunicamycin 280-291 mitogen-activated protein kinase 1 Mus musculus 145-182 23373714-1 2013 BACKGROUND AND PURPOSE: Endoplasmic reticulum (ER) stress has been implicated in the pathogeneses of insulin resistance and type 2 diabetes, and extracellular signal-regulated kinase (ERK) antagonist is an insulin sensitizer that can restore muscle insulin responsiveness in both tunicamycin-treated muscle cells and type 2 diabetic mice. Tunicamycin 280-291 mitogen-activated protein kinase 1 Mus musculus 184-187 23537656-8 2013 OxLDL stimulated apoE and CETP secretion, while tunicamycin determined a reduction of the secreted apoE and CETP, both in control and lipid-loaded macrophages. Tunicamycin 48-59 apolipoprotein E Homo sapiens 99-103 23537656-8 2013 OxLDL stimulated apoE and CETP secretion, while tunicamycin determined a reduction of the secreted apoE and CETP, both in control and lipid-loaded macrophages. Tunicamycin 48-59 cholesteryl ester transfer protein Homo sapiens 108-112 23537656-9 2013 The addition of HDL3 to the culture medium of tunicamycin-treated cells induced: (i) the reduction of ER stress, expressed as decreased levels of eIF-2alpha and SAPK/JNK, and (ii) a partial recovery of the secreted apoE and CETP levels in lipid-loaded macrophages. Tunicamycin 46-57 HDL3 Homo sapiens 16-20 23537656-9 2013 The addition of HDL3 to the culture medium of tunicamycin-treated cells induced: (i) the reduction of ER stress, expressed as decreased levels of eIF-2alpha and SAPK/JNK, and (ii) a partial recovery of the secreted apoE and CETP levels in lipid-loaded macrophages. Tunicamycin 46-57 eukaryotic translation initiation factor 2A Homo sapiens 146-156 23537656-9 2013 The addition of HDL3 to the culture medium of tunicamycin-treated cells induced: (i) the reduction of ER stress, expressed as decreased levels of eIF-2alpha and SAPK/JNK, and (ii) a partial recovery of the secreted apoE and CETP levels in lipid-loaded macrophages. Tunicamycin 46-57 apolipoprotein E Homo sapiens 215-219 23537656-9 2013 The addition of HDL3 to the culture medium of tunicamycin-treated cells induced: (i) the reduction of ER stress, expressed as decreased levels of eIF-2alpha and SAPK/JNK, and (ii) a partial recovery of the secreted apoE and CETP levels in lipid-loaded macrophages. Tunicamycin 46-57 cholesteryl ester transfer protein Homo sapiens 224-228 23638076-8 2013 We demonstrated that endoplasmic reticulum (ER) stress, an important mediator in diabetes-associated complications, was inducible in vitro in normal NK cells and that tunicamycin treatment resulted in a significant decrease in NKG2D expression (P<0.05). Tunicamycin 167-178 killer cell lectin like receptor K1 Homo sapiens 227-232 23261264-2 2013 Expression of VvACBP was detected in grape leaves exposed to tunicamycin-induced endoplasmic reticulum (ER) stress as well as cold and heat shock treatments. Tunicamycin 61-72 acyl-CoA-binding domain-containing protein 3-like Vitis vinifera 14-20 23364800-7 2013 Similarly, the induction of apoptosis was higher in tunicamycin-treated male mice, as measured by the activation of Bax and caspase-3. Tunicamycin 52-63 BCL2-associated X protein Mus musculus 116-119 23364800-7 2013 Similarly, the induction of apoptosis was higher in tunicamycin-treated male mice, as measured by the activation of Bax and caspase-3. Tunicamycin 52-63 caspase 3 Mus musculus 124-133 23403944-6 2013 Thapsigargin or tunicamycin was used to induce ER stress in human cells expressing the leptin receptor. Tunicamycin 16-27 leptin Homo sapiens 87-93 23123503-4 2013 Moreover, intraperitoneal injection of the ER stressor tunicamycin induced hepatic Fgf21 expression in mice and resulted in marked elevation of serum FGF21 levels. Tunicamycin 55-66 fibroblast growth factor 21 Mus musculus 83-88 23123503-4 2013 Moreover, intraperitoneal injection of the ER stressor tunicamycin induced hepatic Fgf21 expression in mice and resulted in marked elevation of serum FGF21 levels. Tunicamycin 55-66 fibroblast growth factor 21 Mus musculus 150-155 23518711-9 2013 Quantitative reverse transcriptase polymerase chain reaction demonstrated that Atf5alpha is the most abundant transcript in adult mouse encephalon and injection of the endoplasmic reticulum stress inducer tunicamycin into adult mouse brain increased neuronal ATF5 levels. Tunicamycin 205-216 activating transcription factor 5 Mus musculus 259-263 23756390-8 2013 Decreased COX-2 after GS-HCl was caused by N-glycosylation inhibition as much as tunicamycin. Tunicamycin 81-92 cytochrome c oxidase II, mitochondrial Rattus norvegicus 10-15 23316062-6 2013 Interestingly, tunicamycin-induced cardiomyocyte mechanical anomalies and cell death were ablated by the CaMKII inhibitor KN93, in a manner reminiscent of catalase. Tunicamycin 15-26 calcium/calmodulin-dependent protein kinase II gamma Mus musculus 105-111 23313137-9 2013 Treatment with tunicamycin, an endoplasmic reticulum stress inducer, increased cleaved caspase-3 and -8 levels in Nogo-B KO MF-HSCs compared with WT MF-HSCs (P < 0.01). Tunicamycin 15-26 caspase 8 Mus musculus 87-103 23313137-9 2013 Treatment with tunicamycin, an endoplasmic reticulum stress inducer, increased cleaved caspase-3 and -8 levels in Nogo-B KO MF-HSCs compared with WT MF-HSCs (P < 0.01). Tunicamycin 15-26 reticulon 4 Mus musculus 114-120 23178931-9 2013 Cultured myotubes exhibited increased levels of PTP1B in response to tunicamycin treatment. Tunicamycin 69-80 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 48-53 23178931-12 2013 However, tunicamycin-induced phosphorylation of eukaryotic initiation factor 2alpha and c-Jun NH(2)-terminal kinase-2 were significantly attenuated in the Ptp1b knockout mice. Tunicamycin 9-20 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 155-160 23178931-13 2013 Treatment with TUDCA or silencing of PTP1B reversed tunicamycin-induced blunted myotube glucose uptake. Tunicamycin 52-63 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 37-42 23270862-5 2013 A spontaneous onset of apoptotic cell death of granulosa cells was induced by thapsigargin or tunicamycin treatment in vitro, which was closely related to the increase of LRF, Luman, CCAAT/enhancer-binding protein homologous protein, and caspase-12 mRNA. Tunicamycin 94-105 CREB3 regulatory factor Mus musculus 171-174 23270862-5 2013 A spontaneous onset of apoptotic cell death of granulosa cells was induced by thapsigargin or tunicamycin treatment in vitro, which was closely related to the increase of LRF, Luman, CCAAT/enhancer-binding protein homologous protein, and caspase-12 mRNA. Tunicamycin 94-105 cAMP responsive element binding protein 3 Mus musculus 176-181 23270862-5 2013 A spontaneous onset of apoptotic cell death of granulosa cells was induced by thapsigargin or tunicamycin treatment in vitro, which was closely related to the increase of LRF, Luman, CCAAT/enhancer-binding protein homologous protein, and caspase-12 mRNA. Tunicamycin 94-105 caspase 12 Mus musculus 238-248 23242184-3 2013 Here we showed that ER stress induced by tunicamycin or thapsigargin suppressed inducible (CoCl(2) or hypoxia) transcription of erythropoietin (EPO), a representative HIF target gene, in HepG2. Tunicamycin 41-52 erythropoietin Rattus norvegicus 128-142 23242184-3 2013 Here we showed that ER stress induced by tunicamycin or thapsigargin suppressed inducible (CoCl(2) or hypoxia) transcription of erythropoietin (EPO), a representative HIF target gene, in HepG2. Tunicamycin 41-52 erythropoietin Rattus norvegicus 144-147 23242184-9 2013 Induction of ER stress in rat liver and kidney by tunicamycin decreased the hepatic and renal mRNA and plasma level of EPO. Tunicamycin 50-61 erythropoietin Rattus norvegicus 119-122 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 eukaryotic translation initiation factor 2A Homo sapiens 71-80 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 23291236-7 2013 We demonstrated that lipin-1 expression was suppressed by the treatment with ER stress inducers (tunicamycin and thapsigargin) at transcriptional level. Tunicamycin 97-108 lipin 1 Homo sapiens 21-28 23123183-9 2013 Administration of tunicamycin to wild-type mice caused intestinal ER stress, which increased when IL-10R1 was blocked. Tunicamycin 18-29 interleukin 10 receptor, alpha Mus musculus 98-105 23473976-6 2013 RESULTS: The result showed that tunicamycin activated p38 mitogen-activated protein kinase (MAPK), while inflammatory cytokines activated p38 MAPK and NFkappaB. Tunicamycin 32-43 mitogen-activated protein kinase 14 Homo sapiens 54-90 23473976-6 2013 RESULTS: The result showed that tunicamycin activated p38 mitogen-activated protein kinase (MAPK), while inflammatory cytokines activated p38 MAPK and NFkappaB. Tunicamycin 32-43 mitogen-activated protein kinase 14 Homo sapiens 54-57 23618865-0 2013 A sigma-1 receptor antagonist (NE-100) prevents tunicamycin-induced cell death via GRP78 induction in hippocampal cells. Tunicamycin 48-59 heat shock protein 5 Mus musculus 83-88 23201481-5 2013 Thapsigargin induced retrotranslocation and rapid degradation of clusterin from the endoplasmic reticulum, whereas tunicamycin failed to degrade but rather retained clusterin in the endoplasmic reticulum. Tunicamycin 115-126 clusterin Homo sapiens 165-174 23123183-10 2013 In LS174T cells, induction of ER stress with tunicamycin and misfolding of MUC2 were reduced by administration of IL-10; this reduction required STAT1 and STAT3. Tunicamycin 45-56 interleukin 10 Homo sapiens 114-119 23123183-11 2013 In LS174T cells incubated with tunicamycin, IL-10 up-regulated genes involved in MUC2 folding and in ER-associated degradation and maintained correct folding of MUC2, its transport from the ER, and its O-glycosylation and secretion. Tunicamycin 31-42 interleukin 10 Homo sapiens 44-49 23123183-11 2013 In LS174T cells incubated with tunicamycin, IL-10 up-regulated genes involved in MUC2 folding and in ER-associated degradation and maintained correct folding of MUC2, its transport from the ER, and its O-glycosylation and secretion. Tunicamycin 31-42 mucin 2, oligomeric mucus/gel-forming Homo sapiens 81-85 23123183-11 2013 In LS174T cells incubated with tunicamycin, IL-10 up-regulated genes involved in MUC2 folding and in ER-associated degradation and maintained correct folding of MUC2, its transport from the ER, and its O-glycosylation and secretion. Tunicamycin 31-42 mucin 2, oligomeric mucus/gel-forming Homo sapiens 161-165 23711492-5 2013 RESULTS: Elevated Klotho levels in HK-2 cells decreased expression of ER stress markers phospho--IRE1, XBP-1s, BiP, CHOP, pJNK, and phospho-p38, all of which were elevated in response to tunicamycin and/or thapsigargin. Tunicamycin 187-198 klotho Homo sapiens 18-24 23106379-7 2013 hnRNP A1 mediates the increase of SREBP-1a protein level and SREBP-1a IRES activity in Hep G2 cells and in rat hepatocytes upon tunicamycin- and thapsigargin-induced ER stress. Tunicamycin 128-139 heterogeneous nuclear ribonucleoprotein A1 Homo sapiens 0-8 23010535-4 2013 Here we report that activation of the UPR response by tunicamycin (TM), an ER stress inducer, leads to accumulation of p27 and G1 cell cycle arrest in melanoma cells. Tunicamycin 54-65 dynactin subunit 6 Homo sapiens 119-122 23010535-4 2013 Here we report that activation of the UPR response by tunicamycin (TM), an ER stress inducer, leads to accumulation of p27 and G1 cell cycle arrest in melanoma cells. Tunicamycin 67-69 dynactin subunit 6 Homo sapiens 119-122 23379566-7 2013 The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription. Tunicamycin 49-60 gastrin releasing peptide Homo sapiens 18-21 23379566-7 2013 The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription. Tunicamycin 49-60 X-box binding protein 1 Homo sapiens 92-96 23379566-7 2013 The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription. Tunicamycin 49-60 activating transcription factor 4 Homo sapiens 98-102 23379566-7 2013 The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription. Tunicamycin 49-60 TNF receptor associated factor 2 Homo sapiens 108-113 23041155-4 2012 In mouse cultured hippocampal HT22 cells, imipramine inhibited cell death and caspase-3 activation induced by tunicamycin, although it did not alter the elevated expressions of 78 kDa glucose-regulated protein (GRP78) and C/EBP-homologous protein (CHOP). Tunicamycin 110-121 caspase 3 Mus musculus 78-87 23437357-8 2013 In this study, eIF3a was down-regulated and recruited into stress granules by iron depletion as well as by the classical stress-inducers, hypoxia and tunicamycin. Tunicamycin 150-161 eukaryotic translation initiation factor 3 subunit J Homo sapiens 15-20 23544152-5 2013 Tunicamycin or thapsigargin was injected into the intravitreal body of oxygen-induced retinopathy (OIR) model mice at postnatal day 14 (P14) and retinal neovascularization was quantified at P17. Tunicamycin 0-11 family with sequence similarity 72, member A Mus musculus 190-193 23544152-8 2013 Tunicamycin enhanced the expression of BiP in HRMEC at both the mRNA level and at the protein level on the cell surface, and increased the formation of a BiP/T-cadherin immunocomplex. Tunicamycin 0-11 heat shock protein 5 Mus musculus 39-42 23544152-8 2013 Tunicamycin enhanced the expression of BiP in HRMEC at both the mRNA level and at the protein level on the cell surface, and increased the formation of a BiP/T-cadherin immunocomplex. Tunicamycin 0-11 heat shock protein 5 Mus musculus 154-157 23544152-8 2013 Tunicamycin enhanced the expression of BiP in HRMEC at both the mRNA level and at the protein level on the cell surface, and increased the formation of a BiP/T-cadherin immunocomplex. Tunicamycin 0-11 cadherin 13 Mus musculus 158-168 23457489-3 2013 Therefore, in order to explore the molecular mechanisms by which CLU inhibited ER stress-induced apoptosis, HCC cell lines were treated with tunicamycin (TN), an ER stress inducer. Tunicamycin 141-152 clusterin Homo sapiens 65-68 23457489-3 2013 Therefore, in order to explore the molecular mechanisms by which CLU inhibited ER stress-induced apoptosis, HCC cell lines were treated with tunicamycin (TN), an ER stress inducer. Tunicamycin 154-156 clusterin Homo sapiens 65-68 23041155-5 2012 Interestingly, in such cells application of imipramine normalized the expression of the sigma-1 receptor, which was decreased by treatment with tunicamycin alone. Tunicamycin 144-155 sigma non-opioid intracellular receptor 1 Mus musculus 88-104 23041155-6 2012 Additionally, NE-100, a selective sigma-1 receptor antagonist, abolished the protective effect of imipramine against such tunicamycin-induced cell death. Tunicamycin 122-133 sigma non-opioid intracellular receptor 1 Mus musculus 34-50 23041155-8 2012 Furthermore, in anesthetized mice intracerebroventricular administration of tunicamycin decreased the number of neuronal cells in the hippocampus, particularly in the CA1 and dentate gyrus (DG) areas, and 7 days" imipramine treatment (10mg/kg/day; i.p.) Tunicamycin 76-87 carbonic anhydrase 1 Mus musculus 167-170 23028052-7 2012 In contrast, other forms of ER stress (e.g., tunicamycin treatment) promote IRF3 phosphorylation independently of stimulator of IFN gene and TANK-binding kinase 1. Tunicamycin 45-56 interferon regulatory factor 3 Mus musculus 76-80 22821029-9 2012 Real-time polymerase chain reaction revealed that ERGIC-53 along with several chaperone proteins was up-regulated after tunicamycin treatment; however, the expression of VIPL was unchanged. Tunicamycin 120-131 lectin, mannose binding 1 Homo sapiens 50-58 22661239-9 2012 Furthermore, whilst hsp-4 was strongly induced by tunicamycin, pre-exposure of C. elegans to low doses of tunicamycin followed by ethanol was not sufficient to induce an additive ER stress response. Tunicamycin 50-61 Endoplasmic reticulum chaperone BiP homolog;Heat shock 70 kDa protein D Caenorhabditis elegans 20-25 22841895-2 2012 In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation. Tunicamycin 23-34 toll-like receptor 4 Mus musculus 117-120 22841895-2 2012 In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation. Tunicamycin 23-34 nitric oxide synthase 2, inducible Mus musculus 131-162 22841895-2 2012 In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation. Tunicamycin 23-34 nitric oxide synthase 2, inducible Mus musculus 164-168 22841895-2 2012 In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation. Tunicamycin 36-38 toll-like receptor 4 Mus musculus 117-120 22841895-2 2012 In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation. Tunicamycin 36-38 nitric oxide synthase 2, inducible Mus musculus 131-162 22841895-2 2012 In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation. Tunicamycin 36-38 nitric oxide synthase 2, inducible Mus musculus 164-168 22893028-11 2012 In contrast, tunicamycin activated a balanced adaptive UPR in association with the maintenance of Xbp1 splicing. Tunicamycin 13-24 X-box binding protein 1 Mus musculus 98-102 23359526-6 2013 14-3-3zeta overexpressing mice were potently protected against cell death caused by intracerebroventricular injection of the ER stressor tunicamycin. Tunicamycin 137-148 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide Mus musculus 0-10 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 mitogen-activated protein kinase 9 Homo sapiens 108-133 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 mitogen-activated protein kinase 9 Homo sapiens 135-139 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 231-234 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 22776647-9 2012 Similarly to the inhibition of OxPAPC effects, knockdown of miR-663 suppressed elevation of ATF4, VEGF and TRIB in response to another inducer of UPR, tunicamycin. Tunicamycin 151-162 microRNA 663a Homo sapiens 60-67 23028052-7 2012 In contrast, other forms of ER stress (e.g., tunicamycin treatment) promote IRF3 phosphorylation independently of stimulator of IFN gene and TANK-binding kinase 1. Tunicamycin 45-56 TANK-binding kinase 1 Mus musculus 141-162 23028052-8 2012 Rather, IRF3 activation by tunicamycin and 2-deoxyglucose was inhibited by 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride, a serine protease inhibitor that blocks activating transcription factor 6 processing. Tunicamycin 27-38 interferon regulatory factor 3 Mus musculus 8-12 22923171-0 2012 Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13 proteins in Caki-2 renal carcinoma cells. Tunicamycin 15-26 ADAM metallopeptidase domain 10 Homo sapiens 146-152 22821197-6 2012 Treatment with tunicamycin, an inhibitor of protein glycosylation, led to the accumulation of the unglycosylated form of TMEM132A in inverse proportion to the glycosylated form; however, both forms were localized at the cell surface at almost equal rates. Tunicamycin 15-26 transmembrane protein 132A Homo sapiens 121-129 22923171-0 2012 Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13 proteins in Caki-2 renal carcinoma cells. Tunicamycin 15-26 matrix metallopeptidase 9 Homo sapiens 154-159 22923171-0 2012 Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13 proteins in Caki-2 renal carcinoma cells. Tunicamycin 15-26 matrix metallopeptidase 13 Homo sapiens 164-170 22923171-3 2012 Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain. Tunicamycin 21-32 caspase 3 Homo sapiens 87-96 22923171-3 2012 Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain. Tunicamycin 21-32 poly(ADP-ribose) polymerase 1 Homo sapiens 98-104 22923171-3 2012 Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain. Tunicamycin 34-36 caspase 3 Homo sapiens 87-96 22923171-3 2012 Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain. Tunicamycin 34-36 poly(ADP-ribose) polymerase 1 Homo sapiens 98-104 22923171-5 2012 Furthermore, induction of matrix metallo-proteinase (MMP)-13, MMP-9 and ADAM10 expression was highly stimulated by tunicamycin in a time- and dose-dependent manner. Tunicamycin 115-126 matrix metallopeptidase 9 Homo sapiens 62-67 22923171-5 2012 Furthermore, induction of matrix metallo-proteinase (MMP)-13, MMP-9 and ADAM10 expression was highly stimulated by tunicamycin in a time- and dose-dependent manner. Tunicamycin 115-126 ADAM metallopeptidase domain 10 Homo sapiens 72-78 23000413-4 2012 In the present study, the results from the cell culture experiments were extended to show that tunicamycin-mediated ER stress in the liver in vivo also induces REDD1 gene expression. Tunicamycin 95-106 DNA damage inducible transcript 4 Homo sapiens 160-165 22959925-4 2012 Here, we investigated the role of Nrf2 in tunicamycin-induced ER stress using a murine insulinoma beta-cell line, betaTC-6. Tunicamycin 42-53 nuclear factor, erythroid derived 2, like 2 Mus musculus 34-38 22959925-5 2012 shRNA-mediated silencing of Nrf2 expression in betaTC-6 cells significantly increased tunicamycin-induced cytotoxicity, elevated the expression of the pro-apoptotic ER stress marker Chop10, and inhibited tunicamycin-inducible expression of the proteasomal catalytic subunits Psmb5 and Psmb6. Tunicamycin 86-97 nuclear factor, erythroid derived 2, like 2 Mus musculus 28-32 22959925-5 2012 shRNA-mediated silencing of Nrf2 expression in betaTC-6 cells significantly increased tunicamycin-induced cytotoxicity, elevated the expression of the pro-apoptotic ER stress marker Chop10, and inhibited tunicamycin-inducible expression of the proteasomal catalytic subunits Psmb5 and Psmb6. Tunicamycin 204-215 nuclear factor, erythroid derived 2, like 2 Mus musculus 28-32 22959925-7 2012 D3T pretreatment reduced tunicamycin cytotoxicity and attenuated the tunicamycin-inducible Chop10 and protein kinase RNA-activated-like ER kinase (Perk). Tunicamycin 69-80 DNA-damage inducible transcript 3 Mus musculus 91-97 22959925-7 2012 D3T pretreatment reduced tunicamycin cytotoxicity and attenuated the tunicamycin-inducible Chop10 and protein kinase RNA-activated-like ER kinase (Perk). Tunicamycin 69-80 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 102-145 22959925-7 2012 D3T pretreatment reduced tunicamycin cytotoxicity and attenuated the tunicamycin-inducible Chop10 and protein kinase RNA-activated-like ER kinase (Perk). Tunicamycin 69-80 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 147-151 22821808-0 2012 Tunicamycin inhibits PDGF-BB-induced proliferation and migration of vascular smooth muscle cells through induction of HO-1. Tunicamycin 0-11 heme oxygenase 1 Homo sapiens 118-122 22705154-3 2012 Here, we show that bestrophin-3 (Best-3), a protein previously associated with Ca(2+)-activated Cl(-) channel activity, is upregulated by the ER stressors, thapsigargin (TG), tunicamycin (TUN) and the toxic metal Cd(2+). Tunicamycin 175-186 bestrophin 3 Rattus norvegicus 19-31 22705154-3 2012 Here, we show that bestrophin-3 (Best-3), a protein previously associated with Ca(2+)-activated Cl(-) channel activity, is upregulated by the ER stressors, thapsigargin (TG), tunicamycin (TUN) and the toxic metal Cd(2+). Tunicamycin 175-186 bestrophin 3 Rattus norvegicus 33-39 23038705-7 2012 The cytoprotective effects of p53 were confirmed by cell viability studies, indicating that p53 deficiency conferred sensitivity against tunicamycin. Tunicamycin 137-148 transformation related protein 53, pseudogene Mus musculus 30-33 23038705-7 2012 The cytoprotective effects of p53 were confirmed by cell viability studies, indicating that p53 deficiency conferred sensitivity against tunicamycin. Tunicamycin 137-148 transformation related protein 53, pseudogene Mus musculus 92-95 22956603-8 2012 Human SEMA4A mutants were expressed in zebrafish embryos with tunicamycin and mRNA of DNA damage-inducible transcript 3 (ddit3) was measured as an ER stress marker. Tunicamycin 62-73 semaphorin 4A Homo sapiens 6-12 23082053-3 2012 RESULTS: Tunicamycin and PNGase F treatment markedly inhibited Axl glycoprotein synthesis and expression, proliferation, invasion, and lymphatic metastasis both in vitro and in vivo. Tunicamycin 9-20 AXL receptor tyrosine kinase Mus musculus 63-66 23038705-3 2012 We found that p53 ablation resulted in a profound sensitivity to tunicamycin that was associated with liver dysfunction, ground glass hepatocyte (GGH) development and nuclear atypia/dysplasia. Tunicamycin 65-76 transformation related protein 53, pseudogene Mus musculus 14-17 23038705-5 2012 Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism. Tunicamycin 0-11 heat shock protein 5 Mus musculus 35-38 23038705-5 2012 Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism. Tunicamycin 0-11 heat shock protein 5 Mus musculus 39-44 23038705-5 2012 Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism. Tunicamycin 0-11 heat shock protein 90, beta (Grp94), member 1 Mus musculus 49-54 23038705-5 2012 Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism. Tunicamycin 0-11 transformation related protein 53, pseudogene Mus musculus 87-90 23038705-5 2012 Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism. Tunicamycin 0-11 transformation related protein 53, pseudogene Mus musculus 185-188 22664345-4 2012 By preincubation with mPL, the cell viabilities were significantly increased in TM or TG treated cells, and caspase-12 activated cells induced by TM or TG treatment were significantly decreased. Tunicamycin 80-82 myeloproliferative leukemia virus oncogene Mus musculus 22-25 22664345-4 2012 By preincubation with mPL, the cell viabilities were significantly increased in TM or TG treated cells, and caspase-12 activated cells induced by TM or TG treatment were significantly decreased. Tunicamycin 146-148 myeloproliferative leukemia virus oncogene Mus musculus 22-25 22664345-4 2012 By preincubation with mPL, the cell viabilities were significantly increased in TM or TG treated cells, and caspase-12 activated cells induced by TM or TG treatment were significantly decreased. Tunicamycin 146-148 caspase 12 Mus musculus 108-118 22781655-4 2012 Retinal pigment epithelial (RPE) cells from alphaB crystallin (-/-) mice, and human RPE cells transfected with alphaB crystallin siRNA, are more vulnerable to ER stress induced by tunicamycin. Tunicamycin 180-191 crystallin, alpha B Mus musculus 111-128 22459357-0 2012 Tunicamycin produces TDP-43 cytoplasmic inclusions in cultured brain organotypic slices. Tunicamycin 0-11 TAR DNA binding protein Mus musculus 21-27 22430940-7 2012 In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively. Tunicamycin 29-40 heat shock protein 5 Mus musculus 81-86 22430940-7 2012 In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively. Tunicamycin 29-40 DNA-damage inducible transcript 3 Mus musculus 101-105 22430940-7 2012 In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively. Tunicamycin 29-40 milk fat globule EGF and factor V/VIII domain containing Mus musculus 107-110 22430940-7 2012 In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively. Tunicamycin 29-40 aldehyde dehydrogenase 2, mitochondrial Mus musculus 178-183 22430940-7 2012 In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively. Tunicamycin 29-40 aldehyde dehydrogenase 2, mitochondrial Mus musculus 211-216 22430940-8 2012 Overexpression of ALDH2 abrogated tunicamycin-induced dephosphorylation Akt. Tunicamycin 34-45 aldehyde dehydrogenase 2, mitochondrial Mus musculus 18-23 22430940-8 2012 Overexpression of ALDH2 abrogated tunicamycin-induced dephosphorylation Akt. Tunicamycin 34-45 thymoma viral proto-oncogene 1 Mus musculus 72-75 22573382-3 2012 In this study, we report lipid accumulation, sterol regulatory element-binding protein-2 (SREBP-2) expression, and ER stress in proximal tubules of kidneys from mice treated with the classic ER stressor tunicamycin (Tm) or in human renal biopsy specimens showing CsA-induced nephrotoxicity. Tunicamycin 203-214 sterol regulatory element binding factor 2 Mus musculus 45-88 22573382-3 2012 In this study, we report lipid accumulation, sterol regulatory element-binding protein-2 (SREBP-2) expression, and ER stress in proximal tubules of kidneys from mice treated with the classic ER stressor tunicamycin (Tm) or in human renal biopsy specimens showing CsA-induced nephrotoxicity. Tunicamycin 216-218 sterol regulatory element binding factor 2 Mus musculus 90-97 22573382-3 2012 In this study, we report lipid accumulation, sterol regulatory element-binding protein-2 (SREBP-2) expression, and ER stress in proximal tubules of kidneys from mice treated with the classic ER stressor tunicamycin (Tm) or in human renal biopsy specimens showing CsA-induced nephrotoxicity. Tunicamycin 216-218 heat shock protein family A (Hsp70) member 9 Homo sapiens 263-266 22742743-10 2012 Using the DPAGT1-specific inhibitor tunicamycin, we show that DPAGT1 is required for efficient glycosylation of acetylcholine-receptor subunits and for efficient export of acetylcholine receptors to the cell surface. Tunicamycin 36-47 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 10-16 22742743-10 2012 Using the DPAGT1-specific inhibitor tunicamycin, we show that DPAGT1 is required for efficient glycosylation of acetylcholine-receptor subunits and for efficient export of acetylcholine receptors to the cell surface. Tunicamycin 36-47 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 62-68 22539597-8 2012 Infusion of tunicamycin in control mice induced ER stress in aorta and MRA, and reduced EDR by a TGF-beta1-dependent mechanism in aorta and reactive oxygen species-dependent mechanism in MRA. Tunicamycin 12-23 transforming growth factor, beta 1 Mus musculus 97-106 22852048-4 2012 Toyocamycin was shown to suppress thapsigargin-, tunicamycin- and 2-deoxyglucose-induced XBP1 mRNA splicing in HeLa cells without affecting activating transcription factor 6 (ATF6) and PKR-like ER kinase (PERK) activation. Tunicamycin 49-60 X-box binding protein 1 Homo sapiens 89-93 22740470-5 2012 The important ER stress regulator 78 kDa glucose-regulated protein (GRP-78 or BiP) was highly upregulated together with several proteins that have been found to form a multiprotein complex with BiP including cyclophilin B, DnaJ homolog subfamily B member 11, endoplasmin, hypoxia upregulated protein 1, protein disulfide isomerase and protein disulfide isomerase A4 upon tunicamycin-induced ER stress. Tunicamycin 371-382 heat shock protein family A (Hsp70) member 5 Homo sapiens 68-74 22740470-5 2012 The important ER stress regulator 78 kDa glucose-regulated protein (GRP-78 or BiP) was highly upregulated together with several proteins that have been found to form a multiprotein complex with BiP including cyclophilin B, DnaJ homolog subfamily B member 11, endoplasmin, hypoxia upregulated protein 1, protein disulfide isomerase and protein disulfide isomerase A4 upon tunicamycin-induced ER stress. Tunicamycin 371-382 heat shock protein family A (Hsp70) member 5 Homo sapiens 78-81 22740470-5 2012 The important ER stress regulator 78 kDa glucose-regulated protein (GRP-78 or BiP) was highly upregulated together with several proteins that have been found to form a multiprotein complex with BiP including cyclophilin B, DnaJ homolog subfamily B member 11, endoplasmin, hypoxia upregulated protein 1, protein disulfide isomerase and protein disulfide isomerase A4 upon tunicamycin-induced ER stress. Tunicamycin 371-382 heat shock protein family A (Hsp70) member 5 Homo sapiens 194-197 22740470-6 2012 Furthermore, seven aminoacyl-tRNA synthetases and five proteins belonging to the Sec61 complex were increased in response to tunicamycin-induced ER stress. Tunicamycin 125-136 SEC61 translocon subunit alpha 1 Homo sapiens 81-86 22497927-8 2012 Tunicamycin, a classical ER stress inductor, also impaired ABCA-1 expression and cholesterol efflux (showing a decrease of 61% and 82%, respectively), confirming the deleterious effect of ER stress in macrophage cholesterol accumulation. Tunicamycin 0-11 ATP binding cassette subfamily A member 1 Homo sapiens 59-65 22571197-5 2012 The lung cancer cell line A549, the gastric carcinoma cell line MKN1 and the immortal cell line HEK (human embryonic kidney)-293 exhibit reduced TGF-beta signalling when either treated with two inhibitors, including tunicamycin (a potent N-linked glycosylation inhibitor) and kifunensine [an inhibitor of ER (endoplasmic reticulum) and Golgi mannosidase I family members], or introduced with a non-glycosylated mutant version of TbetaRII. Tunicamycin 216-227 transforming growth factor beta 1 Homo sapiens 145-153 22571197-5 2012 The lung cancer cell line A549, the gastric carcinoma cell line MKN1 and the immortal cell line HEK (human embryonic kidney)-293 exhibit reduced TGF-beta signalling when either treated with two inhibitors, including tunicamycin (a potent N-linked glycosylation inhibitor) and kifunensine [an inhibitor of ER (endoplasmic reticulum) and Golgi mannosidase I family members], or introduced with a non-glycosylated mutant version of TbetaRII. Tunicamycin 216-227 transforming growth factor beta receptor 2 Homo sapiens 429-437 22459357-10 2012 The induction of TDP-43 cytoplasmic translocation in cerebrocortical slice cultures by tunicamycin provides a platform for further mechanistic investigations of pathological processing of TDP-43. Tunicamycin 87-98 TAR DNA binding protein Mus musculus 17-23 22459357-10 2012 The induction of TDP-43 cytoplasmic translocation in cerebrocortical slice cultures by tunicamycin provides a platform for further mechanistic investigations of pathological processing of TDP-43. Tunicamycin 87-98 TAR DNA binding protein Mus musculus 188-194 25657664-0 2012 Low levels of Bax inhibitor-1 gene expression increase tunicamycin-induced apoptosis in human neuroblastoma SY5Y cells. Tunicamycin 55-66 transmembrane BAX inhibitor motif containing 6 Homo sapiens 14-29 22545589-6 2012 We examined whether the induction of ER stress using tunicamycin, thapsigargin, or palmitate alters the messenger RNA (mRNA) and protein expression of adiponectin and the mRNA expression of chaperones ERP44 and ERO1 in adult-derived human adipocyte stem (ADHAS) cells. Tunicamycin 53-64 adiponectin, C1Q and collagen domain containing Homo sapiens 151-162 25657664-2 2012 In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment. Tunicamycin 26-37 transmembrane BAX inhibitor motif containing 6 Homo sapiens 120-135 25657664-2 2012 In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment. Tunicamycin 267-278 transmembrane BAX inhibitor motif containing 6 Homo sapiens 120-135 22426894-0 2012 Tunicamycin sensitizes human prostate cells to TRAIL-induced apoptosis by upregulation of TRAIL receptors and downregulation of cIAP2. Tunicamycin 0-11 TNF superfamily member 10 Homo sapiens 47-52 22545589-6 2012 We examined whether the induction of ER stress using tunicamycin, thapsigargin, or palmitate alters the messenger RNA (mRNA) and protein expression of adiponectin and the mRNA expression of chaperones ERP44 and ERO1 in adult-derived human adipocyte stem (ADHAS) cells. Tunicamycin 53-64 endoplasmic reticulum protein 44 Homo sapiens 201-206 22545589-9 2012 Our studies indicate that: (1) ER stress markers were increased to a higher degree using tunicamycin or thapsigargin compared to palmitate; (2) ER stress significantly decreased adiponectin mRNA in response to tunicamycin and thapsigargin, but palmitate did not decrease adiponectin mRNA levels. Tunicamycin 89-100 adiponectin, C1Q and collagen domain containing Homo sapiens 178-189 22545589-9 2012 Our studies indicate that: (1) ER stress markers were increased to a higher degree using tunicamycin or thapsigargin compared to palmitate; (2) ER stress significantly decreased adiponectin mRNA in response to tunicamycin and thapsigargin, but palmitate did not decrease adiponectin mRNA levels. Tunicamycin 210-221 adiponectin, C1Q and collagen domain containing Homo sapiens 178-189 22545589-9 2012 Our studies indicate that: (1) ER stress markers were increased to a higher degree using tunicamycin or thapsigargin compared to palmitate; (2) ER stress significantly decreased adiponectin mRNA in response to tunicamycin and thapsigargin, but palmitate did not decrease adiponectin mRNA levels. Tunicamycin 210-221 adiponectin, C1Q and collagen domain containing Homo sapiens 271-282 22511781-3 2012 We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA and protein levels with no change in the expression of the mitochondrial shaping factors Mfn1, Opa1, Drp1, and Fis1. Tunicamycin 71-82 mitofusin 2 Mus musculus 140-144 22511781-3 2012 We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA and protein levels with no change in the expression of the mitochondrial shaping factors Mfn1, Opa1, Drp1, and Fis1. Tunicamycin 71-82 OPA1, mitochondrial dynamin like GTPase Mus musculus 245-249 22511781-3 2012 We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA and protein levels with no change in the expression of the mitochondrial shaping factors Mfn1, Opa1, Drp1, and Fis1. Tunicamycin 71-82 collapsin response mediator protein 1 Mus musculus 251-255 22511781-3 2012 We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA and protein levels with no change in the expression of the mitochondrial shaping factors Mfn1, Opa1, Drp1, and Fis1. Tunicamycin 71-82 fission, mitochondrial 1 Mus musculus 261-265 21922249-11 2012 GRP78 expression and xbp-1 mRNA splicing were enhanced significantly in the presence of IFN-gamma/TNF-alpha and tunicamycin, and they could be dampened by BBR. Tunicamycin 112-123 heat shock protein family A (Hsp70) member 5 Homo sapiens 0-5 21922249-11 2012 GRP78 expression and xbp-1 mRNA splicing were enhanced significantly in the presence of IFN-gamma/TNF-alpha and tunicamycin, and they could be dampened by BBR. Tunicamycin 112-123 X-box binding protein 1 Homo sapiens 21-26 22532439-5 2012 Spontaneous apoptosis was also observed in vitro in granulosa cells induced by serum deprivation or by the ER stress agent tunicamycin, both inducing similar increases in DDIT3 mRNA. Tunicamycin 123-134 DNA damage-inducible transcript 3 protein Capra hircus 171-176 22426894-0 2012 Tunicamycin sensitizes human prostate cells to TRAIL-induced apoptosis by upregulation of TRAIL receptors and downregulation of cIAP2. Tunicamycin 0-11 TNF superfamily member 10 Homo sapiens 102-107 22426894-0 2012 Tunicamycin sensitizes human prostate cells to TRAIL-induced apoptosis by upregulation of TRAIL receptors and downregulation of cIAP2. Tunicamycin 0-11 baculoviral IAP repeat containing 3 Homo sapiens 140-145 22426894-1 2012 The addition of tunicamycin to prostate cancer cells enhances cell death mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Tunicamycin 16-27 TNF superfamily member 10 Homo sapiens 85-140 22426894-1 2012 The addition of tunicamycin to prostate cancer cells enhances cell death mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Tunicamycin 16-27 TNF superfamily member 10 Homo sapiens 142-147 22426894-2 2012 In this study, we investigated whether tunicamycin, an endoplasmic reticulum stress inducer, can potentiate TRAIL-induced apoptosis in human prostate cancer cells. Tunicamycin 39-50 TNF superfamily member 10 Homo sapiens 108-113 22426894-4 2012 The combined treatment with tunicamycin and TRAIL significantly induced apoptosis, and stimulated caspase-3, -8 and -9 activity, as well as the cleavage of poly (ADP-ribose) polymerase. Tunicamycin 28-39 caspase 3 Homo sapiens 98-118 22426894-4 2012 The combined treatment with tunicamycin and TRAIL significantly induced apoptosis, and stimulated caspase-3, -8 and -9 activity, as well as the cleavage of poly (ADP-ribose) polymerase. Tunicamycin 28-39 poly(ADP-ribose) polymerase 1 Homo sapiens 156-184 22426894-5 2012 We found that tunicamycin promoted TRAIL-induced apoptosis by the upregulation of death receptor (DR)4 and DR5 and the downregulation of cellular inhibitor of apoptosis 2 (cIAP2). Tunicamycin 14-25 TNF superfamily member 10 Homo sapiens 35-40 22426894-5 2012 We found that tunicamycin promoted TRAIL-induced apoptosis by the upregulation of death receptor (DR)4 and DR5 and the downregulation of cellular inhibitor of apoptosis 2 (cIAP2). Tunicamycin 14-25 TNF receptor superfamily member 10a Homo sapiens 82-102 22426894-5 2012 We found that tunicamycin promoted TRAIL-induced apoptosis by the upregulation of death receptor (DR)4 and DR5 and the downregulation of cellular inhibitor of apoptosis 2 (cIAP2). Tunicamycin 14-25 baculoviral IAP repeat containing 3 Homo sapiens 137-170 22426894-5 2012 We found that tunicamycin promoted TRAIL-induced apoptosis by the upregulation of death receptor (DR)4 and DR5 and the downregulation of cellular inhibitor of apoptosis 2 (cIAP2). Tunicamycin 14-25 baculoviral IAP repeat containing 3 Homo sapiens 172-177 22335396-1 2012 Arabidopsis bZIP28, an ER membrane-associated transcription factor, is activated in response to conditions that induce ER stress-adverse environmental conditions or exposure to ER stress agents such as tunicamycin and dithiothreitol. Tunicamycin 202-213 Basic-leucine zipper (bZIP) transcription factor family protein Arabidopsis thaliana 12-18 22699051-4 2012 The expressions of Bax, Bcl-2, and GRP78 in cells treated with 3 micromol/L tunicamycin with or without 6.00 micromol/L cisplatin were measured with Western blotting. Tunicamycin 76-87 BCL2 associated X, apoptosis regulator Homo sapiens 19-22 22699051-4 2012 The expressions of Bax, Bcl-2, and GRP78 in cells treated with 3 micromol/L tunicamycin with or without 6.00 micromol/L cisplatin were measured with Western blotting. Tunicamycin 76-87 heat shock protein family A (Hsp70) member 5 Homo sapiens 35-40 22699051-9 2012 Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3. Tunicamycin 14-25 caspase 3 Homo sapiens 233-242 22699051-9 2012 Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3. Tunicamycin 154-165 heat shock protein family A (Hsp70) member 5 Homo sapiens 197-203 22699051-9 2012 Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3. Tunicamycin 154-165 caspase 3 Homo sapiens 233-242 22699051-10 2012 CONCLUSION: Tunicamycin can inhibit the proliferation of CNE-1 and CNE-2 cells and enhance cisplatin-induced cell death, the mechanism of which may involve excessive endoplasmic reticulum stress response and increased activity of caspase-3. Tunicamycin 12-23 caspase 3 Homo sapiens 230-239 22328531-7 2012 The Orm2 protein level responds to ER stress conditions, increasing when cells are treated with tunicamycin or DTT, agents that induce the unfolded protein response (UPR). Tunicamycin 96-107 sphingolipid homeostasis protein ORM2 Saccharomyces cerevisiae S288C 4-8 22524620-6 2012 Treatments of hPBMCs with tunicamycin and deglycosylation enzymes that removed the carbohydrate moieties reduced the secretion of IFN-gamma induction from hPBMCs. Tunicamycin 26-37 interferon gamma Homo sapiens 130-139 22593433-1 2012 BACKGROUND/AIM: Blocking N-glycosylation of the epidermal growth factor receptor (EGFR) by tunicamycin inhibits its cellular accumulation. Tunicamycin 91-102 epidermal growth factor receptor Cricetulus griseus 48-80 22593433-1 2012 BACKGROUND/AIM: Blocking N-glycosylation of the epidermal growth factor receptor (EGFR) by tunicamycin inhibits its cellular accumulation. Tunicamycin 91-102 epidermal growth factor receptor Cricetulus griseus 82-86 22648618-6 2012 In vivo retinal damage in mice following intravitreous injection of tunicamycin was evaluated by counting the cell numbers in the ganglion cell layer (GCL) and measuring the thickness of outer nuclear layer (ONL). Tunicamycin 68-79 germ cell-less, spermatogenesis associated 1 Mus musculus 151-154 22374970-6 2012 Strikingly, exposure of HepG2 cells to prolonged mild ER stress activation induced by low levels of thapsigargin, tunicamycin, or palmitate augmented insulin-stimulated Akt phosphorylation. Tunicamycin 114-125 insulin Homo sapiens 150-157 22466652-7 2012 Treating WT mice with the ER stressor tunicamycin led to marked repression of hepatic sortilin-1 expression, while administration of the chemical chaperone PBA to ob/ob mice led to amelioration of ER stress, increased sortilin-1 expression, and reduced apoB and triglyceride secretion. Tunicamycin 38-49 sortilin 1 Mus musculus 86-96 22326432-7 2012 In cultured cardiac myocytes, treatment with the ER stressor, tunicamycin, or with adenovirus encoding activated ATF6 decreased miR-455 and increased Calr levels, consistent with the effects of ATF6 on miR-455 and Calr, in vivo. Tunicamycin 62-73 microRNA 455 Mus musculus 128-135 22326432-7 2012 In cultured cardiac myocytes, treatment with the ER stressor, tunicamycin, or with adenovirus encoding activated ATF6 decreased miR-455 and increased Calr levels, consistent with the effects of ATF6 on miR-455 and Calr, in vivo. Tunicamycin 62-73 calreticulin Mus musculus 150-154 22326432-7 2012 In cultured cardiac myocytes, treatment with the ER stressor, tunicamycin, or with adenovirus encoding activated ATF6 decreased miR-455 and increased Calr levels, consistent with the effects of ATF6 on miR-455 and Calr, in vivo. Tunicamycin 62-73 calreticulin Mus musculus 214-218 22190710-6 2012 Tunicamycin, an ER stress inducer, induced active XBP1 protein in nuclei of 4-cell embryos. Tunicamycin 0-11 X-box binding protein 1 Homo sapiens 50-54 22648618-10 2012 A-ext., bixin, and Bx-1 significantly inhibited the tunicamycin-induced loss of cells from the GCL, and these materials also suppressed the tunicamycin-induced thinning of ONL. Tunicamycin 52-63 germ cell-less, spermatogenesis associated 1 Mus musculus 95-98 22225575-6 2012 Furthermore, down-regulation of COX-2 expression using the COX-2 inhibitor, celecoxib, increased tunicamycin-induced apoptosis concomitant with the up-regulation of pro-apoptotic transcription factor CHOP (GADD153) and down-regulation of B-cell lymphoma 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, suggesting that inhibition of COX-2 sensitized human hepatoma cells to ER stress-induced apoptosis. Tunicamycin 97-108 prostaglandin-endoperoxide synthase 2 Homo sapiens 59-64 22427561-9 2012 GlcN and tunicamycin reduced the molecular mass of TNF-alpha-induced ICAM-1 in ARPE-19 cells. Tunicamycin 9-20 tumor necrosis factor Homo sapiens 51-60 22427561-9 2012 GlcN and tunicamycin reduced the molecular mass of TNF-alpha-induced ICAM-1 in ARPE-19 cells. Tunicamycin 9-20 intercellular adhesion molecule 1 Homo sapiens 69-75 22225575-6 2012 Furthermore, down-regulation of COX-2 expression using the COX-2 inhibitor, celecoxib, increased tunicamycin-induced apoptosis concomitant with the up-regulation of pro-apoptotic transcription factor CHOP (GADD153) and down-regulation of B-cell lymphoma 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, suggesting that inhibition of COX-2 sensitized human hepatoma cells to ER stress-induced apoptosis. Tunicamycin 97-108 prostaglandin-endoperoxide synthase 2 Homo sapiens 32-37 22442073-4 2012 Inhibiting glycosylation with tunicamycin reduced ASIC1a surface trafficking, dendritic targeting, and acid-activated current density. Tunicamycin 30-41 acid-sensing (proton-gated) ion channel 1 Mus musculus 50-56 22225575-6 2012 Furthermore, down-regulation of COX-2 expression using the COX-2 inhibitor, celecoxib, increased tunicamycin-induced apoptosis concomitant with the up-regulation of pro-apoptotic transcription factor CHOP (GADD153) and down-regulation of B-cell lymphoma 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, suggesting that inhibition of COX-2 sensitized human hepatoma cells to ER stress-induced apoptosis. Tunicamycin 97-108 prostaglandin-endoperoxide synthase 2 Homo sapiens 59-64 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 prostaglandin-endoperoxide synthase 2 Homo sapiens 92-97 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 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 BCL2 apoptosis regulator Homo sapiens 197-202 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 BCL2 associated X, apoptosis regulator Homo sapiens 203-206 22006247-6 2012 RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt). Tunicamycin 50-61 insulin Homo sapiens 72-79 22215680-9 2012 Further, ER stress-inducing agents, including tunicamycin and thapsigargin, induced the expression of CSE in ATF4(+/+) MEFs. Tunicamycin 46-57 cystathionase (cystathionine gamma-lyase) Mus musculus 102-105 22215680-9 2012 Further, ER stress-inducing agents, including tunicamycin and thapsigargin, induced the expression of CSE in ATF4(+/+) MEFs. Tunicamycin 46-57 activating transcription factor 4 Mus musculus 109-113 22215680-10 2012 Consistent with ATF4(-/-) MEFs, CSE(-/-) MEFs showed significantly greater apoptosis when treated with tunicamycin, thapsigargin, and l-Hcy, compared with CSE(+/+) MEFs. Tunicamycin 103-114 cystathionase (cystathionine gamma-lyase) Mus musculus 32-35 21790829-8 2012 In human neuroblastoma cells exposed to Abeta, tunicamycin or H2O2, PACT and pPKR concentrations are increased. Tunicamycin 47-58 amyloid beta precursor protein Homo sapiens 40-45 21790829-8 2012 In human neuroblastoma cells exposed to Abeta, tunicamycin or H2O2, PACT and pPKR concentrations are increased. Tunicamycin 47-58 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 68-72 22215650-9 2012 Tunicamycin significantly upregulated IL-12p40 expression in adipocytes, and IL-12 addition increased ER stress gene expression; conversely, LSF, an IL-12 signaling inhibitor, and an IL-12p40-neutralizing antibody attenuated tunicamycin-induced ER stress. Tunicamycin 0-11 interleukin 12b Mus musculus 38-46 22215650-9 2012 Tunicamycin significantly upregulated IL-12p40 expression in adipocytes, and IL-12 addition increased ER stress gene expression; conversely, LSF, an IL-12 signaling inhibitor, and an IL-12p40-neutralizing antibody attenuated tunicamycin-induced ER stress. Tunicamycin 225-236 interleukin 12b Mus musculus 183-191 22219379-6 2012 Kar2p-sfGFP mobility decreases upon treatment with tunicamycin or dithiothreitol, consistent with increased levels of unfolded proteins and the incorporation of Kar2p-sfGFP into slower-diffusing complexes. Tunicamycin 51-62 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 0-5 22219379-6 2012 Kar2p-sfGFP mobility decreases upon treatment with tunicamycin or dithiothreitol, consistent with increased levels of unfolded proteins and the incorporation of Kar2p-sfGFP into slower-diffusing complexes. Tunicamycin 51-62 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 161-166 22323590-5 2012 After SMCs were exposed to A23187, thapsigargin, or tunicamycin, intracellular calcium level was increased, and CSE translocated from the cytosol to mitochondria. Tunicamycin 52-63 cystathionine gamma-lyase Homo sapiens 112-115 22227571-8 2012 Corroborating this, tunicamycin, a selective inhibitor of N-linked glycosylation, abolished MICA/B surface expression without compromising activation of MICA promoter activity. Tunicamycin 20-31 MHC class I polypeptide-related sequence A Homo sapiens 92-96 22281494-2 2012 Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes. Tunicamycin 29-40 insulin Homo sapiens 80-87 22281494-2 2012 Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes. Tunicamycin 29-40 insulin receptor substrate 1 Homo sapiens 125-130 22281494-2 2012 Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes. Tunicamycin 29-40 mechanistic target of rapamycin kinase Homo sapiens 178-182 22281494-2 2012 Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes. Tunicamycin 29-40 ribosomal protein S6 kinase B1 Homo sapiens 183-187 22063270-9 2012 Furthermore, over-expression of NSMase2 in ER-stressed BAEC lowered cholesterol levels to within control levels as well as nearly doubled the NO production, restoring it to ~74% and 68% of controls using tunicamycin and palmitate, respectively. Tunicamycin 204-215 sphingomyelin phosphodiesterase 3 Homo sapiens 32-39 22006247-6 2012 RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt). Tunicamycin 50-61 thymoma viral proto-oncogene 1 Mus musculus 109-112 22006247-6 2012 RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt). Tunicamycin 50-61 thymoma viral proto-oncogene 1 Mus musculus 117-120 22006247-6 2012 RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt). Tunicamycin 50-61 thymoma viral proto-oncogene 1 Mus musculus 164-167 22006247-10 2012 Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation. Tunicamycin 8-19 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 55-82 22006247-10 2012 Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation. Tunicamycin 8-19 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 84-89 22006247-10 2012 Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation. Tunicamycin 8-19 mitogen-activated protein kinase 8 Homo sapiens 118-121 22006247-10 2012 Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation. Tunicamycin 8-19 insulin receptor substrate 1 Homo sapiens 169-197 22006247-10 2012 Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation. Tunicamycin 8-19 insulin receptor substrate 1 Homo sapiens 199-204 22006247-10 2012 Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation. Tunicamycin 8-19 insulin receptor substrate 1 Homo sapiens 224-229 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 113-117 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 119-125 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 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 127-136 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 22550476-7 2012 While glucolipotoxicity/tunicamycin increased oxidative stress, ER stress, mRNA expression of TRPC-6, and programmed the THP-1 monocytes towards apoptosis, all these molecular perturbations were resisted by PBA. Tunicamycin 24-35 transient receptor potential cation channel subfamily C member 6 Homo sapiens 94-100 22550476-7 2012 While glucolipotoxicity/tunicamycin increased oxidative stress, ER stress, mRNA expression of TRPC-6, and programmed the THP-1 monocytes towards apoptosis, all these molecular perturbations were resisted by PBA. Tunicamycin 24-35 GLI family zinc finger 2 Homo sapiens 121-126 21954231-6 2012 Treatment of neuronal cells with ER stress insults, tunicamycin and thapsigargin, increased mtHTT aggregation via IRE1 activation. Tunicamycin 52-63 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 114-118 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 23209735-12 2012 The significant enhancement in PERK, ATF6 phosphorylated IRE1, BiP and cleaved caspase-3 expression induced by brefeldin A and tunicamycin was partly prevented by glutamine. Tunicamycin 127-138 activating transcription factor 6 Rattus norvegicus 37-41 23209735-12 2012 The significant enhancement in PERK, ATF6 phosphorylated IRE1, BiP and cleaved caspase-3 expression induced by brefeldin A and tunicamycin was partly prevented by glutamine. Tunicamycin 127-138 growth differentiation factor 10 Rattus norvegicus 63-66 23209735-12 2012 The significant enhancement in PERK, ATF6 phosphorylated IRE1, BiP and cleaved caspase-3 expression induced by brefeldin A and tunicamycin was partly prevented by glutamine. Tunicamycin 127-138 caspase 3 Rattus norvegicus 79-88 22859938-6 2012 Tunicamycin or brefeldin A, two ER stress inducers, increased p53 expression in MCF-7 and Hela cells. Tunicamycin 0-11 tumor protein p53 Homo sapiens 62-65 23251594-12 2012 Finally, ER stress induced by tunicamycin was ameliorated by mechanical strain as demonstrated by decreased C/EBPbeta, increased BiP and decreased CHOP protein expression. Tunicamycin 30-41 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 108-117 23251594-12 2012 Finally, ER stress induced by tunicamycin was ameliorated by mechanical strain as demonstrated by decreased C/EBPbeta, increased BiP and decreased CHOP protein expression. Tunicamycin 30-41 heat shock protein 5 Mus musculus 129-132 23251594-12 2012 Finally, ER stress induced by tunicamycin was ameliorated by mechanical strain as demonstrated by decreased C/EBPbeta, increased BiP and decreased CHOP protein expression. Tunicamycin 30-41 DNA-damage inducible transcript 3 Mus musculus 147-151 22815824-8 2012 Compared with wild type mice, CHOP-/- mice showed an enhanced hippocampal cell apoptosis, worse performance in memory-related behavioral tests, and attenuated IRE-1 expression under tunicamycin treatment. Tunicamycin 182-193 DNA-damage inducible transcript 3 Mus musculus 30-34 22815824-8 2012 Compared with wild type mice, CHOP-/- mice showed an enhanced hippocampal cell apoptosis, worse performance in memory-related behavioral tests, and attenuated IRE-1 expression under tunicamycin treatment. Tunicamycin 182-193 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 159-164 22662196-5 2012 COS-7 cells transfected with chIL2/15Rbeta produced proteins of approximately 75 and 62.5 kDa under normal and tunicamycin-treated conditions, respectively. Tunicamycin 111-122 chitinase 3 like 2 Homo sapiens 29-34 22808162-7 2012 Tunicamycin (TM), an ER stress inducer used as a positive control, promoted an increase in the density of nuclear XBP-1 at the one-cell and two-cell stages. Tunicamycin 0-11 X-box binding protein 1 Mus musculus 114-119 22808162-9 2012 Conversely, high concentrations of TM or sorbitol led to reduced nuclear XBP-1 density and significant ER stress-induced apoptosis. Tunicamycin 35-37 X-box binding protein 1 Mus musculus 73-78 22359644-10 2012 Consistently, IRE1a is preferentially required for bZIP60 splicing upon pathogen infection, while IRE1b plays a major role in bZIP60 processing upon Tunicamycin (Tm)-induced stress. Tunicamycin 149-160 inositol requiring 1-1 Arabidopsis thaliana 98-103 22662254-8 2012 In 3T3-L1 adipocytes, 11beta-HSD1 mRNA levels were down-regulated following induction of ER stress by tunicamycin but were up-regulated following inhibition of mTOR by rapamycin. Tunicamycin 102-113 hydroxysteroid 11-beta dehydrogenase 1 Mus musculus 22-33 22359644-10 2012 Consistently, IRE1a is preferentially required for bZIP60 splicing upon pathogen infection, while IRE1b plays a major role in bZIP60 processing upon Tunicamycin (Tm)-induced stress. Tunicamycin 149-160 basic region/leucine zipper motif 60 Arabidopsis thaliana 126-132 21986529-8 2011 In addition, chromatin immunoprecipitation analysis demonstrated that both tunicamycin treatment and ATF3 overexpression inhibited the recruitment of p300 to PDX-1 on the insulin promoter in MIN6N8 cells. Tunicamycin 75-86 E1A binding protein p300 Mus musculus 150-154 22936838-2 2012 Its impairment by tunicamycin [a competitive inhibitor of N-acetylglucosaminyl 1-phosphate transferase (GPT)] has been known to inhibit neo-vascularization (i.e., angiogenesis) in humanized breast tumor due to an induction of ER stress-mediated unfolded protein response (UPR). Tunicamycin 18-29 glutamic--pyruvic transaminase Homo sapiens 104-107 22192458-9 2011 RESULTS: Tunicamycin treatment of ALK-positive NB cells resulted in a hypoglycosylated ALK band and in decreased amounts of mature full size receptor. Tunicamycin 9-20 ALK receptor tyrosine kinase Homo sapiens 34-37 22192458-9 2011 RESULTS: Tunicamycin treatment of ALK-positive NB cells resulted in a hypoglycosylated ALK band and in decreased amounts of mature full size receptor. Tunicamycin 9-20 ALK receptor tyrosine kinase Homo sapiens 87-90 22013072-5 2011 Down-regulation of CerS6/C(16)-ceramide, and not its further metabolism to glucosylceramide or sphingomyelin, activated ATF-6 upon treatment with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid). Tunicamycin 165-176 ceramide synthase 6 Homo sapiens 19-24 22013072-5 2011 Down-regulation of CerS6/C(16)-ceramide, and not its further metabolism to glucosylceramide or sphingomyelin, activated ATF-6 upon treatment with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid). Tunicamycin 165-176 activating transcription factor 6 Homo sapiens 120-125 22013072-6 2011 Induction of WT-CerS6 expression, but not its mutant, or ectopic expression of the dominant-negative mutant form of ATF-6 protected cells from apoptosis in response to CerS6 knockdown and tunicamycin or SAHA treatment. Tunicamycin 188-199 activating transcription factor 6 Homo sapiens 116-121 21909975-3 2011 In vitro, IMD(1-53) (10(-9), 10(-8), and 10(-7) mol/l) directly inhibited the upregulation of ERS markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein, and caspase-12 induced by the ERS inducers tunicamycin (Tm, 10 mg/ml) or dithiothreitol (DTT, 2 mmol/l) in cardiac tissue. Tunicamycin 238-249 adrenomedullin 2 Rattus norvegicus 10-13 21909975-3 2011 In vitro, IMD(1-53) (10(-9), 10(-8), and 10(-7) mol/l) directly inhibited the upregulation of ERS markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein, and caspase-12 induced by the ERS inducers tunicamycin (Tm, 10 mg/ml) or dithiothreitol (DTT, 2 mmol/l) in cardiac tissue. Tunicamycin 251-253 adrenomedullin 2 Rattus norvegicus 10-13 21542787-2 2011 RESULTS: Wild-type and transgenic mice with cardiac-specific overexpression of the active mutant of Akt (Myr-Akt) were subjected to the ER stress inducer tunicamycin (1 or 3 mg/kg). Tunicamycin 154-165 thymoma viral proto-oncogene 1 Mus musculus 100-103 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin 15-26 thymoma viral proto-oncogene 1 Mus musculus 49-52 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin 15-26 glycogen synthase kinase 3 beta Mus musculus 79-109 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin 15-26 glycogen synthase kinase 3 beta Mus musculus 111-119 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin 15-26 glycogen synthase kinase 3 beta Mus musculus 147-155 21542787-6 2011 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin 15-26 thymoma viral proto-oncogene 1 Mus musculus 195-198 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 21970967-5 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 22912727-7 2012 Interestingly, nuclear translocation of procaspase-3 (proCASP3) was observed in cells either overexpressing TRB3 or under tunicamycin-induced ER stress. Tunicamycin 122-133 caspase 3 Homo sapiens 40-52 22912727-7 2012 Interestingly, nuclear translocation of procaspase-3 (proCASP3) was observed in cells either overexpressing TRB3 or under tunicamycin-induced ER stress. Tunicamycin 122-133 caspase 3 Homo sapiens 54-62 21932778-5 2011 Experiments using the drug tunicamycin to inhibit the N-linked glycosylation of glypican-1 showed that secretion of anchorless glypican-1 was reduced and that the protein did not accumulate inside the cells. Tunicamycin 27-38 glypican 1 Homo sapiens 80-90 21932778-5 2011 Experiments using the drug tunicamycin to inhibit the N-linked glycosylation of glypican-1 showed that secretion of anchorless glypican-1 was reduced and that the protein did not accumulate inside the cells. Tunicamycin 27-38 glypican 1 Homo sapiens 127-137 22118540-0 2011 Tunicamycin negatively regulates BMP2-induced osteoblast differentiation through CREBH expression in MC3T3E1 cells. Tunicamycin 0-11 bone morphogenetic protein 2 Mus musculus 33-37 22118540-0 2011 Tunicamycin negatively regulates BMP2-induced osteoblast differentiation through CREBH expression in MC3T3E1 cells. Tunicamycin 0-11 cAMP responsive element binding protein 3-like 3 Mus musculus 81-86 22118540-4 2011 In the present study, tunicamycin increased the level of CREBH activation (cleavage) as well as mRNA expression in osteoblast cells. Tunicamycin 22-33 cAMP responsive element binding protein 3-like 3 Mus musculus 57-62 22118540-7 2011 In addition, inhibition of CREBH expression using siRNA reversed the tunicamycin-suppressed ALP and OC expression. Tunicamycin 69-80 cAMP responsive element binding protein 3-like 3 Mus musculus 27-32 22118540-7 2011 In addition, inhibition of CREBH expression using siRNA reversed the tunicamycin-suppressed ALP and OC expression. Tunicamycin 69-80 bone gamma-carboxyglutamate protein 2 Mus musculus 100-102 22340178-2 2011 The present study was designed to characterize the function-unknown gene, C6orf120, and elucidates its primary role in tunicamycin-induced CD4(+) T apoptosis. Tunicamycin 119-130 chromosome 6 open reading frame 120 Homo sapiens 74-82 22340178-2 2011 The present study was designed to characterize the function-unknown gene, C6orf120, and elucidates its primary role in tunicamycin-induced CD4(+) T apoptosis. Tunicamycin 119-130 CD4 molecule Homo sapiens 139-142 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 21677259-4 2011 Under cellular stress induced by hypoxia (1% O(2) or CoCl(2) treatment) or tunicamycin, Prdx6-deficient cells exhibited aberrant activation of ER stress-responsive genes/protein with higher expression of ROS, and died with apoptosis. Tunicamycin 75-86 peroxiredoxin 6 Homo sapiens 88-93 21677259-5 2011 Wild-type cells exposed to tunicamycin or hypoxia remained relatively insensitive with lower expression of ROS and ER-responsive genes than did Prdx6-deficient cells, but upregulation of ER stress responsive proteins or chaperones mimicked the UPR response of Prdx6-deficient or aging cells. Tunicamycin 27-38 peroxiredoxin 6 Homo sapiens 144-149 21677259-5 2011 Wild-type cells exposed to tunicamycin or hypoxia remained relatively insensitive with lower expression of ROS and ER-responsive genes than did Prdx6-deficient cells, but upregulation of ER stress responsive proteins or chaperones mimicked the UPR response of Prdx6-deficient or aging cells. Tunicamycin 27-38 peroxiredoxin 6 Homo sapiens 260-265 21752865-6 2011 Treatment of HEK293 (human embryonic kidney) cells expressing BRI2 with the N-glycosylation inhibitor tunicamycin or mutation of Asn170 to alanine reduced its molecular mass by ~2 kDa. Tunicamycin 102-113 integral membrane protein 2B Homo sapiens 62-66 21896647-7 2011 Treatment with ER stressors, tunicamycin or DTT, rapidly decreased BiP-GFP mobility in mHtt striatal cells and accelerated UPR activation compared with wild-type cells. Tunicamycin 29-40 heat shock protein family A (Hsp70) member 5 Homo sapiens 67-70 21896647-7 2011 Treatment with ER stressors, tunicamycin or DTT, rapidly decreased BiP-GFP mobility in mHtt striatal cells and accelerated UPR activation compared with wild-type cells. Tunicamycin 29-40 huntingtin Mus musculus 87-91 21986529-8 2011 In addition, chromatin immunoprecipitation analysis demonstrated that both tunicamycin treatment and ATF3 overexpression inhibited the recruitment of p300 to PDX-1 on the insulin promoter in MIN6N8 cells. Tunicamycin 75-86 pancreatic and duodenal homeobox 1 Mus musculus 158-163 21832078-2 2011 We demonstrate that CAMP mRNA and protein expression increase in epithelial cells (human primary keratinocytes, HaCaT keratinocytes, and HeLa cells), but not in myeloid (U937 and HL-60) cells, following ER stress generated by two mechanistically different, pharmacological stressors, thapsigargin or tunicamycin. Tunicamycin 300-311 cathelicidin antimicrobial peptide Homo sapiens 20-24 21712074-4 2011 Here we found that application of endoplasmic reticulum stress inducers such as tunicamycin (that prevents protein N-glycosylation) and thapsigargin (that inhibits Ca2+-ATPase) to organotypic slice cultures of the hypothalamus caused preferential loss of orexin-immunoreactive neurons, as compared to melanin-concentrating hormone- or calcitonin gene-related peptide-immunoreactive neurons. Tunicamycin 80-91 hypocretin neuropeptide precursor Homo sapiens 255-261 21712074-5 2011 The decrease in orexin-immunoreactive neurons at early time points (6-24 h) was not accompanied by induction of cell death as indicated by the absence of caspase-3 activation and no significant change in the number of NeuN-positive cells, whereas sustained treatment with tunicamycin for 72 h induced cell death. Tunicamycin 272-283 hypocretin neuropeptide precursor Homo sapiens 16-22 21712074-7 2011 In addition, inhibition of axonal transport by colchicine and inhibition of proteasomal activity by MG132 significantly prevented the decrease in orexin immunoreactivity by tunicamycin. Tunicamycin 173-184 hypocretin neuropeptide precursor Homo sapiens 146-152 21605081-3 2011 The aim of the present study was to investigate the role of L-PTP1B (liver-specific PTP1B) in chronically HFD (high-fat diet) and pharmacologically induced (tunicamycin and thapsigargin) ER-stress response signalling in vitro and in vivo. Tunicamycin 157-168 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 62-67 21841811-7 2011 RESULTS: Tunicamycin-induced chronic ER stress attenuated IR tyrosine phosphorylation in a time-dependent manner, whereas over-expression of ATF6 protected IR from desensitization. Tunicamycin 9-20 insulin receptor Homo sapiens 58-60 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 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 21605081-3 2011 The aim of the present study was to investigate the role of L-PTP1B (liver-specific PTP1B) in chronically HFD (high-fat diet) and pharmacologically induced (tunicamycin and thapsigargin) ER-stress response signalling in vitro and in vivo. Tunicamycin 157-168 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 84-89 21731954-6 2011 HAC1 is central to the unfolded protein response (UPR) and in its absence, i.e. the absence of UPR, emc1Delta-, emc3Delta-, emc4Delta-, emc5Delta-hac1Delta double mutants were specifically hypersensitive to ER-stress (tunicamycin) lending credence to the usefulness of the high content microscope screening for discovery of functional effects of single mutants. Tunicamycin 218-229 transcription factor HAC1 Saccharomyces cerevisiae S288C 0-4 21725197-6 2011 NTSR-1 glycosylation was confirmed by pharmacological (tunicamycin) and chemical (PGNaseF and O-type glycosidase) approaches. Tunicamycin 55-66 neurotensin receptor 1 Homo sapiens 0-6 21736484-3 2011 The leakage of EC-SOD through the retinal endothelial cell layer was elevated by the treatment with thapsigargin or tunicamycin. Tunicamycin 116-127 superoxide dismutase 3 Homo sapiens 15-21 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 21640381-5 2011 In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH). Tunicamycin 39-50 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 136-186 21640381-5 2011 In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH). Tunicamycin 39-50 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 256-265 21640381-5 2011 In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH). Tunicamycin 39-50 activating transcription factor 6 Homo sapiens 268-301 21640381-5 2011 In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH). Tunicamycin 39-50 activating transcription factor 6 Homo sapiens 303-307 21640381-5 2011 In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH). Tunicamycin 39-50 cAMP responsive element binding protein 3 like 3 Homo sapiens 381-386 21640381-9 2011 Moreover, in mice treated with the ER stress inducer tunicamycin, CORM administration reduced serum levels of CRP and the expression of CRP mRNA in the liver. Tunicamycin 53-64 C-reactive protein, pentraxin-related Mus musculus 110-113 21640381-9 2011 Moreover, in mice treated with the ER stress inducer tunicamycin, CORM administration reduced serum levels of CRP and the expression of CRP mRNA in the liver. Tunicamycin 53-64 C-reactive protein, pentraxin-related Mus musculus 136-139 21640381-5 2011 In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH). Tunicamycin 39-50 C-reactive protein Homo sapiens 99-102 21676868-7 2011 A 3.8-fold increased expression of TSP-1, an endogenous angiogenesis inhibitor in Matrigel(TM) implants correlated with that in tunicamycin (32 h)-treated capillary endothelial cells. Tunicamycin 128-139 tumor suppressor region 1 Mus musculus 35-40 21294793-8 2011 Although tunicamycin upregulated XBP1 splicing in cultured chondrocytes, its impact on XBP1 splicing was weakened at higher concentrations. Tunicamycin 9-20 X-box binding protein 1 Homo sapiens 33-37 21294793-8 2011 Although tunicamycin upregulated XBP1 splicing in cultured chondrocytes, its impact on XBP1 splicing was weakened at higher concentrations. Tunicamycin 9-20 X-box binding protein 1 Homo sapiens 87-91 21677192-0 2011 A haploid genetic screen identifies the major facilitator domain containing 2A (MFSD2A) transporter as a key mediator in the response to tunicamycin. Tunicamycin 137-148 major facilitator superfamily domain containing 2A Homo sapiens 80-86 21538441-5 2011 The prolonged treatment of wild-type larvae with tunicamycin (TN), which caused chronic ER stress, phenocopied foigr. Tunicamycin 49-60 trafficking protein particle complex subunit 11 Danio rerio 111-116 21535396-8 2011 RESULTS: Tunicamycin treatment reduced TF activity at the endothelial cell surface; however, this reduction was found to be the result of decreased TF protein production in tunicamycin-treated cells. Tunicamycin 9-20 coagulation factor III, tissue factor Homo sapiens 39-41 21535396-8 2011 RESULTS: Tunicamycin treatment reduced TF activity at the endothelial cell surface; however, this reduction was found to be the result of decreased TF protein production in tunicamycin-treated cells. Tunicamycin 9-20 coagulation factor III, tissue factor Homo sapiens 148-150 21535396-8 2011 RESULTS: Tunicamycin treatment reduced TF activity at the endothelial cell surface; however, this reduction was found to be the result of decreased TF protein production in tunicamycin-treated cells. Tunicamycin 173-184 coagulation factor III, tissue factor Homo sapiens 148-150 21677192-1 2011 Tunicamycin (TM) inhibits eukaryotic asparagine-linked glycosylation, protein palmitoylation, ganglioside production, proteoglycan synthesis, 3-hydroxy-3-methylglutaryl coenzyme-A reductase activity, and cell wall biosynthesis in bacteria. Tunicamycin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 142-189 21677192-1 2011 Tunicamycin (TM) inhibits eukaryotic asparagine-linked glycosylation, protein palmitoylation, ganglioside production, proteoglycan synthesis, 3-hydroxy-3-methylglutaryl coenzyme-A reductase activity, and cell wall biosynthesis in bacteria. Tunicamycin 13-15 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 142-189 21762510-4 2011 RESULTS: Expression in the presence of either tunicamycin or furin inhibitor showed that a substantial portion of recombinant intracellular E1 and precursor E3E2 was glycosylated, but that a smaller fraction of E3E2 was processed by furin into mature E3 and E2. Tunicamycin 46-57 small nucleolar RNA, H/ACA box 73A Homo sapiens 140-161 21527262-4 2011 Time-dependent induction of the ER chaperones, glucose-regulated protein (GRP) 78 and GRP94, was observed after treatment with tunicamycin (TM) (80 mug/mL). Tunicamycin 140-142 heat shock protein 90 beta family member 1 Homo sapiens 86-91 21439722-3 2011 PrP(C) confers resistance against oxidative stress-apoptosis as indicated by MTT assay, Annexin V-FITC/PI and DCFH-DA staining, but this property is abolished upon N-glycosylation inhibition by tunicamycin. Tunicamycin 194-205 prion protein Homo sapiens 0-6 21527262-4 2011 Time-dependent induction of the ER chaperones, glucose-regulated protein (GRP) 78 and GRP94, was observed after treatment with tunicamycin (TM) (80 mug/mL). Tunicamycin 127-138 heat shock protein family A (Hsp70) member 5 Homo sapiens 47-81 21389343-8 2011 However, tunicamycin-induced HSPA5 expression was significantly lowered in these cells when pretreated with E(2) (P < 0.01 and P < 0.05, respectively). Tunicamycin 9-20 heat shock protein family A (Hsp70) member 5 Homo sapiens 29-34 20927523-0 2011 Inhibition of N-linked glycosylation by tunicamycin induces E-cadherin-mediated cell-cell adhesion and inhibits cell proliferation in undifferentiated human colon cancer cells. Tunicamycin 40-51 cadherin 1 Homo sapiens 60-70 20927523-9 2011 Interestingly, tunicamycin, but not swainsonine, was able to induce functional E-cadherin-mediated cell-cell adhesion in undifferentiated HCT-116 cells, as shown by the increased association of E-cadherin with the actin cytoskeleton. Tunicamycin 15-26 cadherin 1 Homo sapiens 79-89 20927523-9 2011 Interestingly, tunicamycin, but not swainsonine, was able to induce functional E-cadherin-mediated cell-cell adhesion in undifferentiated HCT-116 cells, as shown by the increased association of E-cadherin with the actin cytoskeleton. Tunicamycin 15-26 cadherin 1 Homo sapiens 194-204 21527262-4 2011 Time-dependent induction of the ER chaperones, glucose-regulated protein (GRP) 78 and GRP94, was observed after treatment with tunicamycin (TM) (80 mug/mL). Tunicamycin 127-138 heat shock protein 90 beta family member 1 Homo sapiens 86-91 22093624-9 2011 With exposure to tunicamycin (3 micromol/L) for 12, 24, 36 hours the Bim protein levels were not increased in Mel-RM and MM200 cells. Tunicamycin 17-28 BCL2 like 11 Homo sapiens 69-72 21527262-4 2011 Time-dependent induction of the ER chaperones, glucose-regulated protein (GRP) 78 and GRP94, was observed after treatment with tunicamycin (TM) (80 mug/mL). Tunicamycin 140-142 heat shock protein family A (Hsp70) member 5 Homo sapiens 47-81 21605547-5 2011 TUDCA efficiently inhibited the expression of UPR dependent genes like GRP78 triggered by the ER stressor tunicamycin in the small intestinal epithelial cell line Mode-K. TUDCA inhibited upstream signaling events in all three branches of the UPR cascade and diminished binding of UPR activated transcription factors to the grp78 promoter. Tunicamycin 106-117 heat shock protein family A (Hsp70) member 5 Homo sapiens 71-76 21605547-5 2011 TUDCA efficiently inhibited the expression of UPR dependent genes like GRP78 triggered by the ER stressor tunicamycin in the small intestinal epithelial cell line Mode-K. TUDCA inhibited upstream signaling events in all three branches of the UPR cascade and diminished binding of UPR activated transcription factors to the grp78 promoter. Tunicamycin 106-117 heat shock protein family A (Hsp70) member 5 Homo sapiens 323-328 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 21252914-3 2011 We demonstrate here that AMF/PGI also protects against thapsigargin (TG)- and tunicamycin (TUN)-induced ER stress and apoptosis. Tunicamycin 78-89 glucose-6-phosphate isomerase Homo sapiens 29-32 21600878-4 2011 In this work, we have examined the effect of metformin on the expression of UPR-related markers (GRP94 and CHOP) induced by glucosamine (GlcN), 2-deoxyglucose (2-DOG) and tunicamycin (TUNI) in renal proximal tubular epithelial cells and in murine mesangial cells. Tunicamycin 171-182 heat shock protein 90 beta family member 1 Canis lupus familiaris 97-102 20726815-7 2011 Tunicamycin and thapsigargin, irrespective of the dose, induced sufficient ER stress, as evidenced by the increased phosphorylation or activation of eIF2alpha and PERK. Tunicamycin 0-11 eukaryotic translation initiation factor 2A Rattus norvegicus 149-158 21252914-3 2011 We demonstrate here that AMF/PGI also protects against thapsigargin (TG)- and tunicamycin (TUN)-induced ER stress and apoptosis. Tunicamycin 91-94 glucose-6-phosphate isomerase Homo sapiens 29-32 21279413-8 2011 These antibodies also reacted to a glycosylation-disturbed full-length nephrin protein (inhibited by tunicamycin), but did not react to either a native nephrin protein or a fully glycosylated conformational nephrin protein. Tunicamycin 101-112 NPHS1 adhesion molecule, nephrin Rattus norvegicus 71-78 21590646-6 2011 After exposure to TN, phospho-Akt protein levels were repressed whereas total Akt protein levels were not changed. Tunicamycin 18-20 AKT serine/threonine kinase 1 Rattus norvegicus 30-33 21590646-6 2011 After exposure to TN, phospho-Akt protein levels were repressed whereas total Akt protein levels were not changed. Tunicamycin 18-20 AKT serine/threonine kinase 1 Rattus norvegicus 78-81 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 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 BCL2 associated X, apoptosis regulator Rattus norvegicus 96-99 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 BCL2, apoptosis regulator Rattus norvegicus 134-139 21310902-6 2011 On stress induction, HTRA1 and VEGFA were upregulated in human fetal RPE cells treated by tunicamycin and dithiothreitol, but reduced after treatment by MG132. Tunicamycin 90-101 HtrA serine peptidase 1 Homo sapiens 21-26 21310902-6 2011 On stress induction, HTRA1 and VEGFA were upregulated in human fetal RPE cells treated by tunicamycin and dithiothreitol, but reduced after treatment by MG132. Tunicamycin 90-101 vascular endothelial growth factor A Homo sapiens 31-36 21321189-5 2011 The tunicamycin-induced splicing of X-box binding protein-1 and expression of GRP78 and CHOP were reduced by resveratrol in cultured cells in a SIRT1-dependent manner. Tunicamycin 4-15 X-box binding protein 1 Mus musculus 36-59 21454560-8 2011 Inhibitors of N-linked glycosylation (tunicamycin, deoxymannojirimycin, and deoxynojirimycin) also markedly attenuated the inhibitory effect of IGF-I on beta-glycerophosphate-induced mineralization (p < 0.05) and activation of Akt and MAPK. Tunicamycin 38-49 insulin like growth factor 1 Homo sapiens 144-149 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 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 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 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 eukaryotic translation initiation factor 2A Rattus norvegicus 175-184 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 apolipoprotein B Rattus norvegicus 229-236 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 apolipoprotein B Rattus norvegicus 229-233 21321189-5 2011 The tunicamycin-induced splicing of X-box binding protein-1 and expression of GRP78 and CHOP were reduced by resveratrol in cultured cells in a SIRT1-dependent manner. Tunicamycin 4-15 heat shock protein 5 Mus musculus 78-83 21321189-5 2011 The tunicamycin-induced splicing of X-box binding protein-1 and expression of GRP78 and CHOP were reduced by resveratrol in cultured cells in a SIRT1-dependent manner. Tunicamycin 4-15 DNA-damage inducible transcript 3 Mus musculus 88-92 21321189-5 2011 The tunicamycin-induced splicing of X-box binding protein-1 and expression of GRP78 and CHOP were reduced by resveratrol in cultured cells in a SIRT1-dependent manner. Tunicamycin 4-15 sirtuin 1 Mus musculus 144-149 21321189-6 2011 Conversely, SIRT1-deficient mouse embryonic fibroblasts challenged with tunicamycin exhibited markedly increased mTORC1 activity and impaired ER homeostasi and insulin signaling. Tunicamycin 72-83 CREB regulated transcription coactivator 1 Mus musculus 113-119 21242807-1 2011 We investigated the effects of endoplasmic reticulum (ER) stress inducers thapsigargin (TG) and tunicamycin (Tm) on immunostimulant lipopolysaccharide/interferon (LPS/IFN)-induced expression of isoform of nitric oxide synthase (iNOS) and nitric oxide (NO) production in vascular smooth muscle cells. Tunicamycin 96-107 interferon regulatory factor 6 Homo sapiens 132-170 22069719-7 2011 However, RTA inhibited both phosphorylation of inositol-requiring enzyme 1 (IRE1) and splicing of X-box binding protein1 mRNA by the UPR-inducing agent tunicamycin (Tm). Tunicamycin 152-163 RNA binding fox-1 homolog 2 Homo sapiens 9-12 22069719-7 2011 However, RTA inhibited both phosphorylation of inositol-requiring enzyme 1 (IRE1) and splicing of X-box binding protein1 mRNA by the UPR-inducing agent tunicamycin (Tm). Tunicamycin 152-163 X-box binding protein 1 Homo sapiens 98-120 21241252-5 2011 Tunicamycin-treated Bak-/-Bax-/- cells remain viable, but cease growth, arresting in G1-phase and undergoing autophagy in the absence of apoptosis. Tunicamycin 0-11 BCL2 antagonist/killer 1 Homo sapiens 20-23 21241252-5 2011 Tunicamycin-treated Bak-/-Bax-/- cells remain viable, but cease growth, arresting in G1-phase and undergoing autophagy in the absence of apoptosis. Tunicamycin 0-11 BCL2 associated X, apoptosis regulator Homo sapiens 26-29 21241252-11 2011 Importantly, the effects of tunicamycin on cellular metabolic processes may be related to a reduction in cell-surface GLUT1 (glucose transporter 1) levels which, in turn, may reflect decreased Akt signalling. Tunicamycin 28-39 solute carrier family 2 member 1 Homo sapiens 118-123 21241252-11 2011 Importantly, the effects of tunicamycin on cellular metabolic processes may be related to a reduction in cell-surface GLUT1 (glucose transporter 1) levels which, in turn, may reflect decreased Akt signalling. Tunicamycin 28-39 solute carrier family 2 member 1 Homo sapiens 125-146 21216966-6 2011 PTP1B overexpression or TCPTP knockdown in MIN6 cells mitigated palmitate- or tunicamycin-induced PERK/eIF2alpha ER stress signaling, whereas PTP1B deficiency enhanced ER stress. Tunicamycin 78-89 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 0-5 21151176-6 2011 The combination of ER stress inducers (such as THAPS or tunicamycin) and CDDP effectively induced the translocation of CRT to the plasma membrane, as well as immunogenic cell death, although ER stress or CDDP alone was insufficient to induce CRT exposure and immunogenic cell death. Tunicamycin 56-67 calreticulin Homo sapiens 119-122 21308740-4 2011 Monolayer cultures treated with ER stressors glucose withdrawal (-Glu), tunicamycin (TN), or thapsigargin (TG) up-regulated Grp78 and Gadd153, demonstrating a complete ER stress response. Tunicamycin 72-83 heat shock protein family A (Hsp70) member 5 Bos taurus 124-129 21308740-4 2011 Monolayer cultures treated with ER stressors glucose withdrawal (-Glu), tunicamycin (TN), or thapsigargin (TG) up-regulated Grp78 and Gadd153, demonstrating a complete ER stress response. Tunicamycin 85-87 heat shock protein family A (Hsp70) member 5 Bos taurus 124-129 21216966-6 2011 PTP1B overexpression or TCPTP knockdown in MIN6 cells mitigated palmitate- or tunicamycin-induced PERK/eIF2alpha ER stress signaling, whereas PTP1B deficiency enhanced ER stress. Tunicamycin 78-89 protein tyrosine phosphatase, non-receptor type 2 Mus musculus 24-29 21216966-6 2011 PTP1B overexpression or TCPTP knockdown in MIN6 cells mitigated palmitate- or tunicamycin-induced PERK/eIF2alpha ER stress signaling, whereas PTP1B deficiency enhanced ER stress. Tunicamycin 78-89 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 98-102 21216966-6 2011 PTP1B overexpression or TCPTP knockdown in MIN6 cells mitigated palmitate- or tunicamycin-induced PERK/eIF2alpha ER stress signaling, whereas PTP1B deficiency enhanced ER stress. Tunicamycin 78-89 eukaryotic translation initiation factor 2A Mus musculus 103-112 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 21126579-12 2011 Tunicamycin prevented OCTN2 glycosylation, but it did not impair maturation to the plasma membrane. Tunicamycin 0-11 solute carrier family 22 member 5 Homo sapiens 22-27 20526696-4 2011 Cells expressing PrP-PG9 and PrP-PG12 were sensitive to endoplasmic reticulum (ER) stimuli, tunicamycin, and brefeldin A. ER-stress-related proteins, Grp94, XBP1, TRAF2, and CHOP, were significantly increased in cells expressing PrP-PG9 and PrP-PG12, while Grp78 increased markedly 12 h and pro-caspase-12 decreased sharply 20 h post-transfection. Tunicamycin 92-103 prion protein Homo sapiens 17-20 20526696-4 2011 Cells expressing PrP-PG9 and PrP-PG12 were sensitive to endoplasmic reticulum (ER) stimuli, tunicamycin, and brefeldin A. ER-stress-related proteins, Grp94, XBP1, TRAF2, and CHOP, were significantly increased in cells expressing PrP-PG9 and PrP-PG12, while Grp78 increased markedly 12 h and pro-caspase-12 decreased sharply 20 h post-transfection. Tunicamycin 92-103 prion protein Homo sapiens 29-32 20526696-4 2011 Cells expressing PrP-PG9 and PrP-PG12 were sensitive to endoplasmic reticulum (ER) stimuli, tunicamycin, and brefeldin A. ER-stress-related proteins, Grp94, XBP1, TRAF2, and CHOP, were significantly increased in cells expressing PrP-PG9 and PrP-PG12, while Grp78 increased markedly 12 h and pro-caspase-12 decreased sharply 20 h post-transfection. Tunicamycin 92-103 prion protein Homo sapiens 29-32 20526696-4 2011 Cells expressing PrP-PG9 and PrP-PG12 were sensitive to endoplasmic reticulum (ER) stimuli, tunicamycin, and brefeldin A. ER-stress-related proteins, Grp94, XBP1, TRAF2, and CHOP, were significantly increased in cells expressing PrP-PG9 and PrP-PG12, while Grp78 increased markedly 12 h and pro-caspase-12 decreased sharply 20 h post-transfection. Tunicamycin 92-103 prion protein Homo sapiens 29-32 21150875-2 2011 Since tumor necrosis factor alpha (TNFalpha) plays a role in acute kidney injury, and induces ER stress and cell death in vitro, we examined the contribution of TNFalpha to acute kidney ER stress induced by tunicamycin. Tunicamycin 207-218 tumor necrosis factor Mus musculus 161-169 21150875-3 2011 Contrary to expectation, tunicamycin caused much more severe kidney injury in TNFalpha-/- than in wild-type mice. Tunicamycin 25-36 tumor necrosis factor Mus musculus 78-86 21150875-5 2011 Reconstitution of TNFalpha-/- mice with TNFalpha 24 h before tunicamycin injection reversed the susceptibility. Tunicamycin 61-72 tumor necrosis factor Mus musculus 18-26 21150875-6 2011 When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1). Tunicamycin 56-67 tumor necrosis factor Mus musculus 5-13 21150875-6 2011 When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1). Tunicamycin 56-67 tumor necrosis factor receptor superfamily, member 1a Mus musculus 102-107 21150875-6 2011 When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1). Tunicamycin 56-67 tumor necrosis factor Mus musculus 160-168 21150875-6 2011 When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1). Tunicamycin 56-67 tumor necrosis factor receptor superfamily, member 1a Mus musculus 188-202 21150875-6 2011 When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1). Tunicamycin 56-67 tumor necrosis factor receptor superfamily, member 1a Mus musculus 204-209 21150875-9 2011 Finally, treatment of proximal tubule cells isolated from TNFR1-/- mice with an inhibitor of eIF2alpha phosphatase increased the levels of phosphorylated eIF2alpha and substantially reduced tunicamycin-induced cell death. Tunicamycin 190-201 tumor necrosis factor receptor superfamily, member 1a Mus musculus 58-63 21150875-9 2011 Finally, treatment of proximal tubule cells isolated from TNFR1-/- mice with an inhibitor of eIF2alpha phosphatase increased the levels of phosphorylated eIF2alpha and substantially reduced tunicamycin-induced cell death. Tunicamycin 190-201 eukaryotic translation initiation factor 2A Mus musculus 93-102 21087599-7 2011 In parental HL60 cells, ABC50 KD increased sensitivity to Ec, thapsigargin and tunicamycin but not to serum withdrawal or etoposide. Tunicamycin 79-90 ATP binding cassette subfamily F member 1 Homo sapiens 24-29 21168844-10 2011 Nicorandil significantly attenuated tunicamycin-induced CHOP upregulation in cultured THP-1 macrophages. Tunicamycin 36-47 GLI family zinc finger 2 Homo sapiens 86-91 21298055-6 2011 Analyses of the cell viabilities in the presences of tunicamycin and brefeldin A revealed that expressions of PrP-KDEL and PrP-3AV sensitized the transfected cells to ER stress stimuli. Tunicamycin 53-64 prion protein Homo sapiens 110-113 21029237-6 2011 In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA. Tunicamycin 26-37 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 63-66 21029237-6 2011 In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA. Tunicamycin 26-37 glycogen synthase kinase 3 alpha Homo sapiens 68-77 21029237-6 2011 In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA. Tunicamycin 26-37 microtubule associated protein tau Homo sapiens 89-92 21029237-6 2011 In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA. Tunicamycin 26-37 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 151-154 21029237-6 2011 In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA. Tunicamycin 26-37 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 151-154 21029237-7 2011 Our results demonstrate that neuronal PKR co-localizes with GSK-3beta and tau in AD brains and is able to modulate GSK-3beta activation, tau phosphorylation and apoptosis in neuroblastoma cells exposed to tunicamycin or Abeta. Tunicamycin 205-216 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 38-41 20970123-2 2011 Inhibition of CD44 N- and O-linked glycosylation by using tunicamycin and/or B-GalNAc statistically significantly inhibited endometrial cell attachment to peritoneal mesothelial cells, suggesting a role in establishment of early endometriotic lesions. Tunicamycin 58-69 CD44 molecule (Indian blood group) Homo sapiens 14-18 21298055-6 2011 Analyses of the cell viabilities in the presences of tunicamycin and brefeldin A revealed that expressions of PrP-KDEL and PrP-3AV sensitized the transfected cells to ER stress stimuli. Tunicamycin 53-64 pre-mRNA processing factor 3 Homo sapiens 123-128 21490406-4 2011 Here, we report that acylated ghrelin inhibited tunicamycin- or thapsigargin-triggered ER stress-induced apoptotic cell death in primary rat cortical neurons. Tunicamycin 48-59 ghrelin and obestatin prepropeptide Rattus norvegicus 30-37 21184741-7 2011 Notably, knockdown of Derlin-1 also stabilized the expression of tunicamycin-induced deglycosylated WT BCRP protein, implying the importance of glycosylation state for the recognition of BCRP by Derlin-1. Tunicamycin 65-76 derlin 1 Homo sapiens 22-30 21184741-7 2011 Notably, knockdown of Derlin-1 also stabilized the expression of tunicamycin-induced deglycosylated WT BCRP protein, implying the importance of glycosylation state for the recognition of BCRP by Derlin-1. Tunicamycin 65-76 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 103-107 21184741-7 2011 Notably, knockdown of Derlin-1 also stabilized the expression of tunicamycin-induced deglycosylated WT BCRP protein, implying the importance of glycosylation state for the recognition of BCRP by Derlin-1. Tunicamycin 65-76 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 187-191 21184741-7 2011 Notably, knockdown of Derlin-1 also stabilized the expression of tunicamycin-induced deglycosylated WT BCRP protein, implying the importance of glycosylation state for the recognition of BCRP by Derlin-1. Tunicamycin 65-76 derlin 1 Homo sapiens 195-203 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 21490406-7 2011 Ghrelin also inhibited tunicamycin or thapsigargin induction of PRK-like ER kinase (PERK), eukaryotic translation initiation factor-2alpha (eIF2alpha) and activating transcription factor (ATF) 4. Tunicamycin 23-34 eukaryotic translation initiation factor 2A Rattus norvegicus 91-138 21490406-7 2011 Ghrelin also inhibited tunicamycin or thapsigargin induction of PRK-like ER kinase (PERK), eukaryotic translation initiation factor-2alpha (eIF2alpha) and activating transcription factor (ATF) 4. Tunicamycin 23-34 eukaryotic translation initiation factor 2A Rattus norvegicus 140-149 21490406-7 2011 Ghrelin also inhibited tunicamycin or thapsigargin induction of PRK-like ER kinase (PERK), eukaryotic translation initiation factor-2alpha (eIF2alpha) and activating transcription factor (ATF) 4. Tunicamycin 23-34 activating transcription factor 4 Rattus norvegicus 155-194 21490406-8 2011 Exposure of cells to tunicamycin or thapsigargin resulted in nuclear translocation of forkhead box protein O1 (Foxo1), which was reduced by pretreatment with ghrelin. Tunicamycin 21-32 forkhead box O1 Rattus norvegicus 86-109 21490406-8 2011 Exposure of cells to tunicamycin or thapsigargin resulted in nuclear translocation of forkhead box protein O1 (Foxo1), which was reduced by pretreatment with ghrelin. Tunicamycin 21-32 forkhead box O1 Rattus norvegicus 111-116 21490406-8 2011 Exposure of cells to tunicamycin or thapsigargin resulted in nuclear translocation of forkhead box protein O1 (Foxo1), which was reduced by pretreatment with ghrelin. Tunicamycin 21-32 ghrelin and obestatin prepropeptide Rattus norvegicus 158-165 21432213-5 2011 RESULTS: Gene expression analysis revealed that Ire1beta was up-regulated in astrocytes exposed to aluminum while Ire1alpha was up-regulated by tunicamycin. Tunicamycin 144-155 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 114-123 22174631-0 2011 Tunicamycin depresses P-glycoprotein glycosylation without an effect on its membrane localization and drug efflux activity in L1210 cells. Tunicamycin 0-11 phosphoglycolate phosphatase Mus musculus 22-36 22174631-8 2011 Tunicamycin inhibited P-gp N-glycosylation in both of the P-gp-positive cells. Tunicamycin 0-11 phosphoglycolate phosphatase Mus musculus 22-26 22174631-10 2011 The present paper brings evidence that independently on the mode of P-gp expression (selection with drugs or transfection with a gene encoding P-gp) in L1210 cells, tunicamycin induces inhibition of N-glycosylation of this protein, without altering its function as plasma membrane drug efflux pump. Tunicamycin 165-176 phosphoglycolate phosphatase Mus musculus 68-72 22174631-10 2011 The present paper brings evidence that independently on the mode of P-gp expression (selection with drugs or transfection with a gene encoding P-gp) in L1210 cells, tunicamycin induces inhibition of N-glycosylation of this protein, without altering its function as plasma membrane drug efflux pump. Tunicamycin 165-176 phosphoglycolate phosphatase Mus musculus 143-147 20974203-5 2011 Pretreatment with ER stress inducers, thapsigargin (Tg) and tunicamycin (Tm), promoted GRP78 mRNA induction and ATF4 translation, which are ER stress markers, under our experimental conditions and protected against the cytotoxicity. Tunicamycin 60-71 heat shock protein family A (Hsp70) member 5 Homo sapiens 87-92 21282934-2 2011 Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. Tunicamycin 0-11 caspase 9 Homo sapiens 64-73 21282934-2 2011 Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. Tunicamycin 0-11 caspase 4 Homo sapiens 78-87 21282934-2 2011 Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. Tunicamycin 0-11 caspase 4 Homo sapiens 111-120 21282934-2 2011 Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. Tunicamycin 0-11 caspase 9 Homo sapiens 138-147 32272543-2 2011 Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. Tunicamycin 0-11 caspase 9 Homo sapiens 64-73 32272543-2 2011 Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. Tunicamycin 0-11 caspase 4 Homo sapiens 78-87 32272543-2 2011 Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. Tunicamycin 0-11 caspase 4 Homo sapiens 111-120 32272543-2 2011 Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9. Tunicamycin 0-11 caspase 9 Homo sapiens 138-147 20974203-5 2011 Pretreatment with ER stress inducers, thapsigargin (Tg) and tunicamycin (Tm), promoted GRP78 mRNA induction and ATF4 translation, which are ER stress markers, under our experimental conditions and protected against the cytotoxicity. Tunicamycin 60-71 activating transcription factor 4 Homo sapiens 112-116 20974203-5 2011 Pretreatment with ER stress inducers, thapsigargin (Tg) and tunicamycin (Tm), promoted GRP78 mRNA induction and ATF4 translation, which are ER stress markers, under our experimental conditions and protected against the cytotoxicity. Tunicamycin 73-75 heat shock protein family A (Hsp70) member 5 Homo sapiens 87-92 20974203-5 2011 Pretreatment with ER stress inducers, thapsigargin (Tg) and tunicamycin (Tm), promoted GRP78 mRNA induction and ATF4 translation, which are ER stress markers, under our experimental conditions and protected against the cytotoxicity. Tunicamycin 73-75 activating transcription factor 4 Homo sapiens 112-116 20826801-9 2010 Interestingly, in cells treated with tunicamycin, SIRPalpha dimerization but not CD47 binding was inhibited, suggesting that a SIRPalpha dimer is probably bivalent. Tunicamycin 37-48 signal regulatory protein alpha Homo sapiens 50-59 21698202-4 2011 METHODS: Muscle cells were incubated overnight with tunicamycin or thapsigargin to induce ER stress and the activation of the unfolded protein response, mTORC1 activity at baseline and following insulin and amino acids, as well as amino acid transport were determined. Tunicamycin 52-63 CREB regulated transcription coactivator 1 Mus musculus 153-159 21698202-7 2011 The leucine (2.5-5 mM)-induced phosphorylation of S6K1 on the other hand was repressed by low concentrations of both tunicamycin and thapsigargin. Tunicamycin 117-128 ribosomal protein S6 kinase B1 Homo sapiens 50-54 21698202-10 2011 Tunicamycin and thapsigargin both decreased the basal phosphorylation state of PRAS40. Tunicamycin 0-11 AKT1 substrate 1 Homo sapiens 79-85 22355548-2 2011 We found that a double mutant of Arabidopsis IRE1A and IRE1B (ire1a/ire1b) is more sensitive to the ER stress inducer tunicamycin than the wild-type. Tunicamycin 118-129 Endoribonuclease/protein kinase IRE1-like protein Arabidopsis thaliana 45-50 22355548-2 2011 We found that a double mutant of Arabidopsis IRE1A and IRE1B (ire1a/ire1b) is more sensitive to the ER stress inducer tunicamycin than the wild-type. Tunicamycin 118-129 inositol requiring 1-1 Arabidopsis thaliana 55-60 22355548-2 2011 We found that a double mutant of Arabidopsis IRE1A and IRE1B (ire1a/ire1b) is more sensitive to the ER stress inducer tunicamycin than the wild-type. Tunicamycin 118-129 Endoribonuclease/protein kinase IRE1-like protein Arabidopsis thaliana 62-67 22355548-2 2011 We found that a double mutant of Arabidopsis IRE1A and IRE1B (ire1a/ire1b) is more sensitive to the ER stress inducer tunicamycin than the wild-type. Tunicamycin 118-129 inositol requiring 1-1 Arabidopsis thaliana 68-73 22073243-12 2011 We found that both CeUGGT1 and CeUGGT2 play a protective role under ER stress conditions, since 10 microg/ml tunicamycin arrested development at the L2/L3 stage of both uggt-1(RNAi) and uggt-2(RNAi) but not of control worms. Tunicamycin 109-120 UDP-Glucose Glycoprotein glucosylTransferase Caenorhabditis elegans 19-26 22073243-12 2011 We found that both CeUGGT1 and CeUGGT2 play a protective role under ER stress conditions, since 10 microg/ml tunicamycin arrested development at the L2/L3 stage of both uggt-1(RNAi) and uggt-2(RNAi) but not of control worms. Tunicamycin 109-120 UDP-Glucose Glycoprotein glucosylTransferase Caenorhabditis elegans 31-38 22073243-12 2011 We found that both CeUGGT1 and CeUGGT2 play a protective role under ER stress conditions, since 10 microg/ml tunicamycin arrested development at the L2/L3 stage of both uggt-1(RNAi) and uggt-2(RNAi) but not of control worms. Tunicamycin 109-120 UDP-Glucose Glycoprotein glucosylTransferase Caenorhabditis elegans 169-175 22073243-12 2011 We found that both CeUGGT1 and CeUGGT2 play a protective role under ER stress conditions, since 10 microg/ml tunicamycin arrested development at the L2/L3 stage of both uggt-1(RNAi) and uggt-2(RNAi) but not of control worms. Tunicamycin 109-120 UDP-Glucose Glycoprotein glucosylTransferase Caenorhabditis elegans 186-192 20826801-9 2010 Interestingly, in cells treated with tunicamycin, SIRPalpha dimerization but not CD47 binding was inhibited, suggesting that a SIRPalpha dimer is probably bivalent. Tunicamycin 37-48 signal regulatory protein alpha Homo sapiens 127-136 20933500-4 2010 Here we showed that several well-characterized ER stress inducers (thapsigargin, tunicamycin, and dithiothreitol) increase the expression of TLR2 in epithelial cells. Tunicamycin 81-92 toll-like receptor 2 Mus musculus 141-145 21064031-8 2010 Altered UPR signaling in livers of CD154KO mice was confirmed in tunicamycin (TM) challenge experiments. Tunicamycin 65-76 CD40 ligand Mus musculus 35-42 20933500-6 2010 Furthermore, there was significant increase of TLR2 mRNA level in the livers of tunicamycin-treated mice and high-fat diet-fed mice, suggesting an impact of ER stress in vivo on the expression of TLR2. Tunicamycin 80-91 toll-like receptor 2 Mus musculus 47-51 20933500-6 2010 Furthermore, there was significant increase of TLR2 mRNA level in the livers of tunicamycin-treated mice and high-fat diet-fed mice, suggesting an impact of ER stress in vivo on the expression of TLR2. Tunicamycin 80-91 toll-like receptor 2 Mus musculus 196-200 20685651-3 2010 We found that overexpression of lipid-anchored Rheb enhanced the apoptotic effects induced by UV light, TNFalpha, or tunicamycin in an mTOR complex 1 (mTORC1)-dependent manner. Tunicamycin 117-128 CREB regulated transcription coactivator 1 Mus musculus 151-157 20501874-7 2010 In C(2)C(12) muscle cells, tunicamycin, thapsigargin, and palmitic acid all increased UPR markers and decreased phosphorylation of S6K1 (P < 0.05). Tunicamycin 27-38 ribosomal protein S6 kinase, polypeptide 1 Mus musculus 131-135 20692228-3 2010 The results showed that SelK was regulated by ER stress agents, Tunicamycin (Tm) and beta-Mercaptoethanol (beta-ME), in HepG2 cells. Tunicamycin 64-75 selenoprotein K Homo sapiens 24-28 20628148-8 2010 Manipulating ER signaling by siRNA down-regulation of BiP/GRP78 or treating B-CLL cells with 2 well-known ER stress-inducers, tunicamycin and thapsigargin, increases their apoptosis. Tunicamycin 126-137 heat shock protein family A (Hsp70) member 5 Homo sapiens 58-63 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 21076579-5 2010 METHODS: The effects of tunicamycin and thapsigargin on insulin and TRB3 expression in INS-1 cells were measured by Northern and Western blot analysis, respectively. Tunicamycin 24-35 insulin Homo sapiens 56-63 21076579-5 2010 METHODS: The effects of tunicamycin and thapsigargin on insulin and TRB3 expression in INS-1 cells were measured by Northern and Western blot analysis, respectively. Tunicamycin 24-35 tribbles pseudokinase 3 Rattus norvegicus 68-72 21076579-8 2010 RESULTS: The treatment of INS-1 cells with tunicamycin and thapsigargin decreased insulin mRNA expression, but increased TRB3 protein expression. Tunicamycin 43-54 tribbles pseudokinase 3 Rattus norvegicus 121-125 20886113-4 2010 METHODOLOGY: Forced expression of Hr by transfection decreased the number of apoptotic nuclei, levels of caspase-3 activity, and cytosolic cytochrome C in COS cells exposed to staurosporine and tunicamycin. Tunicamycin 194-205 lysine demethylase and nuclear receptor corepressor Mus musculus 34-36 20688044-9 2010 COX-2 downregulation by E5 could be overcome by thapsigargin or tunicamycin treatments, which initiate ER stress via calcium fluxes and abnormal protein glycosylation respectively, making it unlikely that E5 specifically tempers these pathways. Tunicamycin 64-75 mitochondrially encoded cytochrome c oxidase II Homo sapiens 0-5 20354865-5 2010 Using transfected Chinese hamster ovary (CHO) cells to reconstitute Kv4 complex, we show that the pharmacological inhibition of DPP10 glycosylation by tunicamycin and neuraminidase affects transient outward potassium current (I (to)) kinetics. Tunicamycin 151-162 inactive dipeptidyl peptidase 10 Cricetulus griseus 128-133 20685651-3 2010 We found that overexpression of lipid-anchored Rheb enhanced the apoptotic effects induced by UV light, TNFalpha, or tunicamycin in an mTOR complex 1 (mTORC1)-dependent manner. Tunicamycin 117-128 Ras homolog, mTORC1 binding Homo sapiens 47-51 20685651-3 2010 We found that overexpression of lipid-anchored Rheb enhanced the apoptotic effects induced by UV light, TNFalpha, or tunicamycin in an mTOR complex 1 (mTORC1)-dependent manner. Tunicamycin 117-128 mechanistic target of rapamycin kinase Homo sapiens 135-139 20631254-4 2010 In this report, we burdened mice with intraperitoneal injection of the ER stress-inducing reagent tunicamycin and found that wild-type mice were able to recover from the insult, whereas ATF6alpha-knockout mice exhibited liver dysfunction and steatosis. Tunicamycin 98-109 activating transcription factor 6 Mus musculus 186-195 20631306-7 2010 Depleting MD-2 using small interfering RNA or blocking the N-glycosylation of cells using tunicamycin blocked membrane trafficking of TLR4. Tunicamycin 90-101 toll-like receptor 4 Mus musculus 134-138 20513236-8 2010 The thapsigargin- and tunicamycin-induced UPR (unfolded protein response) also increased SREBP-1 expression in Hep G2 cells, through the cap-independent translation mediated by IRES. Tunicamycin 22-33 sterol regulatory element binding transcription factor 1 Homo sapiens 89-96 20460427-4 2010 RESULTS: N-glycosylation of CN-1 was either inhibited by tunicamycin in pCSII-CN-1-transfected Cos-7 cells or by stepwise deletion of its three putative N-glycosylation sites. Tunicamycin 57-68 carnosine dipeptidase 1 Homo sapiens 28-32 20460427-7 2010 Tunicamycin completely inhibited CN-1 secretion. Tunicamycin 0-11 carnosine dipeptidase 1 Homo sapiens 33-37 20430884-0 2010 The activity of yeast Hog1 MAPK is required during endoplasmic reticulum stress induced by tunicamycin exposure. Tunicamycin 91-102 mitogen-activated protein kinase HOG1 Saccharomyces cerevisiae S288C 22-26 20430884-5 2010 Strains lacking the MAPK Hog1p displayed sensitivity to tunicamycin or beta-mercaptoethanol, whereas hyperactivation of the pathway enhanced their resistance. Tunicamycin 56-67 mitogen-activated protein kinase HOG1 Saccharomyces cerevisiae S288C 25-30 20430884-7 2010 Northern blot analysis demonstrated that Hog1p controls the tunicamycin-induced transcriptional change of GPD1 and that wild-type cells exposed to the drug accumulated glycerol in a Hog1p-dependent manner. Tunicamycin 60-71 mitogen-activated protein kinase HOG1 Saccharomyces cerevisiae S288C 41-46 20430884-7 2010 Northern blot analysis demonstrated that Hog1p controls the tunicamycin-induced transcriptional change of GPD1 and that wild-type cells exposed to the drug accumulated glycerol in a Hog1p-dependent manner. Tunicamycin 60-71 glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1 Saccharomyces cerevisiae S288C 106-110 20430884-7 2010 Northern blot analysis demonstrated that Hog1p controls the tunicamycin-induced transcriptional change of GPD1 and that wild-type cells exposed to the drug accumulated glycerol in a Hog1p-dependent manner. Tunicamycin 60-71 mitogen-activated protein kinase HOG1 Saccharomyces cerevisiae S288C 182-187 20354865-9 2010 The effects of tunicamycin on the native I (to) currents of human atrial myocytes expressing DPP10 were similar to those of the KV4.3/KChIP2/DPP10 complex in CHO cells. Tunicamycin 15-26 dipeptidyl peptidase like 10 Homo sapiens 93-98 20618991-9 2010 N-glycosylation inhibitor tunicamycin was used to deglycosylate the integrin beta1 subunit. Tunicamycin 26-37 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 77-82 20407008-4 2010 In this work, we demonstrated that tunicamycin inhibition of glycosylation of the GLP-1 receptor expressed in CHO cells interfered with biosynthesis and intracellular trafficking, thereby eliminating natural ligand binding. Tunicamycin 35-46 glucagon Homo sapiens 82-87 20457808-3 2010 Knockdown of the oxidase Nox4, expressed on ER endomembranes, or expression of ER-targeted catalase blocked ER H(2)O(2) production by tunicamycin and Tat and prevented the UPR following exposure to these two agonists, but not to thapsigargin or dithiothreitol. Tunicamycin 134-145 NADPH oxidase 4 Homo sapiens 25-29 20413434-9 2010 Molecular analyses of tunicamycin-treated tumors showed reduced levels of EGFR and Met, two RTKs overexpressed in gliomas. Tunicamycin 22-33 epidermal growth factor receptor Homo sapiens 74-78 20450227-7 2010 In further support of a role for glycosylation in receptor function, treatment of RAW 264.7 macrophages with the N-linked glycosylation synthesis inhibitor tunicamycin attenuates P2X(7) agonist-induced, but not phorbol ester-induced, ERK1/2 phosphorylation. Tunicamycin 156-167 purinergic receptor P2X 7 Homo sapiens 179-185 20450227-7 2010 In further support of a role for glycosylation in receptor function, treatment of RAW 264.7 macrophages with the N-linked glycosylation synthesis inhibitor tunicamycin attenuates P2X(7) agonist-induced, but not phorbol ester-induced, ERK1/2 phosphorylation. Tunicamycin 156-167 mitogen-activated protein kinase 3 Homo sapiens 234-240 20368330-3 2010 ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells. Tunicamycin 42-53 matrix metallopeptidase 3 Mus musculus 88-93 20368330-3 2010 ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells. Tunicamycin 42-53 matrix metallopeptidase 3 Mus musculus 88-91 20368330-3 2010 ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells. Tunicamycin 42-53 matrix metallopeptidase 3 Mus musculus 158-163 20368330-3 2010 ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells. Tunicamycin 55-57 matrix metallopeptidase 3 Mus musculus 88-93 20368330-3 2010 ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells. Tunicamycin 55-57 matrix metallopeptidase 3 Mus musculus 88-91 20368330-3 2010 ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells. Tunicamycin 55-57 matrix metallopeptidase 3 Mus musculus 158-163 20235094-5 2010 These transcripts and Nrf2 (Nfe2l2) were increased by systemic application of tunicamycin or the selective olfactotoxic chemical methimazole. Tunicamycin 78-89 nuclear factor, erythroid derived 2, like 2 Mus musculus 22-26 20235094-5 2010 These transcripts and Nrf2 (Nfe2l2) were increased by systemic application of tunicamycin or the selective olfactotoxic chemical methimazole. Tunicamycin 78-89 nuclear factor, erythroid derived 2, like 2 Mus musculus 28-34 20354865-6 2010 Tunicamycin completely blocked DPP10 glycosylation and reduced DPP10 cell surface expression. Tunicamycin 0-11 inactive dipeptidyl peptidase 10 Cricetulus griseus 31-36 20354865-6 2010 Tunicamycin completely blocked DPP10 glycosylation and reduced DPP10 cell surface expression. Tunicamycin 0-11 inactive dipeptidyl peptidase 10 Cricetulus griseus 63-68 20146743-1 2010 EOS1 is required for tolerance to oxidative stress in Saccharomyces cerevisiae; mutants are defective in the gene sensitive to hydrogen peroxide and tolerant to tunicamycin. Tunicamycin 161-172 Eos1p Saccharomyces cerevisiae S288C 0-4 19838798-0 2010 Tunicamycin-induced cell death in the trigeminal ganglion is suppressed by nerve growth factor in the mouse embryo. Tunicamycin 0-11 nerve growth factor Mus musculus 75-94 19951703-6 2010 To evaluate the role of glycosylation in the enzyme activity, we produced unglycosylated UGT1A9 by treating HEK293 cells transiently transfected with expression plasmid with tunicamycin. Tunicamycin 174-185 UDP glucuronosyltransferase family 1 member A9 Homo sapiens 89-95 19838798-1 2010 The effect of nerve growth factor (NGF) on tunicamycin (Tm)-treated neurons in the trigeminal ganglion was investigated by use of caspase-3 immunohistochemistry. Tunicamycin 43-54 nerve growth factor Mus musculus 14-33 19838798-1 2010 The effect of nerve growth factor (NGF) on tunicamycin (Tm)-treated neurons in the trigeminal ganglion was investigated by use of caspase-3 immunohistochemistry. Tunicamycin 43-54 nerve growth factor Mus musculus 35-38 19838798-1 2010 The effect of nerve growth factor (NGF) on tunicamycin (Tm)-treated neurons in the trigeminal ganglion was investigated by use of caspase-3 immunohistochemistry. Tunicamycin 56-58 nerve growth factor Mus musculus 14-33 19838798-1 2010 The effect of nerve growth factor (NGF) on tunicamycin (Tm)-treated neurons in the trigeminal ganglion was investigated by use of caspase-3 immunohistochemistry. Tunicamycin 56-58 nerve growth factor Mus musculus 35-38 20231441-5 2010 Treatment with an inducer of UPR, tunicamycin, resulted in accelerated cell death of AtBAG7-null mutants. Tunicamycin 34-45 BCL-2-associated athanogene 7 Arabidopsis thaliana 85-91 20348923-5 2010 Mice with deletion of p85alpha in liver (L-Pik3r1(-/-)) show a similar attenuated UPR after tunicamycin administration, leading to an increased inflammatory response. Tunicamycin 92-103 phosphoinositide-3-kinase regulatory subunit 1 Mus musculus 22-30 20080976-2 2010 IFRD1 mRNA and protein are elevated in tunicamycin-treated human kidney epithelial cells via stabilization of the mRNA. Tunicamycin 39-50 interferon related developmental regulator 1 Homo sapiens 0-5 20305782-8 2010 A marked increase in PARM-1 expression was observed in response to ER stress inducers such as thapsigargin and tunicamycin, which also induced apoptotic cell death. Tunicamycin 111-122 prostate androgen-regulated mucin-like protein 1 Rattus norvegicus 21-27 19961488-10 2010 Exposure of cells to the endoplasmic reticulum stress inducers thapsigargin and tunicamycin also led to cell apoptosis, which was modulated by Cx43 levels in a way similar to MG132. Tunicamycin 80-91 gap junction protein, alpha 1 Mus musculus 143-147 19782129-5 2010 Tunicamycin prevented the N-linked glycosylation and maturation of PDGFRbeta as well as its activation by PDGF-BB. Tunicamycin 0-11 platelet derived growth factor receptor beta Homo sapiens 67-76 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 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 growth differentiation factor 10 Homo sapiens 161-164 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 AKT serine/threonine kinase 1 Homo sapiens 221-224 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 mitogen-activated protein kinase 1 Homo sapiens 229-232 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 AKT serine/threonine kinase 1 Homo sapiens 264-267 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 mitogen-activated protein kinase 1 Homo sapiens 337-340 20007973-5 2010 FLS2 tolerated mild underglycosylation occurring in stt3a but was sensitive to severe underglycosylation induced by tunicamycin treatment. Tunicamycin 116-127 Leucine-rich receptor-like protein kinase family protein Arabidopsis thaliana 0-4 19901967-9 2010 TCTP also protects cells against the proapoptotic effects of tunicamycin and etoposide, but not against those of arsenite. Tunicamycin 61-72 tumor protein, translationally-controlled 1 Homo sapiens 0-4 20005867-5 2010 Pre-treatment with tunicamycin, which inhibits the biosynthesis of N-linked oligosaccharides, decreased the accumulation of Pt in sensitive cells exposed to oxaliplatin or cisplatin and increased the electrophoretic mobility of MRP1 and MRP4, reproducing the association between decreased glycosylation of MRP1 and MRP4 and decreased Pt accumulation observed in the resistant IGROV-1/OHP cells. Tunicamycin 19-30 ATP binding cassette subfamily C member 1 Homo sapiens 228-232 20005867-5 2010 Pre-treatment with tunicamycin, which inhibits the biosynthesis of N-linked oligosaccharides, decreased the accumulation of Pt in sensitive cells exposed to oxaliplatin or cisplatin and increased the electrophoretic mobility of MRP1 and MRP4, reproducing the association between decreased glycosylation of MRP1 and MRP4 and decreased Pt accumulation observed in the resistant IGROV-1/OHP cells. Tunicamycin 19-30 ATP binding cassette subfamily C member 4 Homo sapiens 237-241 20005867-5 2010 Pre-treatment with tunicamycin, which inhibits the biosynthesis of N-linked oligosaccharides, decreased the accumulation of Pt in sensitive cells exposed to oxaliplatin or cisplatin and increased the electrophoretic mobility of MRP1 and MRP4, reproducing the association between decreased glycosylation of MRP1 and MRP4 and decreased Pt accumulation observed in the resistant IGROV-1/OHP cells. Tunicamycin 19-30 ATP binding cassette subfamily C member 1 Homo sapiens 306-310 20005867-5 2010 Pre-treatment with tunicamycin, which inhibits the biosynthesis of N-linked oligosaccharides, decreased the accumulation of Pt in sensitive cells exposed to oxaliplatin or cisplatin and increased the electrophoretic mobility of MRP1 and MRP4, reproducing the association between decreased glycosylation of MRP1 and MRP4 and decreased Pt accumulation observed in the resistant IGROV-1/OHP cells. Tunicamycin 19-30 ATP binding cassette subfamily C member 4 Homo sapiens 315-319 19782129-6 2010 However, upon tunicamycin treatment, DRD4 continued to signal to ERK1/2 in a tyrphostin A9-sensitive manner. Tunicamycin 14-25 dopamine receptor D4 Homo sapiens 37-41 19782129-6 2010 However, upon tunicamycin treatment, DRD4 continued to signal to ERK1/2 in a tyrphostin A9-sensitive manner. Tunicamycin 14-25 mitogen-activated protein kinase 3 Homo sapiens 65-71 20164584-4 2010 Tunicamycin treatment caused a doubling of PSEN1 holoprotein production in HEK293 cells and an increase in holoprotein production to approximately 180% in GOTO human neuroblastoma and KNS-42 human glioma cell lines, without changing the amounts of PSEN1 N- or C-terminal fragments. Tunicamycin 0-11 presenilin 1 Homo sapiens 43-48 20104019-3 2010 Three widely used ER stress inducers including tunicamycin, DTT and MG132 led to the conversion of LC3-I to LC3-II , a commonly used marker of autophagy, as well as the downregulation of mTOR concurrently. Tunicamycin 47-58 mechanistic target of rapamycin kinase Homo sapiens 187-191 21140004-7 2010 Our data showed that blocking of N-glycan transfer to the nascent polypeptide chain with the antibiotic tunicamycin resulted in the loss of E1 and E2. Tunicamycin 104-115 small nucleolar RNA, H/ACA box 73A Homo sapiens 140-149 19875812-5 2010 Mesangial cells preferentially induced C/EBPbeta after exposure to thapsigargin or tunicamycin; induction of C/EBPdelta was modest and transient, and expression of C/EBPalpha was absent. Tunicamycin 83-94 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 39-48 19773801-8 2010 ER stress agent tunicamycin induced ARMET and CHOP expressions in the primary cultured neurons. Tunicamycin 16-27 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 36-41 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 19773801-9 2010 Treatment with recombinant human ARMET promoted neuron proliferation and prevented from neuron apoptosis induced by tunicamycin. Tunicamycin 116-127 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 33-38 19841481-7 2009 Consistent with a synthetic impairment between challenged ER function and inositol deprivation, increased expression of NTE1 improved the growth of cells exposed to tunicamycin in the absence of inositol. Tunicamycin 165-176 lysophospholipase Saccharomyces cerevisiae S288C 120-124 20022931-4 2010 Western blot analyses performed with or without endoglycosidase H, peptide:N-glycosidase F or tunicamycin treatments and site-directed mutagenesis revealed that MC2R was glycosylated in the N-terminal domain at its two putative N-glycosylation sites (Asn(12)-Asn(13)-Thr(14) and Asn(17)-Asn(18)-Ser(19)). Tunicamycin 94-105 melanocortin 2 receptor Homo sapiens 161-165 19783479-6 2010 These studies uncovered PknB/Stk and Stp as modulators of cell wall structure and susceptibility to cell wall-acting antibiotics such as certain beta-lactams and tunicamycin. Tunicamycin 162-173 macrophage stimulating 1 receptor (c-met-related tyrosine kinase) Mus musculus 29-32 20944397-6 2010 In agreement with increases of TIN1 transcripts, the TIN1 protein accumulated in response to tunicamycin treatment. Tunicamycin 93-104 tunicamycin induced protein Arabidopsis thaliana 31-35 20944397-6 2010 In agreement with increases of TIN1 transcripts, the TIN1 protein accumulated in response to tunicamycin treatment. Tunicamycin 93-104 tunicamycin induced protein Arabidopsis thaliana 53-57 20511722-3 2010 Here we show that tunicamycin, an antibiotic promoting ER stress, suppresses the expression of p21, a tumor suppressor that induces cell cycle arrest and inhibits apoptosis. Tunicamycin 18-29 cyclin dependent kinase inhibitor 1A Homo sapiens 95-98 20511722-5 2010 Consistently with these findings, siRNA-mediated inhibition of p21 levels restored the sensitivity of CHOP-deficient cells to tunicamycin. Tunicamycin 126-137 cyclin dependent kinase inhibitor 1A Homo sapiens 63-66 19834331-7 2010 TUDCA treatment inhibited tunicamycin-induced ER stress as evidenced by the attenuation of phosphorylation of eukaryotic translation initiation factor-2a and glucose reactive protein-78. Tunicamycin 26-37 eukaryotic translation initiation factor 2A Homo sapiens 110-153 20164584-4 2010 Tunicamycin treatment caused a doubling of PSEN1 holoprotein production in HEK293 cells and an increase in holoprotein production to approximately 180% in GOTO human neuroblastoma and KNS-42 human glioma cell lines, without changing the amounts of PSEN1 N- or C-terminal fragments. Tunicamycin 0-11 presenilin 1 Homo sapiens 248-253 20164584-6 2010 HEK293 cells that stably overexpressed PSEN1 holoprotein showed increased resistance to ER stress induced by tunicamycin, but they did not show resistance to ER stress caused by thapsigargin, a specific inhibitor of sarco ER calcium-ATPase (SERCA). Tunicamycin 109-120 presenilin 1 Homo sapiens 39-44 20164584-7 2010 In wild-type HEK293 cells under ER stress induced by tunicamycin, an increased amount of SERCA interacted with PSEN1 holoprotein. Tunicamycin 53-64 presenilin 1 Homo sapiens 111-116 19643964-9 2009 Although caspase-4 inhibitor Z-LEVD-fmk and caspase-1 and -4 inhibitor Z-YVAD-fmk reduced tunicamycin-induced hRPE apoptotic cell death by 59% and 86%, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis. Tunicamycin 90-101 caspase 4 Homo sapiens 9-18 19909340-5 2009 When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38. Tunicamycin 101-112 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 5-10 19909340-5 2009 When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38. Tunicamycin 101-112 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 167-172 19909340-5 2009 When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38. Tunicamycin 101-112 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 167-172 19643964-9 2009 Although caspase-4 inhibitor Z-LEVD-fmk and caspase-1 and -4 inhibitor Z-YVAD-fmk reduced tunicamycin-induced hRPE apoptotic cell death by 59% and 86%, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis. Tunicamycin 90-101 caspase 1 Homo sapiens 44-60 19739097-11 2009 In addition, blockage of N-glycosylation by treatment with tunicamycin eliminated 17 kDa form of intracellular IL-13, but failed to promote IL-13 secretion in BSMC. Tunicamycin 59-70 interleukin 13 Homo sapiens 111-116 19502591-5 2009 ER stress agents thapsigargin and tunicamycin suppressed AdipoR2 and pAMPK levels in Huh7 cells, while fenofibrate and the chemical chaperone 4-phenylbutyrate (PBA) prevented these changes. Tunicamycin 34-45 adiponectin receptor 2 Homo sapiens 57-64 19741092-7 2009 However, we show that TMX-class I HC interaction is enhanced during tunicamycin-induced ER stress, and TMX prevents the ER-to-cytosol retrotranslocation of misfolded class I HC targeted for proteasomal degradation. Tunicamycin 68-79 thioredoxin related transmembrane protein 1 Homo sapiens 22-25 19699254-4 2009 Capsaicin also induced degradation of tumor suppressor p53; this effect was enhanced by the ER stressor tunicamycin. Tunicamycin 104-115 tumor protein p53 Homo sapiens 55-58 19777212-0 2009 Tunicamycin induces resistance to camptothecin and etoposide in human hepatocellular carcinoma cells: role of cell-cycle arrest and GRP78. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 132-137 19777212-11 2009 Furthermore, the cells transfected with GRP78 siRNA were partly resistant to tunicamycin-induced apoptosis but not the inhibitory effect on cell-cycle regulators indicating that GRP78 and G1 arrest are two independent factors to tunicamycin-induced resistance mechanism. Tunicamycin 77-88 heat shock protein family A (Hsp70) member 5 Homo sapiens 40-45 19777212-11 2009 Furthermore, the cells transfected with GRP78 siRNA were partly resistant to tunicamycin-induced apoptosis but not the inhibitory effect on cell-cycle regulators indicating that GRP78 and G1 arrest are two independent factors to tunicamycin-induced resistance mechanism. Tunicamycin 229-240 heat shock protein family A (Hsp70) member 5 Homo sapiens 40-45 19777212-12 2009 In conclusion, the data suggest that tunicamycin induces the resistance to topoisomerase inhibitors through GRP78 up-regulation and G1 arrest of the cell cycle. Tunicamycin 37-48 heat shock protein family A (Hsp70) member 5 Homo sapiens 108-113 19640905-6 2009 In the present study, we show that alpha-actinin-4 K256E upregulates grp94 and CHOP expression in COS cells and significantly exacerbates induction of bip and CHOP in GEC in the presence of tunicamycin. Tunicamycin 190-201 actinin alpha 4 Homo sapiens 35-50 19825181-6 2009 Three generations of barcode microarrays at 30, 8 and 5 microm features sizes independently identified the primary target of tunicamycin to be ALG7. Tunicamycin 125-136 UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase Saccharomyces cerevisiae S288C 143-147 19643964-8 2009 The induced caspase-4 and caspase-3 activities by tunicamycin and the stimulated IL-8 protein expression by IL-1beta were markedly reduced by caspase-4 inhibitor Z-LEVD-fmk. Tunicamycin 50-61 caspase 4 Homo sapiens 12-21 19643964-8 2009 The induced caspase-4 and caspase-3 activities by tunicamycin and the stimulated IL-8 protein expression by IL-1beta were markedly reduced by caspase-4 inhibitor Z-LEVD-fmk. Tunicamycin 50-61 caspase 3 Homo sapiens 26-35 19643964-8 2009 The induced caspase-4 and caspase-3 activities by tunicamycin and the stimulated IL-8 protein expression by IL-1beta were markedly reduced by caspase-4 inhibitor Z-LEVD-fmk. Tunicamycin 50-61 caspase 4 Homo sapiens 142-151 19650649-6 2009 To address the role of Sep15 in protein folding, we analyzed changes in Sep15 expression in murine fibroblast NIH3T3 cells in response to tunicamycin, brefeldin A (brefA), thapsigargin, and DTT that lead to accumulation of unfolded proteins within the ER. Tunicamycin 138-149 selenoprotein F Mus musculus 72-77 19282840-6 2009 Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro. Tunicamycin 97-108 CCAAT enhancer binding protein beta Homo sapiens 238-247 19282840-6 2009 Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro. Tunicamycin 97-108 Kruppel like factor 4 Homo sapiens 249-253 19282840-6 2009 Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro. Tunicamycin 97-108 ATP binding cassette subfamily A member 12 Homo sapiens 259-265 19282840-6 2009 Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro. Tunicamycin 110-112 CCAAT enhancer binding protein beta Homo sapiens 238-247 19282840-6 2009 Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro. Tunicamycin 110-112 Kruppel like factor 4 Homo sapiens 249-253 19282840-6 2009 Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro. Tunicamycin 110-112 ATP binding cassette subfamily A member 12 Homo sapiens 259-265 19724688-4 2009 This was primarily because of the inhibition of Mcl-1 by obatoclax, in that cotreatment with TM and another BH3 mimetic ABT737, which does not antagonize Mcl-1, caused only minimal increases in apoptosis. Tunicamycin 93-95 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 48-53 19561031-4 2009 Our data show that the proteolytic cleavage of the rodent Muc3 SEA module was partially prevented by treatment with tunicamycin, an inhibitor of N-glycosylation. Tunicamycin 116-127 MUC3 Homo sapiens 58-62 19615339-3 2009 CRELD2 mRNA is also shown to be immediately induced by treatment with the ER stress-inducing reagents tunicamycin and brefeldin A. Tunicamycin 102-113 cysteine-rich with EGF-like domains 2 Mus musculus 0-6 19650649-7 2009 We show that expression of this protein is transcriptionally up-regulated in response to adaptive UPR caused by tunicamycin and brefA, whereas acute ER stress caused by DTT and thapsigargin leads to rapid and specific degradation of Sep15 by proteasomes. Tunicamycin 112-123 selenoprotein F Mus musculus 233-238 19501045-5 2009 In neuroepithelial cells treated with tunicamycin, an N-glycosylation inhibitor, unglycosylated form of gp130 was detected. Tunicamycin 38-49 interleukin 6 signal transducer Mus musculus 104-109 19492336-4 2009 Incubation of mesangial cells with ER stress-inducing agents (thapsigargin, tunicamycin, and AB(5) subtilase cytotoxin) resulted in a decrease in connexin 43 (Cx43) expression at both protein and mRNA levels. Tunicamycin 76-87 gap junction protein alpha 1 Homo sapiens 146-157 19130057-0 2009 Activation of ER stress and inhibition of EGFR N-glycosylation by tunicamycin enhances susceptibility of human non-small cell lung cancer cells to erlotinib. Tunicamycin 66-77 epidermal growth factor receptor Homo sapiens 42-46 19130057-5 2009 We found that tunicamycin generated an aglycosylated form of 130 kDa EGFR. Tunicamycin 14-25 epidermal growth factor receptor Homo sapiens 69-73 19130057-6 2009 Tunicamycin additionally affected EGFR activation and subcellular localization. Tunicamycin 0-11 epidermal growth factor receptor Homo sapiens 34-38 19130057-7 2009 Interestingly, the combination of tunicamycin and erlotinib caused more inhibitory effect on EGFR phosphorylation than that of erlotinib alone. Tunicamycin 34-45 epidermal growth factor receptor Homo sapiens 93-97 19130057-9 2009 CONCLUSIONS: Overall, our data demonstrate that tunicamycin significantly enhances the susceptibility of lung cancer cells to erlotinib, particularly sensitizing resistant cell lines to erlotinib, and that such sensitization may be associated with activation of the ER stress pathway and with inhibition of EGFR N-glycosylation. Tunicamycin 48-59 epidermal growth factor receptor Homo sapiens 307-311 19492336-4 2009 Incubation of mesangial cells with ER stress-inducing agents (thapsigargin, tunicamycin, and AB(5) subtilase cytotoxin) resulted in a decrease in connexin 43 (Cx43) expression at both protein and mRNA levels. Tunicamycin 76-87 gap junction protein alpha 1 Homo sapiens 159-163 19411306-0 2009 Knockdown of ERp57 increases BiP/GRP78 induction and protects against hyperoxia and tunicamycin-induced apoptosis. Tunicamycin 84-95 protein disulfide isomerase family A member 3 Homo sapiens 13-18 19411306-6 2009 Transient transfection of ERp57 small interfering RNA significantly knocked down ERp57 expression and reduced hyperoxia- or tunicamycin-induced apoptosis in human endothelial cells. Tunicamycin 124-135 protein disulfide isomerase family A member 3 Homo sapiens 26-31 19411306-8 2009 The activation of caspase-3 induced by hyperoxia or tunicamycin was diminished and immunoglobulin heavy chain-binding protein/glucose-regulated protein 78-kDa (BiP/GRP78) induction was increased in ERp57 knockdown cells. Tunicamycin 52-63 caspase 3 Homo sapiens 18-27 19411306-9 2009 Overexpression of ERp57 exacerbated hyperoxia- or tunicamycin-induced apoptosis in human endothelial cells. Tunicamycin 50-61 protein disulfide isomerase family A member 3 Homo sapiens 18-23 19411306-11 2009 Overexpression of ERp57 also augmented tunicamycin-induced caspase-3 activation and reduced BiP/GRP78 induction. Tunicamycin 39-50 protein disulfide isomerase family A member 3 Homo sapiens 18-23 19411306-11 2009 Overexpression of ERp57 also augmented tunicamycin-induced caspase-3 activation and reduced BiP/GRP78 induction. Tunicamycin 39-50 caspase 3 Homo sapiens 59-68 19411306-13 2009 It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction. Tunicamycin 85-96 protein disulfide isomerase family A member 3 Homo sapiens 29-34 19411306-13 2009 It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction. Tunicamycin 85-96 caspase 3 Homo sapiens 132-141 19411306-13 2009 It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction. Tunicamycin 85-96 heat shock protein family A (Hsp70) member 5 Homo sapiens 172-175 19242657-0 2009 Tunicamycin suppresses cisplatin-induced HepG2 cell apoptosis via enhancing p53 protein nuclear export. Tunicamycin 0-11 tumor protein p53 Homo sapiens 76-79 19242657-4 2009 In order to further explore the mechanism underlying tumor resistance to cisplatin, we observed that increased nuclear export of endogenous p53 protein by pharmacological inducers of ER stress, such as tunicamycin, was associated with the suppression of cisplatin-induced apoptosis. Tunicamycin 202-213 tumor protein p53 Homo sapiens 140-143 19443639-6 2009 Bsg isolated from HL-60 cells bound to E-selectin, and tunicamycin treatment to abolish N-linked glycans from Bsg abrogated this binding. Tunicamycin 55-66 basigin (Ok blood group) Homo sapiens 110-113 19411306-13 2009 It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction. Tunicamycin 85-96 heat shock protein family A (Hsp70) member 5 Homo sapiens 176-181 19276076-8 2009 Mesangial cell cultures treated with poly(I:C) or tunicamycin in normal glucose media synthesized monocyte-adhesive hyaluronan matrices but with concurrent down-regulation of cyclin D3. Tunicamycin 50-61 cyclin D3 Rattus norvegicus 175-184 19454717-8 2009 The suppression of NF-kappaB was reproduced by other inducers of UPR including AB(5) subtilase cytotoxin, tunicamycin, thapsigargin, and A23187. Tunicamycin 106-117 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 19-28 19582722-7 2009 The 2-D apoB profile obtained from the media of HepG2 cells treated in the presence of agents (tunicamycin and glucosamine) known to modulate the PTM of apoB was distinct from that of control cells. Tunicamycin 95-106 apolipoprotein B Homo sapiens 8-12 19582722-7 2009 The 2-D apoB profile obtained from the media of HepG2 cells treated in the presence of agents (tunicamycin and glucosamine) known to modulate the PTM of apoB was distinct from that of control cells. Tunicamycin 95-106 apolipoprotein B Homo sapiens 153-157 19251702-6 2009 Conversely, the hypersensitivity of lrk-1 mutant animals to the endoplasmic reticulum stressor tunicamycin was reduced in a pink-1 mutant background. Tunicamycin 95-106 Leucine-rich repeat serine/threonine-protein kinase 1 Caenorhabditis elegans 36-41 19251702-6 2009 Conversely, the hypersensitivity of lrk-1 mutant animals to the endoplasmic reticulum stressor tunicamycin was reduced in a pink-1 mutant background. Tunicamycin 95-106 PTEN induced kinase 1 Homo sapiens 124-130 19424594-5 2009 Importantly, both PI3K inhibitor LY294002 and dominant-negative Akt construct promoted tunicamycin- and thapsigargin-induced ERK phosphorylation. Tunicamycin 87-98 AKT serine/threonine kinase 1 Homo sapiens 64-67 19424594-5 2009 Importantly, both PI3K inhibitor LY294002 and dominant-negative Akt construct promoted tunicamycin- and thapsigargin-induced ERK phosphorylation. Tunicamycin 87-98 mitogen-activated protein kinase 1 Homo sapiens 125-128 19369942-2 2009 We found that the FG-specific Kss1 MAPK is activated by a combination of an O-glycosylation defect caused by disruption of the gene encoding the protein O-mannosyltransferase Pmt4, and an N-glycosylation defect induced by tunicamycin. Tunicamycin 222-233 mitogen-activated serine/threonine-protein kinase KSS1 Saccharomyces cerevisiae S288C 30-34 19406177-7 2009 Furthermore, in vitro, ghrelin directly inhibited the myocardial ERS response induced by tunicamycin or dithiothreitol in rat cardiac tissue. Tunicamycin 89-100 ghrelin and obestatin prepropeptide Rattus norvegicus 23-30 19307757-0 2009 Tunicamycin enhances TRAIL-induced apoptosis by inhibition of cyclin D1 and the subsequent downregulation of survivin. Tunicamycin 0-11 TNF superfamily member 10 Homo sapiens 21-26 19307757-0 2009 Tunicamycin enhances TRAIL-induced apoptosis by inhibition of cyclin D1 and the subsequent downregulation of survivin. Tunicamycin 0-11 cyclin D1 Homo sapiens 62-71 19307757-3 2009 In this study, we showed that tunicamycin, a naturally occurring antibiotic, was a potent enhancer of TRAIL-induced apoptosis through downregulation of survivin. Tunicamycin 30-41 TNF superfamily member 10 Homo sapiens 102-107 19307757-4 2009 The tunicamycin-mediated sensitization to TRAIL was efficiently reduced by forced expression of survivin, suggesting that the sensitization was mediated at least in part through inhibition of survivin expression. Tunicamycin 4-15 TNF superfamily member 10 Homo sapiens 42-47 19307757-5 2009 Tunicamycin also repressed expression of cyclin D1, a cell cycle regulator commonly overexpressed in thyroid carcinoma. Tunicamycin 0-11 cyclin D1 Homo sapiens 41-50 19307757-6 2009 Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin. Tunicamycin 182-193 cyclin D1 Homo sapiens 161-170 19307757-6 2009 Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin. Tunicamycin 182-193 TNF superfamily member 10 Homo sapiens 206-211 19307757-7 2009 Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin. Tunicamycin 44-55 TNF superfamily member 10 Homo sapiens 65-70 19307757-7 2009 Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin. Tunicamycin 44-55 cyclin D1 Homo sapiens 140-149 19347031-3 2009 We targeted Bcl-2 to mitochondria or endoplasmic reticulum (ER) and induced apoptosis using several apoptotic stimuli that initiate ER and/or mitochondrial signaling pathways (UV radiation, TNF and cycloheximide, staurosporine, thapsigargin and tunicamycin). Tunicamycin 245-256 BCL2 apoptosis regulator Homo sapiens 12-17 19338771-5 2009 Tunicamycin-evoked changes in cellular Ca2+ fluxes coincided with decreased glycosylation of STIM1 protein. Tunicamycin 0-11 stromal interaction molecule 1 Homo sapiens 93-98 19188482-3 2009 Tunicamycin caused early activation of caspase-2, -3, -4, and -8, followed by apoptosis, whereas caspase-9 was slowly activated. Tunicamycin 0-11 caspase 2 Homo sapiens 39-64 19188482-5 2009 Tunicamycin induced apoptosis independently of the mitochondrial pathway but caused lysosomal destabilization followed by lysosomal membrane permeabilization (LMP), cathepsin B relocation from lysosomes to the cytosol, and caspase-8 and -3 activation. Tunicamycin 0-11 cathepsin B Homo sapiens 165-176 19188482-5 2009 Tunicamycin induced apoptosis independently of the mitochondrial pathway but caused lysosomal destabilization followed by lysosomal membrane permeabilization (LMP), cathepsin B relocation from lysosomes to the cytosol, and caspase-8 and -3 activation. Tunicamycin 0-11 caspase 8 Homo sapiens 223-239 19188482-9 2009 Activating GSK-3beta caused K562 cells to be susceptible to tunicamycin-induced apoptosis. Tunicamycin 60-71 glycogen synthase kinase 3 beta Homo sapiens 11-20 19360472-3 2009 The nuclear translocation of DHFR protein during apoptosis was independent of the cellular context, but it was more sensitive in cell death induction by DNA damaging agents such as doxorubicin, etoposide and ultraviolent radiation than endoplasmic reticulum stressors (brefeldin-A and tunicamycin) and anti-microtubule agents (paclitaxel and nocodozole). Tunicamycin 285-296 dihydrofolate reductase Homo sapiens 29-33 18661133-10 2009 In addition, the sensitivity to cytochalasin H and tunicamycin of breast cancer cell lines with low KSR1 expression, (HS578T and MDA-MB-231/ATCC), was increased relative to the sensitivity of breast cancer cells with higher levels of KSR1 (MCF7). Tunicamycin 51-62 kinase suppressor of ras 1 Homo sapiens 100-104 18661133-10 2009 In addition, the sensitivity to cytochalasin H and tunicamycin of breast cancer cell lines with low KSR1 expression, (HS578T and MDA-MB-231/ATCC), was increased relative to the sensitivity of breast cancer cells with higher levels of KSR1 (MCF7). Tunicamycin 51-62 kinase suppressor of ras 1 Homo sapiens 234-238 18661133-7 2009 Cytotoxicity of two agents, cytochalasin H and tunicamycin, identified through the COMPARE analysis of KSR1 expression and drug sensitivity, was also examined in wild type (KSR(+/+)) mouse embryo fibroblasts (MEFs) and MEFs deficient in KSR1 expression (KSR1(-/-)). Tunicamycin 47-58 kinase suppressor of ras 1 Mus musculus 103-107 18661133-7 2009 Cytotoxicity of two agents, cytochalasin H and tunicamycin, identified through the COMPARE analysis of KSR1 expression and drug sensitivity, was also examined in wild type (KSR(+/+)) mouse embryo fibroblasts (MEFs) and MEFs deficient in KSR1 expression (KSR1(-/-)). Tunicamycin 47-58 kinase suppressor of ras 1 Mus musculus 103-106 19302790-3 2009 X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts. Tunicamycin 95-106 X-box binding protein 1 Homo sapiens 0-15 18661133-8 2009 These studies demonstrated enhanced sensitivity, as well as increased ERK activation, in KSR(-/-) MEFs following exposure to tunicamycin or cytochalasin H compared to KSR(+/+) MEFs. Tunicamycin 125-136 kinase suppressor of ras 1 Homo sapiens 89-92 18661133-9 2009 Furthermore, restoration of KSR1 expression in KSR(-/-) MEFs following stable transduction of cells with a KSR1 expression vector, enhanced sensitivity of cells to tunicamycin and cytochalasin H and decreased ERK1/2 activation following exposure to these drugs. Tunicamycin 164-175 kinase suppressor of ras 1 Homo sapiens 28-32 18661133-9 2009 Furthermore, restoration of KSR1 expression in KSR(-/-) MEFs following stable transduction of cells with a KSR1 expression vector, enhanced sensitivity of cells to tunicamycin and cytochalasin H and decreased ERK1/2 activation following exposure to these drugs. Tunicamycin 164-175 kinase suppressor of ras 1 Homo sapiens 28-31 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 calpain 2 Rattus norvegicus 204-213 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 1B Rattus norvegicus 215-220 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 90 beta family member 1 Rattus norvegicus 222-227 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 19367787-7 2009 Pretreatment with 50 microg/kg tunicamycin significantly reduced HSP70 in cortical tissue samples taken from sham-operated rats and appeared to attenuate the threshold for activation of m-calpain in rats undergoing 4 h of MCAO. Tunicamycin 31-42 heat shock protein family A (Hsp70) member 1B Rattus norvegicus 65-70 19367787-7 2009 Pretreatment with 50 microg/kg tunicamycin significantly reduced HSP70 in cortical tissue samples taken from sham-operated rats and appeared to attenuate the threshold for activation of m-calpain in rats undergoing 4 h of MCAO. Tunicamycin 31-42 calpain 2 Rattus norvegicus 186-195 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 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 90 beta family member 1 Rattus norvegicus 244-249 19302790-0 2009 ATM blocks tunicamycin-induced endoplasmic reticulum stress. Tunicamycin 11-22 ATM serine/threonine kinase Homo sapiens 0-3 19302790-2 2009 We present here conclusive data showing that ATM blocks ER-stress induced by tunicamycin or ionizing radiation (IR). Tunicamycin 77-88 ATM serine/threonine kinase Homo sapiens 45-48 19122239-4 2009 ERdj5 promoted apoptosis in tunicamycin, thapsigargin, and bortezomib-treated cells. Tunicamycin 28-39 DnaJ heat shock protein family (Hsp40) member C10 Homo sapiens 0-5 19302790-3 2009 X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts. Tunicamycin 95-106 X-box binding protein 1 Homo sapiens 17-22 19302790-3 2009 X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts. Tunicamycin 95-106 heat shock protein family A (Hsp70) member 5 Homo sapiens 34-39 19302790-3 2009 X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts. Tunicamycin 95-106 ATM serine/threonine kinase Homo sapiens 116-119 19302790-4 2009 Activation of caspase-12 and caspase-3 by tunicamycin was significantly reduced in cells transfected with wild-type Atm (AT5BIVA/wtATM). Tunicamycin 42-53 caspase 3 Homo sapiens 29-38 19302790-4 2009 Activation of caspase-12 and caspase-3 by tunicamycin was significantly reduced in cells transfected with wild-type Atm (AT5BIVA/wtATM). Tunicamycin 42-53 ATM serine/threonine kinase Homo sapiens 116-119 19302790-4 2009 Activation of caspase-12 and caspase-3 by tunicamycin was significantly reduced in cells transfected with wild-type Atm (AT5BIVA/wtATM). Tunicamycin 42-53 ATM serine/threonine kinase Homo sapiens 121-134 19302790-5 2009 Atm knockdown by siRNA, however, noticeably elevated ER-stress and chemosensitivity to tunicamycin. Tunicamycin 87-98 ATM serine/threonine kinase Homo sapiens 0-3 18990090-8 2009 Lastly, the ER stressors tunicamycin, thapsigargin and Brefeldin A were found to inhibit basal Nrf1 activity by approximately 25%, and almost completely prevented induction of Nrf1-mediated transactivation by tBHQ. Tunicamycin 25-36 nuclear respiratory factor 1 Rattus norvegicus 95-99 19100962-4 2009 Both thapsigargin and tunicamycin elevated the mRNA level of MMP13 and phosphorylation of p38 MAPK. Tunicamycin 22-33 matrix metallopeptidase 13 Homo sapiens 61-66 19100962-4 2009 Both thapsigargin and tunicamycin elevated the mRNA level of MMP13 and phosphorylation of p38 MAPK. Tunicamycin 22-33 mitogen-activated protein kinase 14 Homo sapiens 90-93 18990090-8 2009 Lastly, the ER stressors tunicamycin, thapsigargin and Brefeldin A were found to inhibit basal Nrf1 activity by approximately 25%, and almost completely prevented induction of Nrf1-mediated transactivation by tBHQ. Tunicamycin 25-36 nuclear respiratory factor 1 Rattus norvegicus 176-180 19005738-4 2009 GDNF secretion was augmented by stimulation with high potassium, while it was inhibited by treatment with either tunicamycin, an inhibitor of protein glycosylation, or brefeldin A, a disturbing factor of ER-Golgi transport. Tunicamycin 113-124 glial cell derived neurotrophic factor Homo sapiens 0-4 19180501-10 2009 Incubation with 2 agents that induce endoplasmic reticulum stress, tunicamycin and thapsigargin, increased TRB3 levels in normal cells. Tunicamycin 67-78 tribbles pseudokinase 3 Homo sapiens 107-111 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 19567124-6 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 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 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 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 DNA-damage inducible transcript 3 Rattus norvegicus 80-84 19166345-12 2009 Inhibition of hH(4)R glycosylation by tunicamycin reduced the [(3)H]HA binding B(max) value. Tunicamycin 38-49 histamine receptor H4 Homo sapiens 14-20 18840095-2 2009 The present study shows that ASNS (asparagine synthetase) transcription activity was up-regulated in HepG2 cells treated with the UPR activators thapsigargin and tunicamycin. Tunicamycin 162-173 asparagine synthetase (glutamine-hydrolyzing) Homo sapiens 29-33 18840095-2 2009 The present study shows that ASNS (asparagine synthetase) transcription activity was up-regulated in HepG2 cells treated with the UPR activators thapsigargin and tunicamycin. Tunicamycin 162-173 asparagine synthetase (glutamine-hydrolyzing) Homo sapiens 35-56 18814142-4 2009 Exposure to adrenaline not only increased cAMP formation, phosphorylation of cAMP responsive element (CRE) binding protein (CREB) on serine133 and CRE reporter activity in a manner sensitive to propranolol, but also rendered C3H10T1/2 cells resistant to the cytotoxicity of hydrogen peroxide, but not of either 2,4-dinitirophenol or tunicamycin. Tunicamycin 333-344 cAMP responsive element binding protein 1 Mus musculus 124-128 18978361-0 2009 Tunicamycin enhances the apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand in endometriotic stromal cells. Tunicamycin 0-11 TNF superfamily member 10 Homo sapiens 46-101 18978361-2 2009 In the present study, the effect of tunicamycin, a possible apoptosis enhancer, on TRAIL-induced apoptosis in endometriotic stromal cells (ESC) was determined. Tunicamycin 36-47 TNF superfamily member 10 Homo sapiens 83-88 18978361-8 2009 RESULTS: Tunicamycin increases both DR5 mRNA (P < 0.005) and TRAIL-induced apoptosis (P < 0.0001) in ESC. Tunicamycin 9-20 TNF receptor superfamily member 10b Homo sapiens 36-39 18978361-8 2009 RESULTS: Tunicamycin increases both DR5 mRNA (P < 0.005) and TRAIL-induced apoptosis (P < 0.0001) in ESC. Tunicamycin 9-20 TNF superfamily member 10 Homo sapiens 64-69 18978361-9 2009 The increase in TRAIL-induced apoptosis in ESC by tunicamycin was suppressed (P < 0.05) by z-VAD-fmk. Tunicamycin 50-61 TNF superfamily member 10 Homo sapiens 16-21 18978361-10 2009 Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin. Tunicamycin 43-54 TNF receptor superfamily member 10b Homo sapiens 18-21 18978361-10 2009 Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin. Tunicamycin 43-54 TNF receptor superfamily member 10b Homo sapiens 75-78 18978361-10 2009 Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin. Tunicamycin 146-157 TNF receptor superfamily member 10b Homo sapiens 18-21 18978361-10 2009 Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin. Tunicamycin 146-157 TNF superfamily member 10 Homo sapiens 119-124 18981290-5 2009 Tunicamycin treatment markedly decreased the secretion of ADAMTS13 into the culture medium of transfected cells. Tunicamycin 0-11 A disintegrin and metalloproteinase with thrombospondin motifs 13 Cricetulus griseus 58-66 19007793-6 2009 Reconstitution of PKR and PACT expression in the null cells renders them sensitive to tunicamycin, thus demonstrating that PACT-induced PKR activation plays an essential function in induction of apoptosis. Tunicamycin 86-97 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 18-21 19007793-6 2009 Reconstitution of PKR and PACT expression in the null cells renders them sensitive to tunicamycin, thus demonstrating that PACT-induced PKR activation plays an essential function in induction of apoptosis. Tunicamycin 86-97 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 26-30 19007793-0 2009 Essential role of PACT-mediated PKR activation in tunicamycin-induced apoptosis. Tunicamycin 50-61 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 18-22 19007793-6 2009 Reconstitution of PKR and PACT expression in the null cells renders them sensitive to tunicamycin, thus demonstrating that PACT-induced PKR activation plays an essential function in induction of apoptosis. Tunicamycin 86-97 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 123-127 19007793-0 2009 Essential role of PACT-mediated PKR activation in tunicamycin-induced apoptosis. Tunicamycin 50-61 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 32-35 19007793-6 2009 Reconstitution of PKR and PACT expression in the null cells renders them sensitive to tunicamycin, thus demonstrating that PACT-induced PKR activation plays an essential function in induction of apoptosis. Tunicamycin 86-97 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 136-139 19007793-3 2009 In this study, we examined the involvement of double-stranded RNA (dsRNA)-activated protein kinase (PKR) and its protein activator PACT in tunicamycin-induced apoptosis. Tunicamycin 139-150 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 100-103 19026635-5 2009 In the present study, we show that glycosylation is an essential requirement for surface nucleolin expression, since it is prevented when cells are cultured in the presence of tunicamycin, an inhibitor of N-glycosylation. Tunicamycin 176-187 nucleolin Homo sapiens 89-98 19007793-3 2009 In this study, we examined the involvement of double-stranded RNA (dsRNA)-activated protein kinase (PKR) and its protein activator PACT in tunicamycin-induced apoptosis. Tunicamycin 139-150 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 131-135 19007793-4 2009 We demonstrate for the first time that PACT is phosphorylated in response to tunicamycin and is responsible for PKR activation by direct interaction. Tunicamycin 77-88 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 39-43 19007793-4 2009 We demonstrate for the first time that PACT is phosphorylated in response to tunicamycin and is responsible for PKR activation by direct interaction. Tunicamycin 77-88 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 112-115 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 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 13-17 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 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 26-29 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 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 95-99 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 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 111-114 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 eukaryotic translation initiation factor 2A Homo sapiens 183-192 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 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 152-163 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 13-17 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 152-163 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 26-29 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 152-163 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 111-114 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 152-163 protein activator of interferon induced protein kinase EIF2AK2 Homo sapiens 13-17 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 152-163 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 26-29 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 152-163 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 111-114 19124762-3 2009 Priming of the cells with ER stress inducers (tunicamycin, thapsigargin, A23187, and AB5 subtilase cytotoxin) caused blunted induction of MCP-1 in response to TNF-alpha, IL-1beta, macrophage-derived factors, or bystander macrophages. Tunicamycin 46-57 C-C motif chemokine ligand 2 Homo sapiens 138-143 19047052-10 2009 We have found that Nrf3 is activated by the ER stressors tunicamycin and brefeldin A, and that NHB1 is required for this response. Tunicamycin 57-68 nuclear factor, erythroid derived 2, like 3 Mus musculus 19-23 19124762-3 2009 Priming of the cells with ER stress inducers (tunicamycin, thapsigargin, A23187, and AB5 subtilase cytotoxin) caused blunted induction of MCP-1 in response to TNF-alpha, IL-1beta, macrophage-derived factors, or bystander macrophages. Tunicamycin 46-57 tumor necrosis factor Homo sapiens 159-168 19124762-3 2009 Priming of the cells with ER stress inducers (tunicamycin, thapsigargin, A23187, and AB5 subtilase cytotoxin) caused blunted induction of MCP-1 in response to TNF-alpha, IL-1beta, macrophage-derived factors, or bystander macrophages. Tunicamycin 46-57 interleukin 1 beta Homo sapiens 170-178 19239156-6 2009 After tunicamycin-mediated ERS, the expression of the key molecular chaperone, Bip, increased in both cell lines. Tunicamycin 6-17 heat shock protein 5 Mus musculus 79-82 19239156-7 2009 The chaperone, GRP94, responded differently to extended tunicamycin treatment, with protein levels remaining largely unchanged in 3T3L1 cells but falling in C2C12 cells. Tunicamycin 56-67 heat shock protein 90, beta (Grp94), member 1 Mus musculus 15-20 18650099-7 2008 Following tunicamycin treatment the secretion of additional proteins as well as ER-resident chaperones from the Hsp70 and Hsp90 families outside the protoplasts was noted. Tunicamycin 10-21 heat shock protein 70 Arabidopsis thaliana 112-117 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 tribbles pseudokinase 3 Rattus norvegicus 30-56 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 tribbles pseudokinase 3 Rattus norvegicus 58-62 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 18757512-1 2009 PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. Tunicamycin 167-178 heat shock protein 5 Mus musculus 83-88 18757512-1 2009 PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. Tunicamycin 167-178 heat shock protein 5 Mus musculus 90-132 18757512-1 2009 PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. Tunicamycin 167-178 heat shock protein 5 Mus musculus 134-137 18757512-1 2009 PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. Tunicamycin 167-178 heat shock protein 5 Mus musculus 139-142 18757512-1 2009 PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. Tunicamycin 252-263 heat shock protein 5 Mus musculus 83-88 18757512-1 2009 PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. Tunicamycin 252-263 heat shock protein 5 Mus musculus 90-132 18757512-1 2009 PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. Tunicamycin 252-263 heat shock protein 5 Mus musculus 134-137 18757512-1 2009 PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. Tunicamycin 252-263 heat shock protein 5 Mus musculus 139-142 18757512-3 2009 The effect of BIX on tunicamycin (at 2 microg/mL)-induced damage was evaluated by measuring the cell-death rate and CHOP protein expression. Tunicamycin 21-32 DNA-damage inducible transcript 3 Mus musculus 116-120 18757512-5 2009 The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression. Tunicamycin 35-46 germ cell-less, spermatogenesis associated 1 Mus musculus 123-126 18757512-5 2009 The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression. Tunicamycin 35-46 deoxynucleotidyltransferase, terminal Mus musculus 139-180 18757512-5 2009 The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression. Tunicamycin 35-46 deoxynucleotidyltransferase, terminal Mus musculus 182-185 18757512-5 2009 The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression. Tunicamycin 35-46 DNA-damage inducible transcript 3 Mus musculus 241-245 18757512-7 2009 BIX (1 and 5 microM) significantly reduced tunicamycin-induced cell death, and BIX (5 microM) significantly reduced tunicamycin-induced CHOP protein expression. Tunicamycin 116-127 DNA-damage inducible transcript 3 Mus musculus 136-140 18757512-9 2009 Co-administration of BIX (5 nmol) significantly reduced both the retinal cell death and the CHOP protein expression in GCL induced by intravitreal injection of tunicamycin or NMDA. Tunicamycin 160-171 DNA-damage inducible transcript 3 Mus musculus 92-96 18757512-9 2009 Co-administration of BIX (5 nmol) significantly reduced both the retinal cell death and the CHOP protein expression in GCL induced by intravitreal injection of tunicamycin or NMDA. Tunicamycin 160-171 germ cell-less, spermatogenesis associated 1 Mus musculus 119-122 18778408-5 2008 Interestingly, when cells are depleted of cholesterol and treated with tunicamycin, treatments that by themselves do not affect PLAP sorting, PLAP is not able to oligomerize and is missorted to the basolateral surface, thus supporting an indirect role of N-glycosylation, possibly mediated by a raft-associated glycosylated interactor. Tunicamycin 71-82 alkaline phosphatase, placental Homo sapiens 142-146 18768906-4 2008 Tunicamycin treatment or expression in the stt3a-2 mutant relieved the folding block, and migration to Golgi stacks resumed. Tunicamycin 0-11 staurosporin and temperature sensitive 3-like A Arabidopsis thaliana 43-48 19028522-4 2009 Pretreatment with 100 microM alpha-mannosidase inhibitor 1-deoxymannojirimycin (DMJ) in PC-12 cells significantly attenuated the cytotoxicity by ER stressors tunicamycin (TM), thapsigargin (TG), and amyloid beta1-42 (Abeta1-42), and reduced caspase-3 activation by TM and TG. Tunicamycin 171-173 caspase 3 Rattus norvegicus 241-250 18691157-2 2008 Addressing the cytoprotective functions of PON2, we observed that PON2 overexpression provided significant resistance to ER-stress-induced caspase 3 activation when the ER stress was induced by interference with protein modification (by tunicamycin or dithiothreitol), but not when ER stress was induced by disturbance of Ca(2+) homoeostasis (by thapsigargin or A23187). Tunicamycin 237-248 paraoxonase 2 Homo sapiens 66-70 18691157-4 2008 However, only tunicamycin and dithiothreitol resulted in increased PON2 mRNA and protein levels. Tunicamycin 14-25 paraoxonase 2 Homo sapiens 67-71 18791174-4 2008 Effects of tunicamycin and thapsigargin on IL-1beta- and TNF-alpha-stimulated MCP-1 mRNA expression and protein production were further examined by RT-PCR and ELISA, respectively. Tunicamycin 11-22 interleukin 1 beta Homo sapiens 43-51 18791174-4 2008 Effects of tunicamycin and thapsigargin on IL-1beta- and TNF-alpha-stimulated MCP-1 mRNA expression and protein production were further examined by RT-PCR and ELISA, respectively. Tunicamycin 11-22 tumor necrosis factor Homo sapiens 57-66 18791174-4 2008 Effects of tunicamycin and thapsigargin on IL-1beta- and TNF-alpha-stimulated MCP-1 mRNA expression and protein production were further examined by RT-PCR and ELISA, respectively. Tunicamycin 11-22 C-C motif chemokine ligand 2 Homo sapiens 78-83 18791174-8 2008 Compared to Cys and IL-10, the ER stress activators tunicamycin and thapsigargin were even more potent enhancers of hRPE caspase-12S gene expression. Tunicamycin 52-63 ribulose-5-phosphate-3-epimerase Homo sapiens 116-120 18799549-6 2008 In tumor necrosis factor (TNF)-alpha-treated cells, suppression of MCP-1 by indomethacin was inversely correlated with induction of UPR, and other inducers of UPR including tunicamycin, thapsigargin, and A23187 reproduced the suppressive effect. Tunicamycin 173-184 tumor necrosis factor Mus musculus 3-36 18626793-6 2008 Since PAC1-R mRNA expression was induced by NGF, PACAP exhibited neuroprotective effect against tunicamycin-induced cell death in the differentiated PC12 cells. Tunicamycin 96-107 ADCYAP receptor type I Rattus norvegicus 6-12 18626793-6 2008 Since PAC1-R mRNA expression was induced by NGF, PACAP exhibited neuroprotective effect against tunicamycin-induced cell death in the differentiated PC12 cells. Tunicamycin 96-107 adenylate cyclase activating polypeptide 1 Rattus norvegicus 49-54 19017746-6 2008 The bZIP60 protein resides in the ER membrane under unstressed condition and is cleaved in response to ER stress caused by either tunicamycin or DTT. Tunicamycin 130-141 basic region/leucine zipper motif 60 Arabidopsis thaliana 4-10 18839021-2 2008 METHODS: rNav1.3 was expressed in Xenopus oocyte, with glycosylation inhibition by using tunicamycin. Tunicamycin 89-100 sodium voltage-gated channel alpha subunit 3 Rattus norvegicus 9-16 18847488-4 2008 RESULTS: Tunicamycin treatment demonstrated that human OSTalpha is glycosylated. Tunicamycin 9-20 solute carrier family 51 subunit alpha Homo sapiens 55-63 18847488-6 2008 Immunofluorescence of both cells indicated that, in the presence of OSTbeta, the alpha subunit could still be expressed on the plasma membrane after tunicamycin treatment. Tunicamycin 149-160 solute carrier family 51 subunit beta Homo sapiens 68-75 18838865-3 2008 Here, we show by epistatic analysis that p53 inhibition results in a maximum level of autophagy that cannot be further enhanced by a variety of different autophagy inducers including lithium, tunicamycin-induced stress of the endoplasmic reticulum (ER) or inhibition of Bcl-2 and Bcl-X(L) with the BH3 mimetic ABT737. Tunicamycin 192-203 tumor protein p53 Homo sapiens 41-44 18838865-4 2008 Chemical inducers of autophagy (including rapamycin, lithium, tunicamycin and ABT737) induced rapid depletion of the p53 protein. Tunicamycin 62-73 tumor protein p53 Homo sapiens 117-120 18788711-3 2008 Both Chinese propolis and chrysin concentration-dependently inhibited such cell death, the tunicamycin-induced activation of caspase-3, and the effects of tunicamycin on mitochondria [release of cytochrome c into the cytosol and disruption of the mitochondrial membrane potential (DeltaPsim)]. Tunicamycin 91-102 caspase 3 Homo sapiens 125-134 18788711-3 2008 Both Chinese propolis and chrysin concentration-dependently inhibited such cell death, the tunicamycin-induced activation of caspase-3, and the effects of tunicamycin on mitochondria [release of cytochrome c into the cytosol and disruption of the mitochondrial membrane potential (DeltaPsim)]. Tunicamycin 155-166 cytochrome c, somatic Homo sapiens 195-207 18704925-7 2008 However, upon treatment with tunicamycin, which induces an endoplasmic reticulum (ER)-stress response, CrebH(-/-) mice displayed reduced expression of acute phase response proteins. Tunicamycin 29-40 cAMP responsive element binding protein 3-like 3 Mus musculus 103-108 18701708-8 2008 Apoptotic death caused by tunicamycin was dramatically reduced in a strain expressing endogenous levels of calnexin lacking its TM and cytosolic tail. Tunicamycin 26-37 calnexin Homo sapiens 107-115 18549807-2 2008 In HEK293-corin cells, the inhibition of N-glycosylation, with tunicamycin, reduced the cell-surface expression of murine corin, but did not alter the total expression. Tunicamycin 63-74 corin, serine peptidase Mus musculus 10-15 18718935-4 2008 Tunicamycin treatment of Arabidopsis cells, which causes ER stress, led to up-regulation of AtERdj3A, AtERdj3B, AtP58(IPK) and AtERdj2B. Tunicamycin 0-11 DNAJ heat shock N-terminal domain-containing protein Arabidopsis thaliana 92-100 18718935-4 2008 Tunicamycin treatment of Arabidopsis cells, which causes ER stress, led to up-regulation of AtERdj3A, AtERdj3B, AtP58(IPK) and AtERdj2B. Tunicamycin 0-11 DNAJ heat shock family protein Arabidopsis thaliana 102-110 18718935-4 2008 Tunicamycin treatment of Arabidopsis cells, which causes ER stress, led to up-regulation of AtERdj3A, AtERdj3B, AtP58(IPK) and AtERdj2B. Tunicamycin 0-11 DnaJ / Sec63 Brl domains-containing protein Arabidopsis thaliana 127-135 18602013-2 2008 We have characterized the global transcriptional response of Candida albicans to ER stresses (dithiothreitol and tunicamycin) and established the impact of the transcription factor Hac1 upon this response. Tunicamycin 113-124 transcription factor HAC1 Saccharomyces cerevisiae S288C 181-185 18628206-7 2008 Expression of ERp16 in HeLa cells inhibited the induction of apoptosis by agents that elicit ER stress, including brefeldin A, tunicamycin, and dithiothreitol. Tunicamycin 127-138 thioredoxin domain containing 12 Homo sapiens 14-19 18682497-5 2008 Unglycosylated CFTR, generated by removal of glycosylation sites or treatment of cells with the N-glycosylation inhibitor tunicamycin, did not bind calnexin, but did traffic to the cell surface and exhibited chloride channel activity. Tunicamycin 122-133 CF transmembrane conductance regulator Homo sapiens 15-19 18549807-2 2008 In HEK293-corin cells, the inhibition of N-glycosylation, with tunicamycin, reduced the cell-surface expression of murine corin, but did not alter the total expression. Tunicamycin 63-74 corin, serine peptidase Mus musculus 122-127 18549807-3 2008 Therefore, tunicamycin treatment likely caused the intracellular accumulation of non-glycosylated corin. Tunicamycin 11-22 corin, serine peptidase Mus musculus 98-103 18549807-4 2008 Tunicamycin treatment also significantly reduced corin activity (pro-ANP cleavage) in these cells. Tunicamycin 0-11 corin, serine peptidase Mus musculus 49-54 18604159-6 2008 Several distinct autophagy inducers (e.g., starvation, rapamycin, lithium, tunicamycin and thapsigargin) stimulate the rapid degradation of p53. Tunicamycin 75-86 tumor protein p53 Homo sapiens 140-143 18701495-3 2008 Inhibition of Mcl-1 by small interference RNA (siRNA) rendered melanoma cells sensitive to apoptosis induced by the ER stress inducers thapsigargin and tunicamycin, but this sensitization was partially reversed by siRNA knockdown of PUMA or Noxa, as shown in Mcl-1-deficient melanoma cells. Tunicamycin 152-163 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 14-19 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 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 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 157-161 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 protein phosphatase 1 regulatory subunit 15A Homo sapiens 163-169 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 175-179 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 X-box binding protein 1 Homo sapiens 195-199 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 eukaryotic translation initiation factor 2A Homo sapiens 268-277 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 mitogen-activated protein kinase 8 Homo sapiens 279-283 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 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 289-294 18690846-3 2008 Immunoblots of whole cell lysates, subcellular fractionation and tunicamycin treatment of human tumor cells indicated that 4Ig-hB7H3 is a approximately 100-kDa N-linked glycosylated membrane protein. Tunicamycin 65-76 CD276 molecule Homo sapiens 123-132 18503006-8 2008 Grx6 and Grx7 have measurable oxidoreductase activity in vivo, which is increased in the presence of tunicamycin. Tunicamycin 101-112 glutathione-disulfide reductase GRX6 Saccharomyces cerevisiae S288C 0-4 18503006-8 2008 Grx6 and Grx7 have measurable oxidoreductase activity in vivo, which is increased in the presence of tunicamycin. Tunicamycin 101-112 glutathione-disulfide reductase GRX7 Saccharomyces cerevisiae S288C 9-13 18503006-8 2008 Grx6 and Grx7 have measurable oxidoreductase activity in vivo, which is increased in the presence of tunicamycin. Tunicamycin 101-112 oxidoreductase Saccharomyces cerevisiae S288C 30-44 18477628-7 2008 We observed that nicotine suppressed the Tm-induced, but not Tg-induced, splicing of XBP1 mRNA, and also suppressed the Tm-induced, but not Tg-induced, production of cleaved ATF6 in PC12 cells. Tunicamycin 41-43 X-box binding protein 1 Rattus norvegicus 85-89 18555216-9 2008 In contrast, tunicamycin (TM) strongly inhibited N-glycans incorporation into OA protein. Tunicamycin 13-24 glycoprotein (transmembrane) nmb Mus musculus 78-80 18555216-9 2008 In contrast, tunicamycin (TM) strongly inhibited N-glycans incorporation into OA protein. Tunicamycin 26-28 glycoprotein (transmembrane) nmb Mus musculus 78-80 18561914-8 2008 Overexpression of Armet/MANF inhibited cell proliferation and improved cell viability under glucose-free conditions and tunicamycin treatment. Tunicamycin 120-131 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 18-23 18561914-8 2008 Overexpression of Armet/MANF inhibited cell proliferation and improved cell viability under glucose-free conditions and tunicamycin treatment. Tunicamycin 120-131 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 24-28 18339707-7 2008 In addition, it was found that DHCR24 exerted cytoprotective effects in the tunicamycin-induced endoplasmic reticulum stress by eliminating ROS. Tunicamycin 76-87 24-dehydrocholesterol reductase Mus musculus 31-37 18376137-6 2008 We showed that during induction of autophagy by rapamycin, tunicamycin or starvation to amino acids, fluorescence intensity of GFP-LC3 is reduced in a time-dependent manner. Tunicamycin 59-70 microtubule associated protein 1 light chain 3 alpha Homo sapiens 131-134 18436549-8 2008 The Atcrt1a mutants exhibited increased sensitivity to the drug tunicamycin, an inducer of the unfolded protein response. Tunicamycin 64-75 calreticulin 1a Arabidopsis thaliana 4-11 18308848-4 2008 Silencing of MEKK-1 gene expression in betaTC-6 and human dispersed islet cells, using in vitro-generated diced small interfering RNA, resulted in protection from DETA/NO, STZ, H2O2, and tunicamycin induced cell death. Tunicamycin 187-198 mitogen-activated protein kinase kinase kinase 1 Homo sapiens 13-19 18064635-10 2008 Taking into account that induction of ER stress by tunicamycin and brefeldin A, without altering intracellular calcium concentrations, also increased HIF-1alpha mRNA, suggests that ER stress pathways enhanced transcription of HIF-1alpha mRNA. Tunicamycin 51-62 hypoxia inducible factor 1 subunit alpha Homo sapiens 150-160 18064635-10 2008 Taking into account that induction of ER stress by tunicamycin and brefeldin A, without altering intracellular calcium concentrations, also increased HIF-1alpha mRNA, suggests that ER stress pathways enhanced transcription of HIF-1alpha mRNA. Tunicamycin 51-62 hypoxia inducible factor 1 subunit alpha Homo sapiens 226-236 18600068-0 2008 Tunicamycin-induced ER stress upregulates the expression of mitochondrial HtrA2 and promotes apoptosis through the cytosolic release of HtrA2. Tunicamycin 0-11 HtrA serine peptidase 2 Homo sapiens 74-79 18600068-0 2008 Tunicamycin-induced ER stress upregulates the expression of mitochondrial HtrA2 and promotes apoptosis through the cytosolic release of HtrA2. Tunicamycin 0-11 HtrA serine peptidase 2 Homo sapiens 136-141 18600068-3 2008 In the present study, we have demonstrated that the HtrA2 protein level was gradually and significantly increased by up to 10-fold in the mitochondria under tunicamycin (Tm)-induced ER stress, which eventually promoted cell death through the release of HtrA2 into the cytoplasm. Tunicamycin 157-168 HtrA serine peptidase 2 Homo sapiens 52-57 18600068-3 2008 In the present study, we have demonstrated that the HtrA2 protein level was gradually and significantly increased by up to 10-fold in the mitochondria under tunicamycin (Tm)-induced ER stress, which eventually promoted cell death through the release of HtrA2 into the cytoplasm. Tunicamycin 157-168 HtrA serine peptidase 2 Homo sapiens 253-258 18600068-3 2008 In the present study, we have demonstrated that the HtrA2 protein level was gradually and significantly increased by up to 10-fold in the mitochondria under tunicamycin (Tm)-induced ER stress, which eventually promoted cell death through the release of HtrA2 into the cytoplasm. Tunicamycin 170-172 HtrA serine peptidase 2 Homo sapiens 52-57 18600068-3 2008 In the present study, we have demonstrated that the HtrA2 protein level was gradually and significantly increased by up to 10-fold in the mitochondria under tunicamycin (Tm)-induced ER stress, which eventually promoted cell death through the release of HtrA2 into the cytoplasm. Tunicamycin 170-172 HtrA serine peptidase 2 Homo sapiens 253-258 18356160-5 2008 Induction of ER stress by treatment with either thapsigargin or tunicamycin activated autophagy in immortalized hepatocytes as monitored by the conversion LC3-I to LC3-II, clustering of LC3 into dot-like cytoplasmic structures, and electron microscopic detection of autophagosomes. Tunicamycin 64-75 microtubule associated protein 1 light chain 3 alpha Homo sapiens 155-158 18356160-5 2008 Induction of ER stress by treatment with either thapsigargin or tunicamycin activated autophagy in immortalized hepatocytes as monitored by the conversion LC3-I to LC3-II, clustering of LC3 into dot-like cytoplasmic structures, and electron microscopic detection of autophagosomes. Tunicamycin 64-75 microtubule associated protein 1 light chain 3 alpha Homo sapiens 164-167 18356160-5 2008 Induction of ER stress by treatment with either thapsigargin or tunicamycin activated autophagy in immortalized hepatocytes as monitored by the conversion LC3-I to LC3-II, clustering of LC3 into dot-like cytoplasmic structures, and electron microscopic detection of autophagosomes. Tunicamycin 64-75 microtubule associated protein 1 light chain 3 alpha Homo sapiens 164-167 18466333-4 2008 Treatment of cultures with the endoplasmic reticulum (ER) stressor tunicamycin caused an increase in levels of 14-3-3 zeta within the ER-containing microsomal fraction, along with up-regulation of Lys-Asp-Glu-Leu-containing proteins and calnexin, and the selective death of dentate granule cells. Tunicamycin 67-78 tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide Mus musculus 111-122 18425424-6 2008 Inhibition of N-glycosylation by tunicamycin reduced both the enzymatic activity of extracellular NEP2 and the molecular size of intracellular NEP2. Tunicamycin 33-44 membrane metallo-endopeptidase-like 1 Mus musculus 98-102 18425424-6 2008 Inhibition of N-glycosylation by tunicamycin reduced both the enzymatic activity of extracellular NEP2 and the molecular size of intracellular NEP2. Tunicamycin 33-44 membrane metallo-endopeptidase-like 1 Mus musculus 143-147 18436549-9 2008 We therefore conclude that AtCRT1a is an alleviator of the tunicamycin-induced unfolded protein response, and propose that the use of the mouse crt-/- fibroblasts as a calreticulin expression system may prove useful to assess functionalities of calreticulins from different species. Tunicamycin 59-70 calreticulin 1a Arabidopsis thaliana 27-34 18483264-5 2008 Using the N-linked glycosylation inhibitor, tunicamycin, we show that expression levels of several RTKS (EGFR, ErbB2, ErbB3, and IGF-IR) are exquisitely sensitive to inhibition of N-linked glycosylation. Tunicamycin 44-55 epidermal growth factor receptor Homo sapiens 105-109 18483264-5 2008 Using the N-linked glycosylation inhibitor, tunicamycin, we show that expression levels of several RTKS (EGFR, ErbB2, ErbB3, and IGF-IR) are exquisitely sensitive to inhibition of N-linked glycosylation. Tunicamycin 44-55 erb-b2 receptor tyrosine kinase 2 Homo sapiens 111-116 18483264-5 2008 Using the N-linked glycosylation inhibitor, tunicamycin, we show that expression levels of several RTKS (EGFR, ErbB2, ErbB3, and IGF-IR) are exquisitely sensitive to inhibition of N-linked glycosylation. Tunicamycin 44-55 erb-b2 receptor tyrosine kinase 3 Homo sapiens 118-123 18483264-5 2008 Using the N-linked glycosylation inhibitor, tunicamycin, we show that expression levels of several RTKS (EGFR, ErbB2, ErbB3, and IGF-IR) are exquisitely sensitive to inhibition of N-linked glycosylation. Tunicamycin 44-55 insulin like growth factor 1 receptor Homo sapiens 129-135 17988239-9 2008 Provoking SA in vitro in the presence of the N-linked glycosylation blocker tunicamycin abrogated the activity-dependent increase of HCN1/HCN2 heteromerization. Tunicamycin 76-87 hyperpolarization activated cyclic nucleotide gated potassium channel 1 Homo sapiens 133-137 18395193-2 2008 We evaluated the effect of a selective inducer of immunoglobulin heavy chain binding protein (BiP) (BiP inducer X; BIX) against both tunicamycin-induced cell death (in SH-SY5Y cells) and the effects of global transient forebrain ischemia (in gerbils). Tunicamycin 133-144 heat shock protein family A (Hsp70) member 5 Homo sapiens 50-92 18395193-2 2008 We evaluated the effect of a selective inducer of immunoglobulin heavy chain binding protein (BiP) (BiP inducer X; BIX) against both tunicamycin-induced cell death (in SH-SY5Y cells) and the effects of global transient forebrain ischemia (in gerbils). Tunicamycin 133-144 heat shock protein family A (Hsp70) member 5 Homo sapiens 94-97 17624530-9 2008 In addition, IPI-504 also blocks the tunicamycin-induced phosphorylation of eIF2 by PERK. Tunicamycin 37-48 eukaryotic translation initiation factor 2 subunit beta Homo sapiens 76-80 17624530-9 2008 In addition, IPI-504 also blocks the tunicamycin-induced phosphorylation of eIF2 by PERK. Tunicamycin 37-48 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 84-88 18256359-7 2008 Of note, pretreatment with tunicamycin or thapsigargin decreased the excessive ER stress-induced intracellular signaling observed in anti-Thy1 nephritis. Tunicamycin 27-38 Thy-1 cell surface antigen Rattus norvegicus 138-142 18280615-3 2008 Analysis of propidium iodide uptake showed that TM-induced neuronal death in a concentration-dependent manner (20-80 microg/mL) and that the rank order of vulnerability among hippocampal subregions was dentate gyrus (DG)>CA1>CA3. Tunicamycin 48-50 carbonic anhydrase 1 Rattus norvegicus 224-227 18280615-3 2008 Analysis of propidium iodide uptake showed that TM-induced neuronal death in a concentration-dependent manner (20-80 microg/mL) and that the rank order of vulnerability among hippocampal subregions was dentate gyrus (DG)>CA1>CA3. Tunicamycin 48-50 carbonic anhydrase 3 Rattus norvegicus 231-234 18649184-6 2008 The temporal differences of Panx1 trafficking correlate with spatial differences of intracellular localizations induced by Golgi blockage by Brefeldin-A or glycosylation prevention by tunicamycin. Tunicamycin 184-195 pannexin 1 Homo sapiens 28-33 18375764-4 2008 We show that deglycosylation of cell surface proteins by glycosidase treatment, or inhibition of protein N-glycosylation by tunicamycin, ablates CyaA binding and penetration of CD11b-expressing cells. Tunicamycin 124-135 integrin subunit alpha M Homo sapiens 177-182 18379069-4 2008 Using primary cultured rat cortical neurons, we here examined whether expression of PLC-beta 1 and -gamma 1 was altered in ER stress-loaded neurons induced by tunicamycin (Tm). Tunicamycin 159-170 phospholipase C beta 1 Rattus norvegicus 84-107 18379069-4 2008 Using primary cultured rat cortical neurons, we here examined whether expression of PLC-beta 1 and -gamma 1 was altered in ER stress-loaded neurons induced by tunicamycin (Tm). Tunicamycin 172-174 phospholipase C beta 1 Rattus norvegicus 84-107 17988239-9 2008 Provoking SA in vitro in the presence of the N-linked glycosylation blocker tunicamycin abrogated the activity-dependent increase of HCN1/HCN2 heteromerization. Tunicamycin 76-87 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Homo sapiens 138-142 18216284-5 2008 We showed that ER stress induced by tunicamycin or high temperature resulted in increased transcription of apy-1. Tunicamycin 36-47 Apyrase apy-1 Caenorhabditis elegans 107-112 18160625-12 2008 In contrast, ER-Bcl-2 protected against apoptosis during tunicamycin-induced ER stress. Tunicamycin 57-68 BCL2 apoptosis regulator Homo sapiens 16-21 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 cyclin D1 Homo sapiens 39-48 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 cyclin A2 Homo sapiens 53-61 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 98-130 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 18228003-8 2008 Cyclin A was the most sensitive regulator to tunicamycin-triggered degradation mechanism. Tunicamycin 45-56 cyclin A2 Homo sapiens 0-8 18228003-9 2008 The association of p27(Kip1) with cyclin D1/cyclin-dependent kinase (Cdk) 4 was also increased by tunicamycin. Tunicamycin 98-109 interferon alpha inducible protein 27 Homo sapiens 19-22 18228003-9 2008 The association of p27(Kip1) with cyclin D1/cyclin-dependent kinase (Cdk) 4 was also increased by tunicamycin. Tunicamycin 98-109 cyclin dependent kinase inhibitor 1B Homo sapiens 23-27 18228003-9 2008 The association of p27(Kip1) with cyclin D1/cyclin-dependent kinase (Cdk) 4 was also increased by tunicamycin. Tunicamycin 98-109 proliferating cell nuclear antigen Homo sapiens 34-40 18228003-9 2008 The association of p27(Kip1) with cyclin D1/cyclin-dependent kinase (Cdk) 4 was also increased by tunicamycin. Tunicamycin 98-109 proliferating cell nuclear antigen Homo sapiens 44-50 18228003-11 2008 The knockdown of GRP78 expression by the siRNA transfection technique moderately increased tunicamycin-induced apoptosis but not the antiproliferative effect by sulforhodamine B assay. Tunicamycin 91-102 heat shock protein family A (Hsp70) member 5 Homo sapiens 17-22 18228003-12 2008 We suggest that tunicamycin induces G1 arrest through down-regulation of cyclins and Cdks, in which cyclin A is more susceptible to ER stress-triggered degradation mechanism in Hep3B cells. Tunicamycin 16-27 cyclin dependent kinase 4 Homo sapiens 85-89 18228003-12 2008 We suggest that tunicamycin induces G1 arrest through down-regulation of cyclins and Cdks, in which cyclin A is more susceptible to ER stress-triggered degradation mechanism in Hep3B cells. Tunicamycin 16-27 cyclin A2 Homo sapiens 100-108 18228003-13 2008 The increased association of p27(Kip1) with cyclin D1/Cdk4 may also contribute to tunicamycin-induced cell-cycle arrest. Tunicamycin 82-93 interferon alpha inducible protein 27 Homo sapiens 29-32 18228003-13 2008 The increased association of p27(Kip1) with cyclin D1/Cdk4 may also contribute to tunicamycin-induced cell-cycle arrest. Tunicamycin 82-93 cyclin dependent kinase inhibitor 1B Homo sapiens 33-37 18228003-13 2008 The increased association of p27(Kip1) with cyclin D1/Cdk4 may also contribute to tunicamycin-induced cell-cycle arrest. Tunicamycin 82-93 cyclin D1 Homo sapiens 44-53 18228003-13 2008 The increased association of p27(Kip1) with cyclin D1/Cdk4 may also contribute to tunicamycin-induced cell-cycle arrest. Tunicamycin 82-93 cyclin dependent kinase 4 Homo sapiens 54-58 18198352-9 2008 Finally, MIN6 cells depleted of GRP78 were more susceptible to tunicamycin-induced apoptosis but not to palmitate-induced apoptosis compared with control cells. Tunicamycin 63-74 heat shock protein 5 Mus musculus 32-37 18211961-10 2008 The thyroid-specific and epithelial dedifferentiation by thapsigargin or tunicamycin were completely prevented by the PP2 inhibitor of Src-family kinases and by stable expression of a dominant-negative Src. Tunicamycin 73-84 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 135-138 17941056-7 2008 Using SH-SY5Y neuroblastoma cells and primary cerebellar granule neurons as in vitro models, we demonstrated that exposure to ethanol alone had little effect on the expression of markers for ER stress; however, ethanol drastically enhanced the expression of GRP78, CHOP, ATF4, ATF6, and phosphorylated PERK and eIF2 alpha when induced by tunicamycin and thapsigargin. Tunicamycin 338-349 heat shock protein family A (Hsp70) member 5 Homo sapiens 258-263 18211961-10 2008 The thyroid-specific and epithelial dedifferentiation by thapsigargin or tunicamycin were completely prevented by the PP2 inhibitor of Src-family kinases and by stable expression of a dominant-negative Src. Tunicamycin 73-84 SRC proto-oncogene, non-receptor tyrosine kinase Rattus norvegicus 202-205 18245485-2 2008 We report in this study that apoptosis was induced by the ER stress inducer thapsigargin or tunicamycin via a caspase-8-mediated pathway in the melanoma cell line Me1007, although the MEK/ERK pathway was activated in this cell line. Tunicamycin 92-103 caspase 8 Homo sapiens 110-119 18065414-5 2008 We found that several well characterized stress inducers (tunicamycin, thapsigargin, and A23187) as well as homocysteine could increase Mthfr mRNA and protein in Neuro-2a cells. Tunicamycin 58-69 methylenetetrahydrofolate reductase Mus musculus 136-141 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 hypoxia up-regulated 1 Rattus norvegicus 0-6 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 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 18041764-2 2008 We found that overexpressing Par-4 by stable transfection sensitizes Caki cells to induction of apoptosis by TRAIL and drugs that induce endoplasmic reticulum (ER) stress [thapsigargin (TG), tunicamycin (TU) and etoposide]. Tunicamycin 191-202 pro-apoptotic WT1 regulator Homo sapiens 29-34 18167147-13 2008 In addition, GmPDIM associated with the alpha" subunit of beta-conglycinin, a seed-storage protein in the presence of tunicamycin. Tunicamycin 118-129 protein disulfide isomerse like protein Glycine max 13-19 18167147-13 2008 In addition, GmPDIM associated with the alpha" subunit of beta-conglycinin, a seed-storage protein in the presence of tunicamycin. Tunicamycin 118-129 alpha subunit of beta conglycinin Glycine max 40-74 18041764-2 2008 We found that overexpressing Par-4 by stable transfection sensitizes Caki cells to induction of apoptosis by TRAIL and drugs that induce endoplasmic reticulum (ER) stress [thapsigargin (TG), tunicamycin (TU) and etoposide]. Tunicamycin 204-206 pro-apoptotic WT1 regulator Homo sapiens 29-34 18089754-7 2008 Treatment of mCAT1/insG-expressing cells with tunicamycin, an N-linked glycosylation inhibitor, increased the transduction titre. Tunicamycin 46-57 solute carrier family 7 (cationic amino acid transporter, y+ system), member 1 Mus musculus 13-18 18283338-6 2008 Cells of the ATL-1 line, which were derived from an Atm-/- mouse thymic lymphoma, were more sensitive to the ER stress inducer tunicamycin than were Atm+/+ thymic leukemia ASL-1 cells. Tunicamycin 127-138 atlastin GTPase 1 Mus musculus 13-18 17928398-9 2008 In addition, cell death is enhanced by approximately 35% in tunicamycin-treated cells expressing an S51A eIF2 alpha mutant that cannot be phosphorylated or in cells lacking PERK (protein kinase regulated by RNA/endoplasmic reticulum-like kinase). Tunicamycin 60-71 eukaryotic translation initiation factor 2A Rattus norvegicus 105-115 17996891-11 2008 Treatment of HL-1 cells with tunicamycin reduced the relative mass of expressed corin. Tunicamycin 29-40 corin, serine peptidase Mus musculus 80-85 18022401-8 2007 We investigated the effect of exogenous UPR inducers thapsigargin (Tg) and tunicamycin (Tu) on Grp78 and ATF6 expression. Tunicamycin 75-86 heat shock protein family A (Hsp70) member 5 Homo sapiens 95-100 18022401-8 2007 We investigated the effect of exogenous UPR inducers thapsigargin (Tg) and tunicamycin (Tu) on Grp78 and ATF6 expression. Tunicamycin 75-86 activating transcription factor 6 Homo sapiens 105-109 18022401-8 2007 We investigated the effect of exogenous UPR inducers thapsigargin (Tg) and tunicamycin (Tu) on Grp78 and ATF6 expression. Tunicamycin 88-90 heat shock protein family A (Hsp70) member 5 Homo sapiens 95-100 18022401-8 2007 We investigated the effect of exogenous UPR inducers thapsigargin (Tg) and tunicamycin (Tu) on Grp78 and ATF6 expression. Tunicamycin 88-90 activating transcription factor 6 Homo sapiens 105-109 18156219-4 2007 One of these factors, bZIP28, an ER-resident transcription factor, is activated in response to treatment by tunicamycin (TM), an agent that blocks N-linked protein glycosylation. Tunicamycin 108-119 Basic-leucine zipper (bZIP) transcription factor family protein Arabidopsis thaliana 22-28 18156219-4 2007 One of these factors, bZIP28, an ER-resident transcription factor, is activated in response to treatment by tunicamycin (TM), an agent that blocks N-linked protein glycosylation. Tunicamycin 121-123 Basic-leucine zipper (bZIP) transcription factor family protein Arabidopsis thaliana 22-28 18029041-2 2008 A time-dependent induction of ER chaperons, glucose regulated protein (GRP)78 and GRP94, was observed after treatment with tunicamycin (TM), and cell death was also induced concomitantly in both cells. Tunicamycin 123-134 heat shock protein family A (Hsp70) member 5 Homo sapiens 71-77 18029041-2 2008 A time-dependent induction of ER chaperons, glucose regulated protein (GRP)78 and GRP94, was observed after treatment with tunicamycin (TM), and cell death was also induced concomitantly in both cells. Tunicamycin 123-134 heat shock protein 90 beta family member 1 Homo sapiens 82-87 17914579-0 2007 Glycosylation modulates TRAIL-R1/death receptor 4 protein: different regulations of two pro-apoptotic receptors for TRAIL by tunicamycin. Tunicamycin 125-136 TNF receptor superfamily member 10a Homo sapiens 24-32 17914579-0 2007 Glycosylation modulates TRAIL-R1/death receptor 4 protein: different regulations of two pro-apoptotic receptors for TRAIL by tunicamycin. Tunicamycin 125-136 TNF receptor superfamily member 10a Homo sapiens 33-49 17914579-0 2007 Glycosylation modulates TRAIL-R1/death receptor 4 protein: different regulations of two pro-apoptotic receptors for TRAIL by tunicamycin. Tunicamycin 125-136 TNF superfamily member 10 Homo sapiens 24-29 17914579-3 2007 Tunicamycin treatment, which is an inducer of endoplasmic reticulum (ER)-stress, generated a lower molecular-weight pattern of DR4, but not DR5 protein in prostate cancer DU145 and PC3 cells. Tunicamycin 0-11 TNF receptor superfamily member 10a Homo sapiens 127-130 17914579-10 2007 These results indicate that tunicamycin regulates DR4 protein size via inhibition of glycosylation. Tunicamycin 28-39 TNF receptor superfamily member 10a Homo sapiens 50-53 17823375-6 2007 Instead, CO prevented X-box binding protein 1 expression and activating transcription factor 6 cleavage induced by ER-stress inducers such as thapsigargin, tunicamycin and homocysteine. Tunicamycin 156-167 X-box binding protein 1 Homo sapiens 22-45 17712038-6 2007 In LNCaP cells, AIbZIP was processed to its transcriptionally active form by drugs that deplete ER calcium stores (i.e., A23187 and caffeine), but it was unaffected by an inhibitor of protein glycosylation (tunicamycin). Tunicamycin 207-218 cAMP responsive element binding protein 3 like 4 Homo sapiens 16-22 17942905-3 2007 Treatment with the ER stress inducer tunicamycin or thapsigargin did not induce significant apoptosis in the majority of melanoma cell lines, but resistance to these agents was reversed by the MEK inhibitor U0126 or MEK1 small interfering RNA (siRNA). Tunicamycin 37-48 mitogen-activated protein kinase kinase 7 Homo sapiens 193-196 17942905-3 2007 Treatment with the ER stress inducer tunicamycin or thapsigargin did not induce significant apoptosis in the majority of melanoma cell lines, but resistance to these agents was reversed by the MEK inhibitor U0126 or MEK1 small interfering RNA (siRNA). Tunicamycin 37-48 mitogen-activated protein kinase kinase 1 Homo sapiens 216-220 17942905-7 2007 Inhibition of MEK/ERK also resulted in down-regulation of GRP78, which was physically associated with caspase-4, before and after treatment with tunicamycin or thapsigargin. Tunicamycin 145-156 mitogen-activated protein kinase kinase 7 Homo sapiens 14-17 17942905-7 2007 Inhibition of MEK/ERK also resulted in down-regulation of GRP78, which was physically associated with caspase-4, before and after treatment with tunicamycin or thapsigargin. Tunicamycin 145-156 mitogen-activated protein kinase 1 Homo sapiens 18-21 17942905-7 2007 Inhibition of MEK/ERK also resulted in down-regulation of GRP78, which was physically associated with caspase-4, before and after treatment with tunicamycin or thapsigargin. Tunicamycin 145-156 heat shock protein family A (Hsp70) member 5 Homo sapiens 58-63 17681378-6 2007 Caspase-3 staining revealed that neuronal death is primarily due to apoptosis in tunicamycin-treated slice cultures. Tunicamycin 81-92 caspase 3 Homo sapiens 0-9 17681378-9 2007 Tunicamycin treatment resulted in upregulation of GRP78/BiP in the neuronal cells. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 50-55 17681378-9 2007 Tunicamycin treatment resulted in upregulation of GRP78/BiP in the neuronal cells. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 Homo sapiens 56-59 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 X-box binding protein 1 Homo sapiens 119-123 17937618-7 2007 Tunicamycin and monensin induced the synthesis of truncated non-glycosylated and partially glycosylated forms of SeP, which were secreted in spite of their impaired glycosylation. Tunicamycin 0-11 selenoprotein P Homo sapiens 113-116 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 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 138-142 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 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 212-216 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 activating transcription factor 6 Homo sapiens 234-267 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 activating transcription factor 6 Homo sapiens 269-273 17660514-8 2007 Treatment of HEK 293 cells expressing rat corin with tunicamycin prevented corin activation and inhibited its pro-atrial natriuretic peptide processing activity. Tunicamycin 53-64 corin, serine peptidase Rattus norvegicus 42-47 17635918-7 2007 Specifically, the effect of low concentration of GS-HCl (1 mM) or of tunicamycin (0.1 microg/ml) to produce the aglycosylated COX-2 was rescued by the proteasomal inhibitor MG132 but not by the lysosomal or caspase inhibitors. Tunicamycin 69-80 mitochondrially encoded cytochrome c oxidase II Homo sapiens 126-131 17660514-8 2007 Treatment of HEK 293 cells expressing rat corin with tunicamycin prevented corin activation and inhibited its pro-atrial natriuretic peptide processing activity. Tunicamycin 53-64 corin, serine peptidase Rattus norvegicus 75-80 17660514-9 2007 Similar effects of tunicamycin on endogenous corin activity were found in HL-1 cells. Tunicamycin 19-30 corin, serine peptidase Homo sapiens 45-50 17588536-3 2007 In this study, we found that the levels of Niban/NIBAN mRNA and protein were induced by treatment with tunicamycin, an inducer of endoplasmic reticulum (ER) stress. Tunicamycin 103-114 niban apoptosis regulator 1 Homo sapiens 43-48 17651753-3 2007 Here we show that in response to a UPR inducing reagent, tunicamycin, the expression of calreticulin (crt-1) is specifically up-regulated in Caenorhabditis elegans. Tunicamycin 57-68 Calreticulin Caenorhabditis elegans 88-100 17651753-3 2007 Here we show that in response to a UPR inducing reagent, tunicamycin, the expression of calreticulin (crt-1) is specifically up-regulated in Caenorhabditis elegans. Tunicamycin 57-68 Calreticulin Caenorhabditis elegans 102-107 17651753-4 2007 Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent. Tunicamycin 0-11 Calreticulin Caenorhabditis elegans 43-48 17651753-4 2007 Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent. Tunicamycin 0-11 Endoribonuclease;Serine/threonine-protein kinase Caenorhabditis elegans 58-63 17651753-4 2007 Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent. Tunicamycin 0-11 BZIP domain-containing protein Caenorhabditis elegans 68-73 17651753-4 2007 Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent. Tunicamycin 0-11 BZIP domain-containing protein Caenorhabditis elegans 81-86 17651753-4 2007 Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent. Tunicamycin 0-11 Eukaryotic translation initiation factor 2-alpha kinase pek-1 Caenorhabditis elegans 91-96 17607300-12 2007 Tunicamycin caused dose-dependent decreases in hepatocyte CD1d, inhibited hepatocyte activation of CD1d-restricted T-cell responses, depleted liver populations of CD1d-reactive NKT cells and promoted Th-1 polarization of hepatic cytokine production. Tunicamycin 0-11 CD1d1 antigen Mus musculus 58-62 17607300-12 2007 Tunicamycin caused dose-dependent decreases in hepatocyte CD1d, inhibited hepatocyte activation of CD1d-restricted T-cell responses, depleted liver populations of CD1d-reactive NKT cells and promoted Th-1 polarization of hepatic cytokine production. Tunicamycin 0-11 CD1d1 antigen Mus musculus 99-103 17607300-12 2007 Tunicamycin caused dose-dependent decreases in hepatocyte CD1d, inhibited hepatocyte activation of CD1d-restricted T-cell responses, depleted liver populations of CD1d-reactive NKT cells and promoted Th-1 polarization of hepatic cytokine production. Tunicamycin 0-11 CD1d1 antigen Mus musculus 99-103 17588536-3 2007 In this study, we found that the levels of Niban/NIBAN mRNA and protein were induced by treatment with tunicamycin, an inducer of endoplasmic reticulum (ER) stress. Tunicamycin 103-114 niban apoptosis regulator 1 Homo sapiens 49-54 17379544-7 2007 When the HeLa cells stably expressing Bcl-2 were treated with tunicamycin, endogenous RTN3 increased in the cell microsomal fraction. Tunicamycin 62-73 BCL2 apoptosis regulator Homo sapiens 38-43 17379544-7 2007 When the HeLa cells stably expressing Bcl-2 were treated with tunicamycin, endogenous RTN3 increased in the cell microsomal fraction. Tunicamycin 62-73 reticulon 3 Homo sapiens 86-90 17652745-8 2007 Immunoblotting analysis showed that tunicamycin at 2 microg/mL induced BiP, ATF4, and CHOP protein production and PKR phosphorylation. Tunicamycin 36-47 heat shock protein 5 Mus musculus 71-74 17652745-8 2007 Immunoblotting analysis showed that tunicamycin at 2 microg/mL induced BiP, ATF4, and CHOP protein production and PKR phosphorylation. Tunicamycin 36-47 activating transcription factor 4 Mus musculus 76-80 17652745-8 2007 Immunoblotting analysis showed that tunicamycin at 2 microg/mL induced BiP, ATF4, and CHOP protein production and PKR phosphorylation. Tunicamycin 36-47 DNA-damage inducible transcript 3 Mus musculus 86-90 17652745-8 2007 Immunoblotting analysis showed that tunicamycin at 2 microg/mL induced BiP, ATF4, and CHOP protein production and PKR phosphorylation. Tunicamycin 36-47 eukaryotic translation initiation factor 2-alpha kinase 2 Mus musculus 114-117 17652745-9 2007 Both the PKR inhibitor (0.03-1 microM) and the PKR knockdown (using siRNA) inhibited tunicamycin-induced RGC-5 cell death. Tunicamycin 85-96 eukaryotic translation initiation factor 2-alpha kinase 2 Mus musculus 9-12 17652745-9 2007 Both the PKR inhibitor (0.03-1 microM) and the PKR knockdown (using siRNA) inhibited tunicamycin-induced RGC-5 cell death. Tunicamycin 85-96 eukaryotic translation initiation factor 2-alpha kinase 2 Mus musculus 47-50 17652745-11 2007 The PKR inhibitor reduced the tunicamycin-induced increase in CHOP but not that in BiP protein production. Tunicamycin 30-41 eukaryotic translation initiation factor 2-alpha kinase 2 Mus musculus 4-7 17652745-11 2007 The PKR inhibitor reduced the tunicamycin-induced increase in CHOP but not that in BiP protein production. Tunicamycin 30-41 DNA-damage inducible transcript 3 Mus musculus 62-66 17827659-2 2007 In eukaryotes, tunicamycins inhibit UDP-N-acetylglucosamine: dolichol phosphate GlcNAc-1-P transferase (GPT) that catalyzes the first step in protein glycosylation. Tunicamycin 15-27 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 80-102 17827659-2 2007 In eukaryotes, tunicamycins inhibit UDP-N-acetylglucosamine: dolichol phosphate GlcNAc-1-P transferase (GPT) that catalyzes the first step in protein glycosylation. Tunicamycin 15-27 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 104-107 17827659-4 2007 Tunicamycins are substrate analog of GPT and MraY, such that the alphabeta-1"",11"-linked GlcNAc residue of the tunicamycins mimics the transferred GlcNAc-1-phosphate. Tunicamycin 0-12 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 37-40 17827659-4 2007 Tunicamycins are substrate analog of GPT and MraY, such that the alphabeta-1"",11"-linked GlcNAc residue of the tunicamycins mimics the transferred GlcNAc-1-phosphate. Tunicamycin 112-124 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 37-40 17416481-4 2007 ER stress inducers (tunicamycin, thapsigargin and oxidized dithiothreitol (DTTox)) resulted in a dose-dependent increase in GRP78 and GRP94 stress protein expression, but the magnitude of induction was cell line- and inducer-dependent. Tunicamycin 20-31 heat shock protein family A (Hsp70) member 5 Sus scrofa 124-129 17416481-4 2007 ER stress inducers (tunicamycin, thapsigargin and oxidized dithiothreitol (DTTox)) resulted in a dose-dependent increase in GRP78 and GRP94 stress protein expression, but the magnitude of induction was cell line- and inducer-dependent. Tunicamycin 20-31 heat shock protein 90 beta family member 1 Sus scrofa 134-139 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 X-box binding protein 1 Homo sapiens 92-96 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 17560726-3 2007 When amyloid-beta protein was combined with tunicamycin (Abeta+TM), cell death was more acute than with TM alone. Tunicamycin 44-55 amyloid beta precursor protein Rattus norvegicus 57-62 17356011-8 2007 Studies with PNGase F and tunicamycin reveal the Slc37a2 protein is posttranslationally modified by addition of N-linked glycans. Tunicamycin 26-37 solute carrier family 37 (glycerol-3-phosphate transporter), member 2 Mus musculus 49-56 17404493-7 2007 In contrast, IRE1 is required for autophagy induced by ER stress-inducing agents such a tunicamycin or thapsigargin. Tunicamycin 88-99 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 13-17 17442667-11 2007 However, the subcellular localization of either a mutant (C236S/C244S) I-MBP, which lacks carbohydrate-binding activity, or the wild-type I-MBP in tunicamycin-treated cells shows an equally diffuse cytoplasmic distribution, suggesting that the unique accumulation of I-MBP in the ER and COPII vesicles is mediated by an N-glycan-lectin interaction. Tunicamycin 147-158 myelin basic protein Homo sapiens 140-143 17586475-10 2007 The glycosylation inhibitor tunicamycin also partially suppresses EpoR surface expression. Tunicamycin 28-39 erythropoietin receptor Homo sapiens 66-70 16904232-6 2007 Moreover, under the tunicamycin treatment, transcripts of BiP, PDI and calnexin in transgenic tomato plants accumulated to a less level than those in non-transgenic tomato plants. Tunicamycin 20-31 luminal-binding protein Solanum lycopersicum 58-61 17655822-1 2007 Experimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release. Tunicamycin 91-102 cytochrome c, somatic Homo sapiens 184-196 17655822-1 2007 Experimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release. Tunicamycin 91-102 BCL2 associated X, apoptosis regulator Homo sapiens 238-241 17655822-1 2007 Experimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release. Tunicamycin 91-102 cytochrome c, somatic Homo sapiens 310-322 17456790-2 2007 Here, we examined the role of inhibin subunit glycosylation in the assembly and secretion of mature inhibin A and activin A. Inhibition of subunit glycosylation by tunicamycin treatment of alpha- and beta(A)-expressing CHO cell lines reduced inhibin but not activin secretion. Tunicamycin 164-175 inhibin alpha chain Cricetulus griseus 100-109 17442667-11 2007 However, the subcellular localization of either a mutant (C236S/C244S) I-MBP, which lacks carbohydrate-binding activity, or the wild-type I-MBP in tunicamycin-treated cells shows an equally diffuse cytoplasmic distribution, suggesting that the unique accumulation of I-MBP in the ER and COPII vesicles is mediated by an N-glycan-lectin interaction. Tunicamycin 147-158 myelin basic protein Homo sapiens 140-143 17347267-6 2007 TC-R delivery to both BLM and BBM was inhibited by Brefeldin A and tunicamycin, but not by wortmannin or leupeptin. Tunicamycin 67-78 CD320 molecule Homo sapiens 0-4 17575157-0 2007 Tunicamycin sensitizes human melanoma cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by up-regulation of TRAIL-R2 via the unfolded protein response. Tunicamycin 0-11 TNF receptor superfamily member 10b Homo sapiens 141-149 17575157-3 2007 We show in this study that the endoplasmic reticulum (ER) stress inducer, tunicamycin, selectively up-regulated the cell surface expression of TRAIL-R2, but not other members of the TNF receptor family, and enhanced TRAIL-induced apoptosis in cultured melanoma cells and fresh melanoma isolates. Tunicamycin 74-85 TNF receptor superfamily member 10b Homo sapiens 143-151 17575157-3 2007 We show in this study that the endoplasmic reticulum (ER) stress inducer, tunicamycin, selectively up-regulated the cell surface expression of TRAIL-R2, but not other members of the TNF receptor family, and enhanced TRAIL-induced apoptosis in cultured melanoma cells and fresh melanoma isolates. Tunicamycin 74-85 TNF superfamily member 10 Homo sapiens 143-148 17575157-4 2007 Tunicamycin-mediated sensitization of melanoma cells to TRAIL-induced apoptosis was associated with increased activation of the caspase cascade and reduction in mitochondrial membrane potential and was inhibited by a recombinant TRAIL-R2/Fc chimeric protein. Tunicamycin 0-11 TNF superfamily member 10 Homo sapiens 56-61 17575157-4 2007 Tunicamycin-mediated sensitization of melanoma cells to TRAIL-induced apoptosis was associated with increased activation of the caspase cascade and reduction in mitochondrial membrane potential and was inhibited by a recombinant TRAIL-R2/Fc chimeric protein. Tunicamycin 0-11 TNF receptor superfamily member 10b Homo sapiens 229-237 17575157-9 2007 Moreover, the transcription factor CCAAT/enhancer-binding protein homologous protein seemed to be involved in the up-regulation of TRAIL-R2 by tunicamycin, but its role varied between different melanoma lines. Tunicamycin 143-154 TNF receptor superfamily member 10b Homo sapiens 131-139 17455306-7 2007 The function of these NMDARs as Ca2+ channels is repressed by tunicamycin, because of the inhibition of NR1, but no NR2A, synthesis. Tunicamycin 62-73 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 104-107 17455306-8 2007 The regulation of NR1 is relevant to the central nervous system, in that a dramatic decrease in synthesis of this subunit and assembly of NMDARs is observed in cortical neurons treated with tunicamycin. Tunicamycin 190-201 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 18-21 17455323-0 2007 Brain-derived neurotrophic factor suppresses tunicamycin-induced upregulation of CHOP in neurons. Tunicamycin 45-56 brain derived neurotrophic factor Homo sapiens 0-33 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 17438523-6 2007 RESULTS: Treatment with tunicamycin induced apoptotic cell death in RGC-5 and also induced production of ER stress-related proteins (BiP, the phosphorylated form of eIF2alpha, and CHOP protein). Tunicamycin 24-35 heat shock protein 5 Mus musculus 133-136 17418825-4 2007 ER stress, induced by Thapsigargin and tunicamycin, elevated a phosphorylated form of eIF2alpha and ATF4, but the cellular fate depended on treatment duration. Tunicamycin 39-50 eukaryotic translation initiation factor 2A Mus musculus 86-95 17418825-4 2007 ER stress, induced by Thapsigargin and tunicamycin, elevated a phosphorylated form of eIF2alpha and ATF4, but the cellular fate depended on treatment duration. Tunicamycin 39-50 activating transcription factor 4 Mus musculus 100-104 17438523-6 2007 RESULTS: Treatment with tunicamycin induced apoptotic cell death in RGC-5 and also induced production of ER stress-related proteins (BiP, the phosphorylated form of eIF2alpha, and CHOP protein). Tunicamycin 24-35 eukaryotic translation initiation factor 2A Mus musculus 165-174 17438523-6 2007 RESULTS: Treatment with tunicamycin induced apoptotic cell death in RGC-5 and also induced production of ER stress-related proteins (BiP, the phosphorylated form of eIF2alpha, and CHOP protein). Tunicamycin 24-35 DNA-damage inducible transcript 3 Mus musculus 180-184 17438523-8 2007 In flatmounted retinas of ERAI mice, the fluorescence intensity arising from the XBP-1-venus fusion protein, indicating ER-stress activation, was increased at 24 h after tunicamycin, NMDA, or IOP elevation. Tunicamycin 170-181 X-box binding protein 1 Mus musculus 81-86 17167073-8 2007 Transient overexpression of wild-type Akt, but not kinase-dead Akt, in JEG-3 cells diminished tunicamycin-OGD reoxygenation-induced apoptosis. Tunicamycin 94-105 AKT serine/threonine kinase 1 Homo sapiens 38-41 17301828-7 2007 Addition of tunicamycin resulted in the resistance of CD23 to Der p I mediated cleavage in CC but no change in TT transfectants. Tunicamycin 12-23 Fc epsilon receptor II Homo sapiens 54-58 17283057-4 2007 The requirement of the p85alpha regulatory subunit for JNK occurs independently of its role as a component of the PI3K heterodimer and occurs only in response to specific stimuli, namely, insulin and tunicamycin, a chemical that induces endoplasmic reticulum stress. Tunicamycin 200-211 phosphoinositide-3-kinase regulatory subunit 1 Homo sapiens 23-31 17283057-4 2007 The requirement of the p85alpha regulatory subunit for JNK occurs independently of its role as a component of the PI3K heterodimer and occurs only in response to specific stimuli, namely, insulin and tunicamycin, a chemical that induces endoplasmic reticulum stress. Tunicamycin 200-211 mitogen-activated protein kinase 8 Homo sapiens 55-58 17314395-2 2007 Yeast mutants lacking Pmr1 show growth sensitivity to multiple drugs (amiodarone, wortmannin, sulfometuron methyl, and tunicamycin) and ions (Mn2+ and Ca2+). Tunicamycin 119-130 Ca(2+)/Mn(2+)-transporting P-type ATPase PMR1 Saccharomyces cerevisiae S288C 22-26 16858427-0 2007 Calnexin-dependent regulation of tunicamycin-induced apoptosis in breast carcinoma MCF-7 cells. Tunicamycin 33-44 calnexin Homo sapiens 0-8 16858427-4 2007 We show that the expression level of the ER chaperone calnexin can directly influence tunicamycin sensitivity in this cell line. Tunicamycin 86-97 calnexin Homo sapiens 54-62 16858427-5 2007 Interestingly, the expression of a calnexin lacking the chaperone domain (DeltaE) partially restores their sensitivity to tunicamycin-induced apoptosis. Tunicamycin 122-133 calnexin Homo sapiens 35-43 16858427-7 2007 Utilizing the ability of MCF-7 cells to resist tunicamycin-induced apoptosis, we have characterized a molecular mechanism by which calnexin regulates ER-stress-mediated apoptosis in a manner independent of its chaperone functions but dependent of its binding to Bap31. Tunicamycin 47-58 calnexin Homo sapiens 131-139 16987996-4 2007 Pharmacological methods such as proteasome inhibition and treatment with brefeldin A and tunicamycin were used to induce ER stress and activate the UPR as monitored by increased levels of spliced XBP1 and BiP mRNA. Tunicamycin 89-100 X-box binding protein 1 Homo sapiens 196-200 16987996-4 2007 Pharmacological methods such as proteasome inhibition and treatment with brefeldin A and tunicamycin were used to induce ER stress and activate the UPR as monitored by increased levels of spliced XBP1 and BiP mRNA. Tunicamycin 89-100 heat shock protein family A (Hsp70) member 5 Homo sapiens 205-208 17131418-0 2007 Role of p53 in neurotoxicity induced by the endoplasmic reticulum stress agent tunicamycin in organotypic slice cultures of rat spinal cord. Tunicamycin 79-90 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 8-11 17187761-5 2007 We found that the deletion of EOS1 enhances tunicamycin tolerance and that in Delta eos1 the transcription level of KAR2, which is the ER stress-inducible gene, was much lower than that in the wild-type strain (BY4741) when exposed to tunicamycin. Tunicamycin 44-55 Eos1p Saccharomyces cerevisiae S288C 30-34 17187761-5 2007 We found that the deletion of EOS1 enhances tunicamycin tolerance and that in Delta eos1 the transcription level of KAR2, which is the ER stress-inducible gene, was much lower than that in the wild-type strain (BY4741) when exposed to tunicamycin. Tunicamycin 235-246 Eos1p Saccharomyces cerevisiae S288C 84-88 17187761-6 2007 The inhibition of the N-glycosylation of carboxypeptidase Y and invertase activity caused by the addition of tunicamycin was depressed in Delta eos1, suggesting that EOS1 may be involved in N-glycosylation of the cellular proteins. Tunicamycin 109-120 Eos1p Saccharomyces cerevisiae S288C 144-148 17187761-6 2007 The inhibition of the N-glycosylation of carboxypeptidase Y and invertase activity caused by the addition of tunicamycin was depressed in Delta eos1, suggesting that EOS1 may be involved in N-glycosylation of the cellular proteins. Tunicamycin 109-120 Eos1p Saccharomyces cerevisiae S288C 166-170 17203246-3 2007 Here, we show that tunicamycin causes significant alteration of calnexin sub-cellular distribution in MCF-7 cells. Tunicamycin 19-30 calnexin Homo sapiens 64-72 17203246-4 2007 Interestingly, this correlates with the absence of both tunicamycin-induced calnexin phosphorylation as well as tunicamycin-induced cell death. Tunicamycin 56-67 calnexin Homo sapiens 76-84 16931790-5 2006 Using the UPR inducing agent tunicamycin and selective siRNA targeting of the ATF4 and XBP1 branches of the UPR, we demonstrate that these transcription factors are essential mediators of IL8, IL6, and MCP1 expression in human aortic ECs required for maximal inflammatory gene expression in the basal state and after oxPAPC treatment. Tunicamycin 29-40 C-X-C motif chemokine ligand 8 Homo sapiens 188-191 17101776-3 2007 Disulfide-bonded ATF6 is reduced upon treatment of cells with not only the reducing reagent dithiothreitol but also the glycosylation inhibitor tunicamycin, and the extent of reduction correlates with that of activation. Tunicamycin 144-155 activating transcription factor 6 Homo sapiens 17-21 17101776-6 2007 ER stress-induced reduction is specific to ATF6 as the oligomeric status of a second ER membrane-bound transcription factor, LZIP/Luman, is not changed upon tunicamycin treatment and LZIP/Luman is well cleaved by S1P in the absence of ER stress. Tunicamycin 157-168 activating transcription factor 6 Homo sapiens 43-47 17031492-4 2006 Furthermore, we demonstrated that endogenous FADD was recruited by ER-bound endogenous RTN3 to the ER membrane under the tunicamycin stimulation. Tunicamycin 121-132 Fas associated via death domain Homo sapiens 45-49 17031492-4 2006 Furthermore, we demonstrated that endogenous FADD was recruited by ER-bound endogenous RTN3 to the ER membrane under the tunicamycin stimulation. Tunicamycin 121-132 reticulon 3 Homo sapiens 87-91 17157811-6 2007 The results showed that ER stress-inducing agent tunicamycin significantly enhanced ERAD in cells that either express endogenous or overexpress gp78. Tunicamycin 49-60 autocrine motility factor receptor Homo sapiens 144-148 17157811-8 2007 Surprisingly, tunicamycin treatment stabilized gp78, an established ERAD E3 and an ERAD substrate as well, for up to 8h. Tunicamycin 14-25 autocrine motility factor receptor Homo sapiens 47-51 17112510-5 2007 We also show by Shb knockdown experiments that Shb regulates c-Abl activity and modulates cell death in response to the genotoxic agent cisplatin and the endoplasmic reticulum stress-inducer tunicamycin. Tunicamycin 191-202 SH2 domain containing adaptor protein B Homo sapiens 16-19 17112510-5 2007 We also show by Shb knockdown experiments that Shb regulates c-Abl activity and modulates cell death in response to the genotoxic agent cisplatin and the endoplasmic reticulum stress-inducer tunicamycin. Tunicamycin 191-202 SH2 domain containing adaptor protein B Homo sapiens 47-50 17112510-5 2007 We also show by Shb knockdown experiments that Shb regulates c-Abl activity and modulates cell death in response to the genotoxic agent cisplatin and the endoplasmic reticulum stress-inducer tunicamycin. Tunicamycin 191-202 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 61-66 17127020-0 2007 Toxicogenomics of endoplasmic reticulum stress inducer tunicamycin in the small intestine and liver of Nrf2 knockout and C57BL/6J mice. Tunicamycin 55-66 nuclear factor, erythroid derived 2, like 2 Mus musculus 103-107 17127020-1 2007 This objective of this study was to investigate the toxicogenomics and the spatial regulation of global gene expression profiles elicited by endoplasmic reticulum (ER) stress inducer tunicamycin (TM) in mouse small intestine and liver as well as to identify TM-modulated nuclear factor-E2-related factor 2 (Nrf2)-dependent genes. Tunicamycin 183-194 nuclear factor, erythroid derived 2, like 2 Mus musculus 307-311 17346424-6 2007 In vitro cell viability experiments using Hepatocellular Carcinoma HuH7 cells treated with ERdj5 small interfering RNA showed that ERdj5 knockdown cells exhibited less resistance to Doxorubicin (chemotherapy drug), but more resistance to Tunicamycin (Endoplasmic Stress inducer), compared to control cells. Tunicamycin 238-249 DnaJ heat shock protein family (Hsp40) member C10 Homo sapiens 131-136 16841181-8 2007 Moreover, MCF-7 cells stably transfected with CD38wt cDNA, also revealed the presence of cross-linked oligomers when treated with a N-linked glycosylation inhibitor tunicamycin (TM). Tunicamycin 165-176 CD38 molecule Homo sapiens 46-50 16841181-8 2007 Moreover, MCF-7 cells stably transfected with CD38wt cDNA, also revealed the presence of cross-linked oligomers when treated with a N-linked glycosylation inhibitor tunicamycin (TM). Tunicamycin 178-180 CD38 molecule Homo sapiens 46-50 17055645-5 2006 Treatment with tunicamycin at 2 microg/ml for 24 h induced apoptotic cell death accompanied by nuclear condensation and/or fragmentation, and these cells were positive for YO-PRO-1 (early-phase apoptosis and necrosis indicator). Tunicamycin 15-26 lamin A/C Homo sapiens 175-180 17055645-6 2006 Treatment with the PKR inhibitor at 0.1 or 0.3 microM led to a decrease in the number of apoptotic cells induced by tunicamycin. Tunicamycin 116-127 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 19-22 17055645-7 2006 In the resazurin-reduction test, the PKR inhibitor (at 0.1 and 0.3 microM) concentration-dependently inhibited the tunicamycin-induced decrease in metabolic activity. Tunicamycin 115-126 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 37-40 16931790-5 2006 Using the UPR inducing agent tunicamycin and selective siRNA targeting of the ATF4 and XBP1 branches of the UPR, we demonstrate that these transcription factors are essential mediators of IL8, IL6, and MCP1 expression in human aortic ECs required for maximal inflammatory gene expression in the basal state and after oxPAPC treatment. Tunicamycin 29-40 interleukin 6 Homo sapiens 193-196 16931790-5 2006 Using the UPR inducing agent tunicamycin and selective siRNA targeting of the ATF4 and XBP1 branches of the UPR, we demonstrate that these transcription factors are essential mediators of IL8, IL6, and MCP1 expression in human aortic ECs required for maximal inflammatory gene expression in the basal state and after oxPAPC treatment. Tunicamycin 29-40 C-C motif chemokine ligand 2 Homo sapiens 202-206 17200012-7 2006 Tunicamycin, an inhibitor of N-terminal glycoprotein synthesis, was added into the culture fluid of the FGFR1-IIIb transfected TAKA-1 cells to observe the changes of the FGFR1 bands. Tunicamycin 0-11 fibroblast growth factor receptor 1 Mesocricetus auratus 104-109 17200012-7 2006 Tunicamycin, an inhibitor of N-terminal glycoprotein synthesis, was added into the culture fluid of the FGFR1-IIIb transfected TAKA-1 cells to observe the changes of the FGFR1 bands. Tunicamycin 0-11 fibroblast growth factor receptor 1 Mesocricetus auratus 170-175 16792699-5 2006 To demonstrate N-glycosylation of wild-type Kv3.1 in Sf9 cells, cells were treated with tunicamycin. Tunicamycin 88-99 potassium voltage-gated channel subfamily C member 1 Rattus norvegicus 44-49 16954146-9 2006 Furthermore, in the kidneys of Apaf-1-deficient mice, apoptosis induced by in vivo administration of tunicamycin was remarkably suppressed as compared with wild type mice. Tunicamycin 101-112 apoptotic peptidase activating factor 1 Mus musculus 31-37 16957393-4 2006 Overexpression of ER-sHSP enhanced the resistance of the transgenic plant to tunicamycin (Fig. Tunicamycin 77-88 small heat shock protein Solanum lycopersicum 18-25 16957393-6 2006 Tunicamycin treatment induced an increase in mRNA level of BiP and calnexin in plant cell, but mRNAs of these two genes in transgenic plants were accumulated to a much smaller extent than those in non-transgenic plants (Fig. Tunicamycin 0-11 luminal-binding protein Solanum lycopersicum 59-62 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 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 caspase 12 Rattus norvegicus 120-130 16781668-4 2006 Transcripts for beta-glucuronidase (GUS) driven by BiP promoter respond to tunicamycin and sugar, being similar with endogenous BiP transcripts in transgenic A. thaliana. Tunicamycin 75-86 Heat shock protein 70 (Hsp 70) family protein Arabidopsis thaliana 51-54 16673398-3 2006 Overexpression of Galpha(s-L) to a level twice that of the vector-transfected cells did not directly affect cell viability but significantly increased the sensitivity to induction of cell death by serum deprivation and other apoptotic stimuli, including staurosporine, H(2)O(2), and tunicamycin. Tunicamycin 283-294 succinate-CoA ligase GDP/ADP-forming subunit alpha Homo sapiens 18-28 16701639-3 2006 Here we show that brefeldin A and tunicamycin-mediated ER stress lead to caspase-dependent apoptosis involving caspase-2. Tunicamycin 34-45 caspase 2 Homo sapiens 111-120 16687406-10 2006 Treatment with tunicamycin, an endoplasmic reticulum stress inducer, caused an accumulation of a smaller form of Nrf1 that correlated with detection of Nrf1 in the nucleus by biochemical fractionation and immunofluorescent analysis. Tunicamycin 15-26 nuclear respiratory factor 1 Homo sapiens 113-117 16687406-10 2006 Treatment with tunicamycin, an endoplasmic reticulum stress inducer, caused an accumulation of a smaller form of Nrf1 that correlated with detection of Nrf1 in the nucleus by biochemical fractionation and immunofluorescent analysis. Tunicamycin 15-26 nuclear respiratory factor 1 Homo sapiens 152-156 16765953-0 2006 Novel potential of tunicamycin as an activator of the aryl hydrocarbon receptor -- dioxin responsive element signaling pathway. Tunicamycin 19-30 aryl hydrocarbon receptor Homo sapiens 54-79 16765953-2 2006 We found that tunicamycin induced expression of cytochrome P450 1A1 in a dose-dependent manner. Tunicamycin 14-25 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 48-67 16765953-5 2006 Pharmacological and genetic inhibition of the aryl hydrocarbon receptor (AhR) significantly attenuated activation of DRE by tunicamycin. Tunicamycin 124-135 aryl hydrocarbon receptor Homo sapiens 46-71 16765953-5 2006 Pharmacological and genetic inhibition of the aryl hydrocarbon receptor (AhR) significantly attenuated activation of DRE by tunicamycin. Tunicamycin 124-135 aryl hydrocarbon receptor Homo sapiens 73-76 16765953-6 2006 These results elucidated the novel potential of tunicamycin as an activator of the AhR -- DRE signaling pathway. Tunicamycin 48-59 aryl hydrocarbon receptor Homo sapiens 83-86 16456185-5 2006 Exposure to tunicamycin to inhibit SP1 glycosylation reduces ClC-2 expression. Tunicamycin 12-23 chloride voltage-gated channel 2 Homo sapiens 61-66 16291577-5 2006 Inhibition of glycosylation with tunicamycin in wild-type NKCC2-injected oocytes resulted in an 80% reduction of NKCC2 activity. Tunicamycin 33-44 solute carrier family 12 member 1 L homeolog Xenopus laevis 58-63 16723486-6 2006 Treatment with the N-glycosylation inhibitor tunicamycin induces an epithelioid phenotype in clone-YH, like time in culture but disrupts the hTERT-RPE1 phenotype. Tunicamycin 45-56 telomerase reverse transcriptase Homo sapiens 141-151 16291577-5 2006 Inhibition of glycosylation with tunicamycin in wild-type NKCC2-injected oocytes resulted in an 80% reduction of NKCC2 activity. Tunicamycin 33-44 solute carrier family 12 member 1 L homeolog Xenopus laevis 113-118 16513638-8 2006 Treatment with tunicamycin, an inhibitor of N-linked glycosylation, induced the appearance of the unglycosylated 115-kDa CaR form, which was further increased by exposure to MG132, or upon transfection with a dorfin dominant negative construct, suggesting that dorfin-mediated proteasomal degradation of immature CaR occurs from the endoplasmic reticulum. Tunicamycin 15-26 calcium sensing receptor Homo sapiens 121-124 16513638-8 2006 Treatment with tunicamycin, an inhibitor of N-linked glycosylation, induced the appearance of the unglycosylated 115-kDa CaR form, which was further increased by exposure to MG132, or upon transfection with a dorfin dominant negative construct, suggesting that dorfin-mediated proteasomal degradation of immature CaR occurs from the endoplasmic reticulum. Tunicamycin 15-26 calcium sensing receptor Homo sapiens 313-316 16754299-5 2006 By treatment with tunicamycin (TM), an inhibitor of N-glycosylation, the expression level of HG-CD147 decreased and the LG-CD147 disappeared completely in HcaF cells. Tunicamycin 18-29 basigin Mus musculus 96-101 16645094-3 2006 DKO mice responded abnormally to tunicamycin-induced ER stress in the liver, with extensive tissue damage and decreased expression of the IRE1 substrate X-box-binding protein 1 and its target genes. Tunicamycin 33-44 endoplasmic reticulum (ER) to nucleus signalling 2 Mus musculus 138-142 16645094-3 2006 DKO mice responded abnormally to tunicamycin-induced ER stress in the liver, with extensive tissue damage and decreased expression of the IRE1 substrate X-box-binding protein 1 and its target genes. Tunicamycin 33-44 X-box binding protein 1 Mus musculus 153-176 16533755-7 2006 Cells treated with tunicamycin, an inhibitor of glycosylation, prevented TLR3-induced NF-kappaB activation, confirming that N-linked glycosylation is required for bioactivity of this receptor. Tunicamycin 19-30 toll like receptor 3 Homo sapiens 73-77 16564150-10 2006 ER stress inducers tunicamycin and thapsigargin down-regulate cell cycle proteins ppRb and cyclin D1 in differentiated neuroblastoma cells. Tunicamycin 19-30 cyclin D1 Homo sapiens 91-100 16564150-11 2006 In contrast, protein levels of p27, a cyclin dependent kinase inhibitor, are increased after induction of ER-stress using tunicamycin. Tunicamycin 122-133 dynactin subunit 6 Homo sapiens 31-34 16525726-4 2006 Tunicamycin reduces MUC1 concentration on the cellular surface more than benzylglycoside, and greatly reduces glycosylation of glycoproteins, causing an increase in cell adhesion in both types of cancer cells. Tunicamycin 0-11 mucin 1, cell surface associated Homo sapiens 20-24 16754299-5 2006 By treatment with tunicamycin (TM), an inhibitor of N-glycosylation, the expression level of HG-CD147 decreased and the LG-CD147 disappeared completely in HcaF cells. Tunicamycin 18-29 basigin Mus musculus 123-128 16754299-5 2006 By treatment with tunicamycin (TM), an inhibitor of N-glycosylation, the expression level of HG-CD147 decreased and the LG-CD147 disappeared completely in HcaF cells. Tunicamycin 31-33 basigin Mus musculus 96-101 16754299-5 2006 By treatment with tunicamycin (TM), an inhibitor of N-glycosylation, the expression level of HG-CD147 decreased and the LG-CD147 disappeared completely in HcaF cells. Tunicamycin 31-33 basigin Mus musculus 123-128 16375864-4 2006 Treatment with tunicamycin or thapsigargin, ER stress inducers, caused dephosphorylation of Akt from 12 to 24 h and induced cell death. Tunicamycin 15-26 AKT serine/threonine kinase 1 Homo sapiens 92-95 16388830-10 2006 Thapsigargin and tunicamycin each significantly activated caspase-3, -9, and -2 in the intrinsic apoptotic pathway in SH-SY5Y cells. Tunicamycin 17-28 caspase 3 Homo sapiens 58-79 16332684-8 2006 Unexpectedly, we found that one of the mutants activates transcription of both Xbp-1-specific and non-Xbp-1-dependent UPR targets in response to tunicamycin treatment, even more potently than does wild type Xbp-1. Tunicamycin 145-156 X-box binding protein 1 Homo sapiens 79-84 16332684-8 2006 Unexpectedly, we found that one of the mutants activates transcription of both Xbp-1-specific and non-Xbp-1-dependent UPR targets in response to tunicamycin treatment, even more potently than does wild type Xbp-1. Tunicamycin 145-156 X-box binding protein 1 Homo sapiens 102-107 16332684-8 2006 Unexpectedly, we found that one of the mutants activates transcription of both Xbp-1-specific and non-Xbp-1-dependent UPR targets in response to tunicamycin treatment, even more potently than does wild type Xbp-1. Tunicamycin 145-156 X-box binding protein 1 Homo sapiens 102-107 16541468-7 2006 We observed that ammonium chloride and tunicamycin blocked TNF-alpha-EGFP fusion protein delivery to secretory granules. Tunicamycin 39-50 tumor necrosis factor Homo sapiens 59-68 16581801-2 2006 Here, we use tunicamycin (Tn) to investigate ER stress-triggered changes in the translation of cytochrome c, a pivotal regulator of apoptosis. Tunicamycin 13-24 cytochrome c, somatic Homo sapiens 95-107 16526095-3 2006 Tat expression also resulted in protection from Tunicamycin-induced apoptosis as determined by DNA staining and TUNEL assays. Tunicamycin 48-59 tyrosine aminotransferase Homo sapiens 0-3 16316999-10 2006 Induction of the endoplasmic reticulum stress response by anoxia/recovery or tunicamycin (monitored by induction of Bip or Grp94 expression, phosphorylation of eukaryotic translation initiation factor 2alpha subunit, expression of CHOP, and activation of caspase-12) was attenuated in cells that overexpress SLK. Tunicamycin 77-88 heat shock protein family A (Hsp70) member 5 Homo sapiens 116-119 16271832-11 2006 Indeed, tunicamycin, known to inhibit N-linked glycosylation in the ER, was found to induce a similar inverse correlation between GRP78 overexpression and HSP72/73 under-expression. Tunicamycin 8-19 heat shock protein family A (Hsp70) member 5 Homo sapiens 130-135 16271832-11 2006 Indeed, tunicamycin, known to inhibit N-linked glycosylation in the ER, was found to induce a similar inverse correlation between GRP78 overexpression and HSP72/73 under-expression. Tunicamycin 8-19 heat shock protein family A (Hsp70) member 1A Homo sapiens 155-160 16357177-4 2005 Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism. Tunicamycin 90-101 mitogen-activated protein kinase 8 Homo sapiens 126-153 16357177-4 2005 Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism. Tunicamycin 90-101 mitogen-activated protein kinase 8 Homo sapiens 155-158 16316340-5 2005 METHODS: The expression of ER stress inducible proteins (ORP150, GRP78, or GRP94) in cultured podocytes treated with tunicamycin, A23187, SNAP, hypoxia, or hyperglycemia, and the renal tissues or isolated glomeruli from megsin transgenic rats was analyzed by Western blotting analysis, immunohistochemistry, or confocal microscopy. Tunicamycin 117-128 hypoxia up-regulated 1 Rattus norvegicus 57-63 16316340-5 2005 METHODS: The expression of ER stress inducible proteins (ORP150, GRP78, or GRP94) in cultured podocytes treated with tunicamycin, A23187, SNAP, hypoxia, or hyperglycemia, and the renal tissues or isolated glomeruli from megsin transgenic rats was analyzed by Western blotting analysis, immunohistochemistry, or confocal microscopy. Tunicamycin 117-128 heat shock protein 90 beta family member 1 Rattus norvegicus 75-80 16107336-6 2005 Conversely, the UPR induced by tunicamycin substantially suppresses TNFalpha-induced ROS accumulation and cell death by inhibiting reduction of cellular glutathione levels. Tunicamycin 31-42 tumor necrosis factor Mus musculus 68-76 16014566-2 2005 In COS-7 cells transiently transfected with GPVI, deglycosylation with peptide-N-glycosidase F (PNGase F; specific for complex N-linked glycans) or tunicamycin decreases the molecular weight of GPVI and reduces transfected COS-7 cell binding to both CRP and CVX. Tunicamycin 148-159 glycoprotein VI platelet Homo sapiens 44-48 16014566-2 2005 In COS-7 cells transiently transfected with GPVI, deglycosylation with peptide-N-glycosidase F (PNGase F; specific for complex N-linked glycans) or tunicamycin decreases the molecular weight of GPVI and reduces transfected COS-7 cell binding to both CRP and CVX. Tunicamycin 148-159 glycoprotein VI platelet Homo sapiens 194-198 16014566-2 2005 In COS-7 cells transiently transfected with GPVI, deglycosylation with peptide-N-glycosidase F (PNGase F; specific for complex N-linked glycans) or tunicamycin decreases the molecular weight of GPVI and reduces transfected COS-7 cell binding to both CRP and CVX. Tunicamycin 148-159 C-reactive protein Homo sapiens 250-253 16118201-5 2005 Conditional nup1 and nup82 mutations are partially suppressed by the glycosylation inhibitor tunicamycin, while nic96 and nup116 alleles are hypersensitive to tunicamycin treatment, further implicating glycosylation in NPC function. Tunicamycin 93-104 FG-nucleoporin NUP1 Saccharomyces cerevisiae S288C 12-16 16118201-5 2005 Conditional nup1 and nup82 mutations are partially suppressed by the glycosylation inhibitor tunicamycin, while nic96 and nup116 alleles are hypersensitive to tunicamycin treatment, further implicating glycosylation in NPC function. Tunicamycin 93-104 linker nucleoporin NUP82 Saccharomyces cerevisiae S288C 21-26 16118201-5 2005 Conditional nup1 and nup82 mutations are partially suppressed by the glycosylation inhibitor tunicamycin, while nic96 and nup116 alleles are hypersensitive to tunicamycin treatment, further implicating glycosylation in NPC function. Tunicamycin 159-170 linker nucleoporin NIC96 Saccharomyces cerevisiae S288C 112-117 16118201-5 2005 Conditional nup1 and nup82 mutations are partially suppressed by the glycosylation inhibitor tunicamycin, while nic96 and nup116 alleles are hypersensitive to tunicamycin treatment, further implicating glycosylation in NPC function. Tunicamycin 159-170 FG-nucleoporin NUP116 Saccharomyces cerevisiae S288C 122-128 16166642-3 2005 Elevated expression of JAMP following UV or tunicamycin treatment results in sustained JNK activity and a higher level of JNK-dependent apoptosis. Tunicamycin 44-55 JNK1/MAPK8 associated membrane protein Homo sapiens 23-27 16180102-5 2005 TGF-beta1 increases the binding of laminin gamma1 to WGA-agarose and the binding is abolished by tunicamycin suggesting that laminin gamma1 is modified by N-linked glycosylation. Tunicamycin 97-108 transforming growth factor, beta 1 Mus musculus 0-9 16180102-5 2005 TGF-beta1 increases the binding of laminin gamma1 to WGA-agarose and the binding is abolished by tunicamycin suggesting that laminin gamma1 is modified by N-linked glycosylation. Tunicamycin 97-108 laminin, gamma 1 Mus musculus 35-49 16166642-3 2005 Elevated expression of JAMP following UV or tunicamycin treatment results in sustained JNK activity and a higher level of JNK-dependent apoptosis. Tunicamycin 44-55 mitogen-activated protein kinase 8 Homo sapiens 87-90 16180102-5 2005 TGF-beta1 increases the binding of laminin gamma1 to WGA-agarose and the binding is abolished by tunicamycin suggesting that laminin gamma1 is modified by N-linked glycosylation. Tunicamycin 97-108 laminin, gamma 1 Mus musculus 125-139 16166642-3 2005 Elevated expression of JAMP following UV or tunicamycin treatment results in sustained JNK activity and a higher level of JNK-dependent apoptosis. Tunicamycin 44-55 mitogen-activated protein kinase 8 Homo sapiens 122-125 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 16061483-8 2005 Tunicamycin treatment of HeLa cells induced a slow accumulation of calnexin dimers, the appearance of which correlated with enhanced calnexin binding to deglycosylated MHC class I heavy chains. Tunicamycin 0-11 calnexin Homo sapiens 67-75 16061483-8 2005 Tunicamycin treatment of HeLa cells induced a slow accumulation of calnexin dimers, the appearance of which correlated with enhanced calnexin binding to deglycosylated MHC class I heavy chains. Tunicamycin 0-11 calnexin Homo sapiens 133-141 16081652-8 2005 The results showed that various ER stressors (thapsigargin, A23187, tunicamycin, brefeldin A, and cisplatin) provoked a dramatic change in the localization of PSP from outside of the nucleus to inside the nucleus within 3 h. Moreover, the ER stressors induced PSP expression. Tunicamycin 68-79 reactive intermediate imine deaminase A homolog Homo sapiens 159-162 15845869-9 2005 Agents that perturb the synthesis and/or activity of ER chaperones such as tunicamycin and calcium ionophore A23187, have different effects on the solubility and degradation of alpha1-AT Z as well as on its residual secretion. Tunicamycin 75-86 serpin family A member 1 Homo sapiens 177-186 16091421-8 2005 Treatment of rat islets with both chronic high glucose and two ER stress inducers, thapsigargin and tunicamycin, enhanced SREBP-1 binding to the human IRS2 promoter. Tunicamycin 100-111 sterol regulatory element binding transcription factor 1 Rattus norvegicus 122-129 16091421-8 2005 Treatment of rat islets with both chronic high glucose and two ER stress inducers, thapsigargin and tunicamycin, enhanced SREBP-1 binding to the human IRS2 promoter. Tunicamycin 100-111 insulin receptor substrate 2 Homo sapiens 151-155 16081652-8 2005 The results showed that various ER stressors (thapsigargin, A23187, tunicamycin, brefeldin A, and cisplatin) provoked a dramatic change in the localization of PSP from outside of the nucleus to inside the nucleus within 3 h. Moreover, the ER stressors induced PSP expression. Tunicamycin 68-79 reactive intermediate imine deaminase A homolog Homo sapiens 260-263 15978049-9 2005 Phosphorylation of initiation factor-2alpha, which was inhibited by P58(IPK), was decreased in tunicamycin-treated plantlets. Tunicamycin 95-106 DnaJ P58IPK-like protein Arabidopsis thaliana 72-75 16024639-2 2005 In this study, we showed that tunicamycin, a naturally occurring antibiotic, is a potent enhancer of TRAIL-induced apoptosis through up-regulation of DR5 expression. Tunicamycin 30-41 TNF superfamily member 10 Homo sapiens 101-106 16024639-2 2005 In this study, we showed that tunicamycin, a naturally occurring antibiotic, is a potent enhancer of TRAIL-induced apoptosis through up-regulation of DR5 expression. Tunicamycin 30-41 TNF receptor superfamily member 10b Homo sapiens 150-153 16024639-3 2005 Tunicamycin significantly sensitized PC-3, androgen-independent human prostate cancer cells, to TRAIL-induced apoptosis. Tunicamycin 0-11 TNF superfamily member 10 Homo sapiens 96-101 16024639-4 2005 The tunicamycin-mediated enhancement of TRAIL-induced apoptosis was markedly blocked by a recombinant human DR5/Fc chimeric protein. Tunicamycin 4-15 TNF superfamily member 10 Homo sapiens 40-45 16024639-4 2005 The tunicamycin-mediated enhancement of TRAIL-induced apoptosis was markedly blocked by a recombinant human DR5/Fc chimeric protein. Tunicamycin 4-15 TNF receptor superfamily member 10b Homo sapiens 108-111 16024639-5 2005 Tunicamycin and TRAIL cooperatively activated caspase-8, -10, -9, and -3 and Bid cleavage and this activation was also blocked in the presence of the DR5/Fc chimera. Tunicamycin 0-11 caspase 8 Homo sapiens 46-72 16024639-5 2005 Tunicamycin and TRAIL cooperatively activated caspase-8, -10, -9, and -3 and Bid cleavage and this activation was also blocked in the presence of the DR5/Fc chimera. Tunicamycin 0-11 BH3 interacting domain death agonist Homo sapiens 77-80 16024639-5 2005 Tunicamycin and TRAIL cooperatively activated caspase-8, -10, -9, and -3 and Bid cleavage and this activation was also blocked in the presence of the DR5/Fc chimera. Tunicamycin 0-11 TNF receptor superfamily member 10b Homo sapiens 150-153 16024639-6 2005 Tunicamycin up-regulated DR5 expression at the mRNA and protein levels in a dose-dependent manner. Tunicamycin 0-11 TNF receptor superfamily member 10b Homo sapiens 25-28 16024639-7 2005 Furthermore, the tunicamycin-mediated sensitization to TRAIL was efficiently reduced by DR5 small interfering RNA, suggesting that the sensitization was mediated through induction of DR5 expression. Tunicamycin 17-28 TNF superfamily member 10 Homo sapiens 55-60 16024639-7 2005 Furthermore, the tunicamycin-mediated sensitization to TRAIL was efficiently reduced by DR5 small interfering RNA, suggesting that the sensitization was mediated through induction of DR5 expression. Tunicamycin 17-28 TNF receptor superfamily member 10b Homo sapiens 88-91 16024639-7 2005 Furthermore, the tunicamycin-mediated sensitization to TRAIL was efficiently reduced by DR5 small interfering RNA, suggesting that the sensitization was mediated through induction of DR5 expression. Tunicamycin 17-28 TNF receptor superfamily member 10b Homo sapiens 183-186 16024639-8 2005 Tunicamycin increased DR5 promoter activity and this enhanced activity was diminished by mutation of a CHOP-binding site. Tunicamycin 0-11 TNF receptor superfamily member 10b Homo sapiens 22-25 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 16024639-9 2005 In addition, suppression of CHOP expression by small interfering RNA reduced the tunicamycin-mediated induction of DR5. Tunicamycin 81-92 TNF receptor superfamily member 10b Homo sapiens 115-118 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 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 TNF receptor superfamily member 10b Homo sapiens 52-55 15864808-3 2005 Treatment targeting the ER with tunicamycin or thapsigargin induced the phosphorylation of Hsp27 but not of alphaB-crystallin in U373 MG cells, increase being observed after 2-10 h and decline at 24 h. Similar phosphorylation of Hsp27 by ER stress was also observed with U251 MG and HeLa but not in COS cells and could be blocked using SB203580, an inhibitor of p38 MAP kinase. Tunicamycin 32-43 heat shock protein family B (small) member 1 Homo sapiens 91-96 15864808-3 2005 Treatment targeting the ER with tunicamycin or thapsigargin induced the phosphorylation of Hsp27 but not of alphaB-crystallin in U373 MG cells, increase being observed after 2-10 h and decline at 24 h. Similar phosphorylation of Hsp27 by ER stress was also observed with U251 MG and HeLa but not in COS cells and could be blocked using SB203580, an inhibitor of p38 MAP kinase. Tunicamycin 32-43 heat shock protein family B (small) member 1 Homo sapiens 229-234 15864808-3 2005 Treatment targeting the ER with tunicamycin or thapsigargin induced the phosphorylation of Hsp27 but not of alphaB-crystallin in U373 MG cells, increase being observed after 2-10 h and decline at 24 h. Similar phosphorylation of Hsp27 by ER stress was also observed with U251 MG and HeLa but not in COS cells and could be blocked using SB203580, an inhibitor of p38 MAP kinase. Tunicamycin 32-43 mitogen-activated protein kinase 14 Homo sapiens 362-365 15864808-5 2005 Prolonged treatment with tunicamycin but not thapsigargin for 48 h caused the second induction of the phosphorylation of Hsp27 in U251 MG cells. Tunicamycin 25-36 heat shock protein family B (small) member 1 Homo sapiens 121-126 15994758-13 2005 Treatment of fibroblasts and MIN6 cells with thapsigargin or tunicamycin increased WFS1 mRNA. Tunicamycin 61-72 wolframin ER transmembrane glycoprotein Mus musculus 83-87 15857611-6 2005 Although transcription of the SNK gene was also regulated by tunicamycin, etoposide, or staurosporine, FK506 did not show any effects on these regulations. Tunicamycin 61-72 polo like kinase 2 Homo sapiens 30-33 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 15925308-3 2005 In the present study, rns4 (VPS32/SNF7) gene mutation was identified by complementation of tunicamycin sensitivity. Tunicamycin 91-102 ESCRT-III subunit protein SNF7 Saccharomyces cerevisiae S288C 22-26 15626688-7 2005 Antioxidants superoxide dismutase and catalase prevented the downregulation of NET proteins and induction of ER stress signals produced by NE but not by tunicamycin or thapsigargin. Tunicamycin 153-164 catalase Rattus norvegicus 38-46 15925308-3 2005 In the present study, rns4 (VPS32/SNF7) gene mutation was identified by complementation of tunicamycin sensitivity. Tunicamycin 91-102 ESCRT-III subunit protein SNF7 Saccharomyces cerevisiae S288C 28-33 15925308-3 2005 In the present study, rns4 (VPS32/SNF7) gene mutation was identified by complementation of tunicamycin sensitivity. Tunicamycin 91-102 ESCRT-III subunit protein SNF7 Saccharomyces cerevisiae S288C 34-38 15655246-10 2005 By the use of tunicamycin and endoglycosidase, NAAA was found to be a glycoprotein. Tunicamycin 14-25 N-acylethanolamine acid amidase Homo sapiens 47-51 15760841-5 2005 Sp proteins are constitutively bound to the ERSE; however, activation of GRP78 protein (or reporter gene) by thapsigargin or tunicamycin is inhibited after cotransfection with small inhibitory RNAs for Sp1, Sp3, and Sp4. Tunicamycin 125-136 heat shock protein family A (Hsp70) member 5 Homo sapiens 73-78 15760841-5 2005 Sp proteins are constitutively bound to the ERSE; however, activation of GRP78 protein (or reporter gene) by thapsigargin or tunicamycin is inhibited after cotransfection with small inhibitory RNAs for Sp1, Sp3, and Sp4. Tunicamycin 125-136 Sp3 transcription factor Homo sapiens 207-210 15760841-5 2005 Sp proteins are constitutively bound to the ERSE; however, activation of GRP78 protein (or reporter gene) by thapsigargin or tunicamycin is inhibited after cotransfection with small inhibitory RNAs for Sp1, Sp3, and Sp4. Tunicamycin 125-136 Sp4 transcription factor Homo sapiens 216-219 15823038-3 2005 Treatment of cells with a glycosylation inhibitor tunicamycin significantly impaired LRP folding, although binding to receptor-associated protein (RAP), a specialized chaperone for LRP, was not affected. Tunicamycin 50-61 LDL receptor related protein 1 Homo sapiens 85-88 15823038-4 2005 The effects of tunicamycin on LRP folding were not due to an inhibition of RAP glycosylation since a mutant RAP that harbors a mutation at its sole glycosylation site was still capable of promoting LRP folding. Tunicamycin 15-26 LDL receptor related protein 1 Homo sapiens 30-33 15823038-4 2005 The effects of tunicamycin on LRP folding were not due to an inhibition of RAP glycosylation since a mutant RAP that harbors a mutation at its sole glycosylation site was still capable of promoting LRP folding. Tunicamycin 15-26 LDL receptor related protein associated protein 1 Homo sapiens 108-111 15823038-4 2005 The effects of tunicamycin on LRP folding were not due to an inhibition of RAP glycosylation since a mutant RAP that harbors a mutation at its sole glycosylation site was still capable of promoting LRP folding. Tunicamycin 15-26 LDL receptor related protein 1 Homo sapiens 198-201 15823039-5 2005 The presence of N-glycans was first suggested by sensibility of the 113-kDa nucleolin isoform to tunicamycin treatment. Tunicamycin 97-108 nucleolin Homo sapiens 76-85 15781873-1 2005 Analysis of transcripts of 75 genes encoding putative basic leucine zipper (bZIP) transcription factors in the Arabidopsis genome identified AtbZIP60, which was induced by tunicamycin. Tunicamycin 172-183 basic region/leucine zipper motif 60 Arabidopsis thaliana 141-149 15662046-8 2005 Tunicamycin, an inhibitor of glycosylation, decreased the molecular mass and simultaneously impaired the trafficking of Mrp2 to the canalicular membrane. Tunicamycin 0-11 ATP binding cassette subfamily C member 2 Rattus norvegicus 120-124 15794758-9 2005 Glycosylation of Hu-K4 as shown by treatment with peptide N-glycosidase F or tunicamycin indicates that Hu-K4 has a type 2 transmembrane topology. Tunicamycin 77-88 phospholipase D family member 3 Homo sapiens 17-22 15794758-9 2005 Glycosylation of Hu-K4 as shown by treatment with peptide N-glycosidase F or tunicamycin indicates that Hu-K4 has a type 2 transmembrane topology. Tunicamycin 77-88 phospholipase D family member 3 Homo sapiens 104-109 15576633-3 2005 We showed that both the disruption of the glycosylation sites by mutagenesis and the inhibition of glycosylation by tunicamycin treatment resulted in a nonglycosylated hOAT4, which was unable to target to the cell surface. Tunicamycin 116-127 solute carrier family 22 member 11 Homo sapiens 168-173 15775988-5 2005 Tunicamycin treatment enhanced the TRB3 promoter activity, while dominant-negative forms of CHOP suppressed the tunicamycin-induced activation. Tunicamycin 0-11 tribbles pseudokinase 3 Homo sapiens 35-39 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 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 tribbles pseudokinase 3 Homo sapiens 52-56 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 15775988-6 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 activating transcription factor 4 Homo sapiens 152-156 15775988-7 2005 Knockdown of endogenous ATF4 or CHOP expression dramatically repressed tunicamycin-induced TRB3 induction. Tunicamycin 71-82 activating transcription factor 4 Homo sapiens 24-28 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 15775988-7 2005 Knockdown of endogenous ATF4 or CHOP expression dramatically repressed tunicamycin-induced TRB3 induction. Tunicamycin 71-82 tribbles pseudokinase 3 Homo sapiens 91-95 15320871-12 2005 Tunicamycin inhibited the expression of the 50 and 37 kDa CD83 forms, and also blocked CD83 surface expression on DCs and macrophages. Tunicamycin 0-11 CD83 molecule Homo sapiens 58-62 15557337-9 2005 By contrast, HIF-1alpha-VP16-expressing HT22 cells were more resistant to DNA damage (induced by camptothecin) or endoplasmic reticulum stress (induced by thapsigargin and tunicamycin) than were VP16-expressing cells, and suppression of HIF-1alpha expression using RNA interference rendered HT22 cells more sensitive to death induced by DNA damage or endoplasmic reticulum stress. Tunicamycin 172-183 hypoxia inducible factor 1, alpha subunit Mus musculus 13-23 15458386-5 2005 Treating alk-SMase cDNA-transfected COS-7 cells with tunicamycin rendered the expressed enzyme completely inactive. Tunicamycin 53-64 ectonucleotide pyrophosphatase/phosphodiesterase 7 Homo sapiens 9-18 15320871-12 2005 Tunicamycin inhibited the expression of the 50 and 37 kDa CD83 forms, and also blocked CD83 surface expression on DCs and macrophages. Tunicamycin 0-11 CD83 molecule Homo sapiens 87-91 15522226-4 2004 Another ER-stress inducer, the N-glycosylation inhibitor tunicamycin, also raised WFS1 mRNA but not protein levels. Tunicamycin 57-68 wolframin ER transmembrane glycoprotein Mus musculus 82-86 15733745-10 2005 Moreover, inhibition of IR processing with tunicamycin indicated that the basal interaction of PTP1B with IR occurred during biosynthesis of the IR precursor in the endoplasmic reticulum. Tunicamycin 43-54 insulin receptor Homo sapiens 24-26 15733745-10 2005 Moreover, inhibition of IR processing with tunicamycin indicated that the basal interaction of PTP1B with IR occurred during biosynthesis of the IR precursor in the endoplasmic reticulum. Tunicamycin 43-54 protein tyrosine phosphatase non-receptor type 1 Homo sapiens 95-100 15733745-10 2005 Moreover, inhibition of IR processing with tunicamycin indicated that the basal interaction of PTP1B with IR occurred during biosynthesis of the IR precursor in the endoplasmic reticulum. Tunicamycin 43-54 insulin receptor Homo sapiens 106-108 15733745-10 2005 Moreover, inhibition of IR processing with tunicamycin indicated that the basal interaction of PTP1B with IR occurred during biosynthesis of the IR precursor in the endoplasmic reticulum. Tunicamycin 43-54 insulin receptor Homo sapiens 106-108 15488943-6 2005 mTSLPR produced in presence of tunicamycin migrated with a molecular weight around 40 kDa. Tunicamycin 31-42 cytokine receptor-like factor 2 Mus musculus 0-6 15527836-8 2004 Tunicamycin, an N-glycosylation inhibitor, increased transduction titer in the wild-type rCAT1-expressing cells, but did not do so in the cells expressing either the mCAT1 or rCAT1 mutation 1. Tunicamycin 0-11 solute carrier family 7 member 1 Rattus norvegicus 89-94 15492001-9 2004 Because the cell surface expression of functional DAT requires its oligomerization, misfolded DAT, induced either by the protein glycosylation inhibitor tunicamycin or by its C-terminal truncation, significantly attenuated cell surface expression of native DAT and reduced dopamine uptake. Tunicamycin 153-164 solute carrier family 6 member 3 Homo sapiens 50-53 15492001-9 2004 Because the cell surface expression of functional DAT requires its oligomerization, misfolded DAT, induced either by the protein glycosylation inhibitor tunicamycin or by its C-terminal truncation, significantly attenuated cell surface expression of native DAT and reduced dopamine uptake. Tunicamycin 153-164 solute carrier family 6 member 3 Homo sapiens 94-97 15492001-9 2004 Because the cell surface expression of functional DAT requires its oligomerization, misfolded DAT, induced either by the protein glycosylation inhibitor tunicamycin or by its C-terminal truncation, significantly attenuated cell surface expression of native DAT and reduced dopamine uptake. Tunicamycin 153-164 solute carrier family 6 member 3 Homo sapiens 94-97 15522226-7 2004 Consistent with this, the WFS1 protein was more rapidly degraded in the presence of tunicamycin. Tunicamycin 84-95 wolframin ER transmembrane glycoprotein Mus musculus 26-30 15465829-5 2004 More specifically, JNK activation, XBP-1 splicing, and EDEM (ER degradation-enhancing alpha-mannosidase-like protein) gene induction, as well as ER stress-induced apoptosis, were attenuated in PTP-1B knock-out mouse embryonic fibroblasts in response to two ER stressors, tunicamycin and azetidine-2 carboxylic acid. Tunicamycin 271-282 protein tyrosine phosphatase, non-receptor type 1 Mus musculus 193-199 15601821-6 2004 Furthermore, mice lacking GADD34-directed eIF2alpha dephosphorylation, like CHOP(-/-) mice, are resistant to renal toxicity of the ER stress-inducing drug tunicamycin. Tunicamycin 155-166 protein phosphatase 1, regulatory subunit 15A Mus musculus 26-32 15601821-6 2004 Furthermore, mice lacking GADD34-directed eIF2alpha dephosphorylation, like CHOP(-/-) mice, are resistant to renal toxicity of the ER stress-inducing drug tunicamycin. Tunicamycin 155-166 eukaryotic translation initiation factor 2A Mus musculus 42-51 15601821-6 2004 Furthermore, mice lacking GADD34-directed eIF2alpha dephosphorylation, like CHOP(-/-) mice, are resistant to renal toxicity of the ER stress-inducing drug tunicamycin. Tunicamycin 155-166 DNA-damage inducible transcript 3 Mus musculus 76-80 15572843-9 2004 The tunicamycin-induced up-regulation of GRP78 and GRP94 and phosphorylation of PERK was suppressed by treatment with 4-PBA, indicating that 4-PBA suppresses ER stress responses by decreasing unfolded protein. Tunicamycin 4-15 heat shock protein family A (Hsp70) member 5 Homo sapiens 41-46 15572843-9 2004 The tunicamycin-induced up-regulation of GRP78 and GRP94 and phosphorylation of PERK was suppressed by treatment with 4-PBA, indicating that 4-PBA suppresses ER stress responses by decreasing unfolded protein. Tunicamycin 4-15 heat shock protein 90 beta family member 1 Homo sapiens 51-56 15572843-9 2004 The tunicamycin-induced up-regulation of GRP78 and GRP94 and phosphorylation of PERK was suppressed by treatment with 4-PBA, indicating that 4-PBA suppresses ER stress responses by decreasing unfolded protein. Tunicamycin 4-15 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 80-84 15485913-3 2004 Expression of STC2 gene is rapidly upregulated in cultured cells after exposure to tunicamycin and thapsigargin, by ATF4 after activation of the ER-resident kinase PERK. Tunicamycin 83-94 stanniocalcin 2 Homo sapiens 14-18 15339911-3 2004 Here, we have shown that endogenous Akt and ERK are rapidly activated and act as downstream effectors of phosphatidylinositol 3-kinase in thapsigargin- or tunicamycin-induced ER stress. Tunicamycin 155-166 AKT serine/threonine kinase 1 Homo sapiens 36-39 15339911-3 2004 Here, we have shown that endogenous Akt and ERK are rapidly activated and act as downstream effectors of phosphatidylinositol 3-kinase in thapsigargin- or tunicamycin-induced ER stress. Tunicamycin 155-166 mitogen-activated protein kinase 1 Homo sapiens 44-47 15319438-4 2004 Tunicamycin and brefeldin A, two ER stress inducers, increased the expression of COX-2 in ML-1 or MCF-7 cells. Tunicamycin 0-11 mitochondrially encoded cytochrome c oxidase II Homo sapiens 81-86 15319438-4 2004 Tunicamycin and brefeldin A, two ER stress inducers, increased the expression of COX-2 in ML-1 or MCF-7 cells. Tunicamycin 0-11 interleukin 17F Homo sapiens 90-94 15519674-8 2004 In addition, the levels of mHRD1 mRNA were markedly elevated in glial cells exposed to treatment with tunicamycin (Tm, an ER stress inducer). Tunicamycin 102-113 synovial apoptosis inhibitor 1, synoviolin Mus musculus 27-32 15518647-5 2004 Here, we report that BDNF suppressed the ER stress-mediated cell death in tunicamycin (Tm)-treated cerebral cortical neurons. Tunicamycin 74-85 brain-derived neurotrophic factor Rattus norvegicus 21-25 15518647-5 2004 Here, we report that BDNF suppressed the ER stress-mediated cell death in tunicamycin (Tm)-treated cerebral cortical neurons. Tunicamycin 87-89 brain-derived neurotrophic factor Rattus norvegicus 21-25 15485913-3 2004 Expression of STC2 gene is rapidly upregulated in cultured cells after exposure to tunicamycin and thapsigargin, by ATF4 after activation of the ER-resident kinase PERK. Tunicamycin 83-94 activating transcription factor 4 Homo sapiens 116-120 15648788-3 2004 Expression of GRP78 at both protein and mRNA levels was markedly increased in cardiomyocytes pretreated with tunicamycin, when compared to non-treatment controls. Tunicamycin 109-120 heat shock protein family A (Hsp70) member 5 Homo sapiens 14-19 15342690-2 2004 Reduction in molecular mass of EL after treatment with glycosidases and after treatment of EL-expressing cells with the glycosylation inhibitor tunicamycin demonstrated that EL is a glycosylated protein. Tunicamycin 144-155 lipase G, endothelial type Homo sapiens 91-93 15342690-2 2004 Reduction in molecular mass of EL after treatment with glycosidases and after treatment of EL-expressing cells with the glycosylation inhibitor tunicamycin demonstrated that EL is a glycosylated protein. Tunicamycin 144-155 lipase G, endothelial type Homo sapiens 91-93 15341532-7 2004 This effect was prevented by pretreatment with tunicamycin or brefeldin, suggesting that donepezil affects trafficking and/or maturation of ADAM 10; additionally, this pretreatment significantly decreased sAPPalpha levels. Tunicamycin 47-58 ADAM metallopeptidase domain 10 Homo sapiens 140-147 15383281-5 2004 In cells, calreticulin oligomerization intermediates accumulate in response to conditions that induce protein misfolding (heat shock and tunicamycin treatments), and upon calcium depletion. Tunicamycin 137-148 calreticulin Homo sapiens 10-22 15313195-2 2004 Tunicamycin pretreatment of Madin-Darby canine kidney cells not only preserved E-cadherin staining at the plasma membrane, but also inhibited ATP-depletion-mediated E-cadherin degradation. Tunicamycin 0-11 cadherin 1 Canis lupus familiaris 79-89 15313195-2 2004 Tunicamycin pretreatment of Madin-Darby canine kidney cells not only preserved E-cadherin staining at the plasma membrane, but also inhibited ATP-depletion-mediated E-cadherin degradation. Tunicamycin 0-11 cadherin 1 Canis lupus familiaris 165-175 15313195-3 2004 Electron microscopic analysis, together with the preservation of the staining patterns of the tight junction marker ZO-1, the apical/microvillar marker gp135, and basolateral marker Na/K-ATPase suggested that tunicamycin preserved the junctional complex and the polarized epithelial cell phenotype. Tunicamycin 209-220 podocalyxin like Canis lupus familiaris 152-157 15178695-5 2004 In mouse primary cultured glial cells, edaravone attenuated ER stress as evidenced by inhibition of the induction of glucose regulated protein 78 and CHOP and XBP-1 splicing under treatment with tunicamycin (Tm), which induces ER stress. Tunicamycin 195-206 X-box binding protein 1 Mus musculus 159-164 15178695-5 2004 In mouse primary cultured glial cells, edaravone attenuated ER stress as evidenced by inhibition of the induction of glucose regulated protein 78 and CHOP and XBP-1 splicing under treatment with tunicamycin (Tm), which induces ER stress. Tunicamycin 208-210 DNA-damage inducible transcript 3 Mus musculus 150-154 15178695-5 2004 In mouse primary cultured glial cells, edaravone attenuated ER stress as evidenced by inhibition of the induction of glucose regulated protein 78 and CHOP and XBP-1 splicing under treatment with tunicamycin (Tm), which induces ER stress. Tunicamycin 208-210 X-box binding protein 1 Mus musculus 159-164 15201339-2 2004 We demonstrate that the misfolding agents azetidine-2-carboxylic acid (Azc) and tunicamycin initiate signaling from the ER, resulting in the activation of Jun-N-terminal kinase, p44(MAPK)/extracellular signal-regulated kinase-1 (ERK-1), and p38(MAPK) through IRE1alpha-dependent mechanisms. Tunicamycin 80-91 mitogen activated protein kinase 3 Rattus norvegicus 178-181 15201339-2 2004 We demonstrate that the misfolding agents azetidine-2-carboxylic acid (Azc) and tunicamycin initiate signaling from the ER, resulting in the activation of Jun-N-terminal kinase, p44(MAPK)/extracellular signal-regulated kinase-1 (ERK-1), and p38(MAPK) through IRE1alpha-dependent mechanisms. Tunicamycin 80-91 mitogen activated protein kinase 3 Rattus norvegicus 188-227 15201339-2 2004 We demonstrate that the misfolding agents azetidine-2-carboxylic acid (Azc) and tunicamycin initiate signaling from the ER, resulting in the activation of Jun-N-terminal kinase, p44(MAPK)/extracellular signal-regulated kinase-1 (ERK-1), and p38(MAPK) through IRE1alpha-dependent mechanisms. Tunicamycin 80-91 mitogen activated protein kinase 3 Rattus norvegicus 229-234 15201339-2 2004 We demonstrate that the misfolding agents azetidine-2-carboxylic acid (Azc) and tunicamycin initiate signaling from the ER, resulting in the activation of Jun-N-terminal kinase, p44(MAPK)/extracellular signal-regulated kinase-1 (ERK-1), and p38(MAPK) through IRE1alpha-dependent mechanisms. Tunicamycin 80-91 mitogen activated protein kinase 14 Rattus norvegicus 241-244 15155747-11 2004 Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5. Tunicamycin 67-78 TNF receptor superfamily member 10b Homo sapiens 144-154 15155747-11 2004 Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5. Tunicamycin 67-78 TNF superfamily member 10 Homo sapiens 15-20 15155747-12 2004 Our data suggest that tumor cells may become resistant to TRAIL through regulation of the death receptor cell surface transport and that resistance to TRAIL may be overcome by the glycosylation inhibitor/endoplasmic reticulum stress-inducing agent tunicamycin. Tunicamycin 248-259 TNF superfamily member 10 Homo sapiens 151-156 15155747-11 2004 Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5. Tunicamycin 67-78 TNF superfamily member 10 Homo sapiens 58-63 15155747-11 2004 Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5. Tunicamycin 67-78 TNF receptor superfamily member 10a Homo sapiens 136-139 15304216-3 2004 Cells from BI-1-deficient mice, including fibroblasts, hepatocytes, and neurons, display selective hypersensitivity to apoptosis induced by ER stress agents (thapsigargin, tunicamycin, brefeldin A), but not to stimulators of mitochondrial or TNF/Fas-death receptor apoptosis pathways. Tunicamycin 172-183 transmembrane BAX inhibitor motif containing 6 Mus musculus 11-15 15304216-7 2004 In vivo, bi-1(-/-) mice exhibit increased sensitivity to tissue damage induced by stimuli that trigger ER stress, including stroke and tunicamycin injection. Tunicamycin 135-146 transmembrane BAX inhibitor motif containing 6 Mus musculus 9-13 15294089-5 2004 Analysis of glycosylation status of the J-chain in the transfectant was examined by tunicamycin treatment, endoglycosidase H digestion, and also by treatment with brefeldin A. Tunicamycin 84-95 joining chain of multimeric IgA and IgM Homo sapiens 40-47 15102854-2 2004 The data in the present study document that transcription from the human C/EBPbeta gene is induced in response to endoplasmic reticulum stress, such as glucose deprivation, or treatment of cells with tunicamycin or thapsigargin. Tunicamycin 200-211 CCAAT enhancer binding protein beta Homo sapiens 73-82 14990584-6 2004 Here we show that eIF4E rescued cells from the ER stressors brefeldin A, tunicamycin, thapsigargin, and the Ca(2+) ionophore A23187. Tunicamycin 73-84 eukaryotic translation initiation factor 4E Homo sapiens 18-23 15102851-6 2004 The transcript of uda-1 but not those of two other C. elegans ENTPDase mRNAs (ntp-1 and mig-23) was induced up to 3.5-fold by high temperature, tunicamycin, and ethanol. Tunicamycin 144-155 Nucleoside-diphosphatase uda-1 Caenorhabditis elegans 18-23 14676213-3 2004 Overexpression of Nck-1 enhances protein translation, whereas it abrogates eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation and inhibition of translation in response to tunicamycin or thapsigargin treatment. Tunicamycin 184-195 non-catalytic region of tyrosine kinase adaptor protein 1 Mus musculus 18-23 15063746-3 2004 Glucose deprivation and the ER stress inducers tunicamycin and thapsigargin increased SelS gene expression and protein content several-fold in parallel with glucose-regulated protein 78. Tunicamycin 47-58 selenoprotein S Homo sapiens 86-90 14973138-1 2004 The endoplasmic reticulum (ER) transmembrane proteins, ATF6alpha and ATF6beta, are cleaved in response to ER stress, which can be induced by tunicamycin. Tunicamycin 141-152 activating transcription factor 6 Homo sapiens 55-64 14973138-1 2004 The endoplasmic reticulum (ER) transmembrane proteins, ATF6alpha and ATF6beta, are cleaved in response to ER stress, which can be induced by tunicamycin. Tunicamycin 141-152 activating transcription factor 6 beta Homo sapiens 69-77 14749323-4 2004 274, 1519-1524) that tunicamycin, an inhibitor of asparagine-linked glycosylation, significantly inhibited organic anion transport in COS-7 cells expressing a mouse organic anion transporter (mOAT1), suggesting an important role of glycosylation in mOAT1 function. Tunicamycin 21-32 solute carrier family 22 (organic anion transporter), member 6 Mus musculus 192-197 14749323-4 2004 274, 1519-1524) that tunicamycin, an inhibitor of asparagine-linked glycosylation, significantly inhibited organic anion transport in COS-7 cells expressing a mouse organic anion transporter (mOAT1), suggesting an important role of glycosylation in mOAT1 function. Tunicamycin 21-32 solute carrier family 22 (organic anion transporter), member 6 Mus musculus 249-254 15113843-2 2004 Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity. Tunicamycin 93-104 nerve growth factor Rattus norvegicus 20-39 15113843-2 2004 Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity. Tunicamycin 93-104 nerve growth factor Rattus norvegicus 41-44 15113843-2 2004 Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity. Tunicamycin 93-104 caspase 3 Rattus norvegicus 161-173 14765129-5 2004 The level of nuclear PKR was elevated, but the level of cytoplasmic PKR barely changed in tunicamycin-treated SK-N-SH cells. Tunicamycin 90-101 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 68-71 15006708-0 2004 Fibroblasts from FAD-linked presenilin 1 mutations display a normal unfolded protein response but overproduce Abeta42 in response to tunicamycin. Tunicamycin 133-144 presenilin 1 Homo sapiens 28-40 15006708-5 2004 In contrast, tunicamycin, which allowed exit of APP from the ER, increased secreted Abeta42 only in PS1 mutant fibroblasts. Tunicamycin 13-24 presenilin 1 Homo sapiens 100-103 14765129-6 2004 Furthermore, tunicamycin also raised levels of phosphorylated PKR in the nucleus. Tunicamycin 13-24 eukaryotic translation initiation factor 2 alpha kinase 2 Homo sapiens 62-65 14744598-9 2004 FR167653 also inhibited the transactivation of calreticulin stimulated by two other endoplasmic reticulum stress inducers, tunicamycin and A23187. Tunicamycin 123-134 calreticulin Homo sapiens 47-59 15611953-2 2004 CHOP deficient (chop - / - ) mouse embryonic fibroblasts (MEFs) exposed to ER stresses such as tunicamycin exhibit decreased apoptosis and reduced toxicity when compared to chop + / + control cells. Tunicamycin 95-106 DNA-damage inducible transcript 3 Mus musculus 16-20 14738568-8 2004 RESULTS: We found that glutamine deprivation and treatment with a chemical inducer of ER stress (tunicamycin) caused a marked induction of the secretion of both VEGF and IL-8 protein by a human breast adenocarcinoma cell line (TSE cells). Tunicamycin 97-108 vascular endothelial growth factor A Homo sapiens 161-165 14738568-8 2004 RESULTS: We found that glutamine deprivation and treatment with a chemical inducer of ER stress (tunicamycin) caused a marked induction of the secretion of both VEGF and IL-8 protein by a human breast adenocarcinoma cell line (TSE cells). Tunicamycin 97-108 C-X-C motif chemokine ligand 8 Homo sapiens 170-174 14724446-8 2004 Tunicamycin and endoglycosidase treatments determined the extent of rNKp30 glycosylation. Tunicamycin 0-11 natural cytotoxicity triggering receptor 3 Rattus norvegicus 68-74 15611953-2 2004 CHOP deficient (chop - / - ) mouse embryonic fibroblasts (MEFs) exposed to ER stresses such as tunicamycin exhibit decreased apoptosis and reduced toxicity when compared to chop + / + control cells. Tunicamycin 95-106 DNA-damage inducible transcript 3 Mus musculus 173-177 15611953-8 2004 Enhanced apoptosis and toxicity were observed in chop + / + cells following exposure to tunicamycin or PH mediated PDT when compared to identical treatments in chop - / - cells. Tunicamycin 88-99 DNA-damage inducible transcript 3 Mus musculus 49-53 14690445-3 2003 In contrast, tunicamycin, A23187, and low concentrations of cycloheximide promoted eIF2alpha phosphorylation in Sf9 cells but without apoptosis. Tunicamycin 13-24 eukaryotic translation initiation factor 2A Homo sapiens 83-92 12928435-8 2003 Tunicamycin, an inhibitor of N-linked glycosylation, blocked surface membrane expression of HCN2. Tunicamycin 0-11 hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2 Homo sapiens 92-96 14632661-11 2003 In addition, preincubation of WT-CD16-transfected cells with Tunicamycin (an inhibitor of N-glycosylation) resulted in an increased binding of monomeric IgG whereas N163Q-CD16-transfected cells remained unaffected. Tunicamycin 61-72 Fc gamma receptor IIIa Homo sapiens 33-37 14632661-11 2003 In addition, preincubation of WT-CD16-transfected cells with Tunicamycin (an inhibitor of N-glycosylation) resulted in an increased binding of monomeric IgG whereas N163Q-CD16-transfected cells remained unaffected. Tunicamycin 61-72 Fc gamma receptor IIIa Homo sapiens 171-175 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 14530330-6 2003 Treatment of Ag-pulsed OT-1 CTL with agents that alter cell surface charge, including trypsin, papain, tunicamycin, neuraminidase, and polybrene, allowed Ag-specific TCR capping. Tunicamycin 103-114 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 166-169 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 12738777-5 2003 TDAG51 expression was attenuated in homozygous A/A mutant eukaryotic translation initiation factor 2 alpha mouse embryonic fibroblasts treated with homocysteine or tunicamycin, suggesting that ER stress-induced phosphorylation of eukaryotic translation initiation factor 2 alpha is required for TDAG51 transcriptional activation. Tunicamycin 164-175 pleckstrin homology like domain, family A, member 1 Mus musculus 0-6 14517337-4 2003 ER stress generated in response to miconazole, tunicamycin, or other inhibitors also triggered a transient G2/M arrest that depended upon the Swe1 protein kinase. Tunicamycin 47-58 tyrosine protein kinase SWE1 Saccharomyces cerevisiae S288C 142-146 12950021-6 2003 Tunicamycin diminished the antigenicity of NCR-G3 cells. Tunicamycin 0-11 Neutrophil migration (granulocyte glycoprotein) Homo sapiens 43-46 12913114-4 2003 Microarray analysis of gene expression changes during tunicamycin-induced apoptosis revealed that the Bcl-2 homology domain 3-only family member, Bcl-2 binding component 3/p53 upregulated modulator of apoptosis (Bbc3/PUMA), was the most strongly induced pro-apoptotic gene. Tunicamycin 54-65 BCL2 binding component 3 Homo sapiens 212-216 12736248-7 2003 Furthermore, we demonstrated that dig2 is a novel stress response gene, as its mRNA is induced in response to a variety of cellular stressors including thapsigargin, tunicamycin, and heat shock. Tunicamycin 166-177 DNA-damage-inducible transcript 4 Mus musculus 34-38 12824288-6 2003 The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells. Tunicamycin 190-201 eukaryotic translation initiation factor 2A Mus musculus 23-71 12824288-6 2003 The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells. Tunicamycin 190-201 eukaryotic translation initiation factor 2A Mus musculus 73-82 12824288-6 2003 The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells. Tunicamycin 190-201 protein phosphatase 1, regulatory subunit 15A Mus musculus 141-147 12824288-6 2003 The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells. Tunicamycin 190-201 eukaryotic translation initiation factor 2A Mus musculus 207-216 12824288-6 2003 The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells. Tunicamycin 190-201 protein phosphatase 1, regulatory subunit 15A Mus musculus 264-270 12824288-6 2003 The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells. Tunicamycin 190-201 protein phosphatase 1, regulatory subunit 15A Mus musculus 264-270 12727195-4 2003 Here, we report that the mRNA of lectin ERGIC-53, a cargo receptor for the transport of glycoproteins from ER to ERGIC, and of its related protein VIP36 is induced by the known inducers of ER stress, tunicamycin and thapsigargin. Tunicamycin 200-211 lectin, mannose binding 1 Homo sapiens 40-48 12843613-5 2003 NF-kappaB was activated by ER stress-inducing agents, thapsigargin and tunicamycin. Tunicamycin 71-82 nuclear factor kappa B subunit 1 Homo sapiens 0-9 12805451-7 2003 The R(+) Env protein induced syncytia in XC cells expressing a mutant mCAT1 lacking both of two N glycosylation sites, and tunicamycin treatment suppressed syncytium formation by R(+) Env in those cells. Tunicamycin 123-134 solute carrier family 7 (cationic amino acid transporter, y+ system), member 1 Mus musculus 70-75 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 12808051-6 2003 Conversely, cells carrying a mutation in the Kar2 ATPase domain, in which Kar2 poorly dissociated from Ire1 even in the presence of tunicamycin, a potent inducer of ER stress, were unable to activate the pathway. Tunicamycin 132-143 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 45-49 12727195-4 2003 Here, we report that the mRNA of lectin ERGIC-53, a cargo receptor for the transport of glycoproteins from ER to ERGIC, and of its related protein VIP36 is induced by the known inducers of ER stress, tunicamycin and thapsigargin. Tunicamycin 200-211 lectin, mannose binding 2 Homo sapiens 147-152 12634852-5 2003 Inhibition of insulin-receptor processing using tunicamycin suggests that the basal interaction occurs during insulin-receptor biosynthesis in the ER. Tunicamycin 48-59 insulin receptor Homo sapiens 14-30 12578559-10 2003 However, AE2 expressed in the presence of the glycosylation inhibitor, tunicamycin, was not glycosylated, yet retained 85 +/- 8% of anion-transport activity. Tunicamycin 71-82 NBPF member 3 Homo sapiens 9-12 12754298-4 2003 Cells in which ARMER was overexpressed exhibited protection from multiple apoptotic inducers including serum starvation, doxorubicin, UV irradiation, tumor necrosis factor alpha, and the ER stressors brefeldin A, tunicamycin, and thapsigargin. Tunicamycin 213-224 ADP ribosylation factor like GTPase 6 interacting protein 1 Homo sapiens 15-20 12634852-5 2003 Inhibition of insulin-receptor processing using tunicamycin suggests that the basal interaction occurs during insulin-receptor biosynthesis in the ER. Tunicamycin 48-59 insulin receptor Homo sapiens 110-126 12845220-6 2003 Overproduction of fibronectin and tenascin by HMCs was normalized by tunicamycin and brefeldin A. Tunicamycin 69-80 fibronectin 1 Homo sapiens 18-29 12535667-2 2003 In transgenic plants, tunicamycin stimulated expression of a reporter gene under the control of the BiP promoter and promoter analysis identified a 24 bp sequence crucial to this induction. Tunicamycin 22-33 Heat shock protein 70 (Hsp 70) family protein Arabidopsis thaliana 100-103 12488460-6 2003 Digestion of immunoprecipitated TPP I proenzyme with both N-glycosidase F and endoglycosidase H as well as treatment of the cells with tunicamycin reduced the molecular mass of TPP I proenzyme by approximately 10 kDa, which indicates that all five potential N-glycosylation sites in TPP I are utilized. Tunicamycin 135-146 tripeptidyl peptidase 1 Homo sapiens 32-37 12488460-6 2003 Digestion of immunoprecipitated TPP I proenzyme with both N-glycosidase F and endoglycosidase H as well as treatment of the cells with tunicamycin reduced the molecular mass of TPP I proenzyme by approximately 10 kDa, which indicates that all five potential N-glycosylation sites in TPP I are utilized. Tunicamycin 135-146 tripeptidyl peptidase 1 Homo sapiens 177-182 12488460-6 2003 Digestion of immunoprecipitated TPP I proenzyme with both N-glycosidase F and endoglycosidase H as well as treatment of the cells with tunicamycin reduced the molecular mass of TPP I proenzyme by approximately 10 kDa, which indicates that all five potential N-glycosylation sites in TPP I are utilized. Tunicamycin 135-146 tripeptidyl peptidase 1 Homo sapiens 177-182 12556489-2 2003 In this report, we show that the expression of human GADD34 in cultured cells reversed eIF-2 alpha phosphorylation induced by thapsigargin and tunicamycin, agents that promote protein unfolding in the endoplasmic reticulum (ER). Tunicamycin 143-154 protein phosphatase 1 regulatory subunit 15A Homo sapiens 53-59 12556489-2 2003 In this report, we show that the expression of human GADD34 in cultured cells reversed eIF-2 alpha phosphorylation induced by thapsigargin and tunicamycin, agents that promote protein unfolding in the endoplasmic reticulum (ER). Tunicamycin 143-154 eukaryotic translation initiation factor 2A Homo sapiens 87-98 12845220-6 2003 Overproduction of fibronectin and tenascin by HMCs was normalized by tunicamycin and brefeldin A. Tunicamycin 69-80 tenascin C Homo sapiens 34-42 12845220-6 2003 Overproduction of fibronectin and tenascin by HMCs was normalized by tunicamycin and brefeldin A. Tunicamycin 69-80 MKKS centrosomal shuttling protein Homo sapiens 46-50 12845220-7 2003 Similarly, when HMCs were exposed to exogenous TGF-beta, the increase in fibronectin was reversed by tunicamycin and brefeldin A. Tunicamycin 101-112 MKKS centrosomal shuttling protein Homo sapiens 16-20 12845220-7 2003 Similarly, when HMCs were exposed to exogenous TGF-beta, the increase in fibronectin was reversed by tunicamycin and brefeldin A. Tunicamycin 101-112 transforming growth factor beta 1 Homo sapiens 47-55 12845220-7 2003 Similarly, when HMCs were exposed to exogenous TGF-beta, the increase in fibronectin was reversed by tunicamycin and brefeldin A. Tunicamycin 101-112 fibronectin 1 Homo sapiens 73-84 12943552-3 2003 The influence of N-glycosylation on AtXylT activity has been evaluated using either tunicamycin or mutagenesis of potential N-glycosylation sites. Tunicamycin 84-95 beta-1,2-xylosyltransferase Arabidopsis thaliana 36-42 14643758-4 2003 Treatment with SAC protected these cells against Abeta- and tunicamycin-induced neuronal death, which is mediated predominantly through caspase-12-dependent pathway in a concentration-dependent manner. Tunicamycin 60-71 caspase 12 Rattus norvegicus 136-146 12384508-7 2002 The affinity toward FXa could be restored when the mutants were expressed in the presence of tunicamycin to inhibit glycosylation, indicating the lost FXa affinity to be caused by the added carbohydrates. Tunicamycin 93-104 coagulation factor X Homo sapiens 20-23 12486168-6 2002 Moreover, AIGP1 gene expression in cultured neurons is specifically induced by the endoplasmic reticulum (ER)-Golgi stressors tunicamycin and brefeldin A. Tunicamycin 126-137 serine incorporator 3 Homo sapiens 10-15 12384508-7 2002 The affinity toward FXa could be restored when the mutants were expressed in the presence of tunicamycin to inhibit glycosylation, indicating the lost FXa affinity to be caused by the added carbohydrates. Tunicamycin 93-104 coagulation factor X Homo sapiens 151-154 12515321-0 2002 Effect of 2-fluoropalmitate, cerulenin and tunicamycin on the palmitoylation and intracellular translocation of myelin proteolipid protein. Tunicamycin 43-54 proteolipid protein 1 Rattus norvegicus 112-138 12175333-10 2002 Furthermore, soluble Protein A-CST expressed in the presence of tunicamycin was almost inactive, and accumulated in transfected cells. Tunicamycin 64-75 galactose-3-O-sulfotransferase 1 Mus musculus 31-34 12228224-6 2002 Insulin-like growth factor-1, okadaic acid, calyculin A, and lithium also protected cells from two other inducers of ER stress, tunicamycin and brefeldin A. Tunicamycin 128-139 insulin like growth factor 1 Homo sapiens 0-28 12410842-9 2002 Furthermore, trr1 mutants are resistant to tunicamycin, consistent with their high UPR. Tunicamycin 43-54 thioredoxin-disulfide reductase TRR1 Saccharomyces cerevisiae S288C 13-17 12409609-6 2002 To our knowledge, this is the first report of (i) visualization of the activation of Bid by proteolytic cleavage, with direct observation of the cleavage of YFP-Bid-CFP in the cytoplasm and subsequent translocation of the cleaved Bid to mitochondria and (ii) the absence of Abeta- or tunicamycin-mediated significant activation of caspase 8 in individual living cells. Tunicamycin 284-295 BH3 interacting domain death agonist Homo sapiens 85-88 12409609-6 2002 To our knowledge, this is the first report of (i) visualization of the activation of Bid by proteolytic cleavage, with direct observation of the cleavage of YFP-Bid-CFP in the cytoplasm and subsequent translocation of the cleaved Bid to mitochondria and (ii) the absence of Abeta- or tunicamycin-mediated significant activation of caspase 8 in individual living cells. Tunicamycin 284-295 BH3 interacting domain death agonist Homo sapiens 161-164 12409609-6 2002 To our knowledge, this is the first report of (i) visualization of the activation of Bid by proteolytic cleavage, with direct observation of the cleavage of YFP-Bid-CFP in the cytoplasm and subsequent translocation of the cleaved Bid to mitochondria and (ii) the absence of Abeta- or tunicamycin-mediated significant activation of caspase 8 in individual living cells. Tunicamycin 284-295 BH3 interacting domain death agonist Homo sapiens 161-164 12147617-11 2002 Glucose deprivation or treatment of ARPE-19 cells with tunicamycin, brefeldin A, the calcium ionophore A23187, or thapsigargin increased the expression of VEGF mRNA in these cells by 8- to 10-fold. Tunicamycin 55-66 vascular endothelial growth factor A Homo sapiens 155-159 12235182-2 2002 Substituting Asn residue with Gln at the single glycosylation site within apoB-17 (N(158)) decreased its secretion efficiency to a level equivalent to that of wild-type apoB-17 treated with tunicamycin, but had little effect on its synthesis or intracellular distribution. Tunicamycin 190-201 apolipoprotein B Homo sapiens 74-78 12058017-6 2002 Deletion of COD1 also impaired ER function, causing constitutive activation of the unfolded protein response, hypersensitivity to the glycosylation inhibitor tunicamycin, and synthetic lethality with deletion of the unfolded protein response regulator HAC1. Tunicamycin 158-169 uncharacterized protein Drosophila melanogaster 12-16 11991954-11 2002 Synthesis of the 74-kDa NFIC was also inhibited in this setting by tunicamycin. Tunicamycin 67-78 nuclear factor I/C Mus musculus 24-28 12081137-3 2002 Cells treated with tunicamycin produced only a 25 kDa band, representing a deglycosylated form of PrP. Tunicamycin 19-30 prion protein Homo sapiens 98-101 12021180-5 2002 Cycloheximide treatment, at a dose able to profoundly inhibit protein synthesis in FRTL-5 cells, obliterated the decrease in the level of the inhibitory subunit I kappa B alpha produced by thapsigargin and tunicamycin. Tunicamycin 206-217 NFKB inhibitor alpha Rattus norvegicus 161-176 11559706-6 2001 FPR-C126W differed from FPR-WT and FPR-F110S in migration on SDS-polyacrylamide gels and tunicamycin-sensitive glycosylation. Tunicamycin 89-100 formyl peptide receptor 1 Homo sapiens 0-3 11877404-9 2002 The mobility of wt-CFTR and DeltaF508-CFTR was reduced by maneuvers that alter CFTR processing or interactions with molecular chaperones, including tunicamycin, geldanamycin, and lactacystin. Tunicamycin 148-159 cystic fibrosis transmembrane conductance regulator Cricetulus griseus 19-23 11877404-9 2002 The mobility of wt-CFTR and DeltaF508-CFTR was reduced by maneuvers that alter CFTR processing or interactions with molecular chaperones, including tunicamycin, geldanamycin, and lactacystin. Tunicamycin 148-159 cystic fibrosis transmembrane conductance regulator Cricetulus griseus 38-42 11877404-9 2002 The mobility of wt-CFTR and DeltaF508-CFTR was reduced by maneuvers that alter CFTR processing or interactions with molecular chaperones, including tunicamycin, geldanamycin, and lactacystin. Tunicamycin 148-159 cystic fibrosis transmembrane conductance regulator Cricetulus griseus 38-42 11961028-5 2002 When cells were treated with the N-glycosylation inhibitor, tunicamycin, the molecular weight of nephrin was decreased to a single immunoband of 150 kD, indicating that the shift in the electrophoretic migration of nephrin is due to N-linked carbohydrate moieties. Tunicamycin 60-71 NPHS1 adhesion molecule, nephrin Homo sapiens 97-104 11961028-5 2002 When cells were treated with the N-glycosylation inhibitor, tunicamycin, the molecular weight of nephrin was decreased to a single immunoband of 150 kD, indicating that the shift in the electrophoretic migration of nephrin is due to N-linked carbohydrate moieties. Tunicamycin 60-71 NPHS1 adhesion molecule, nephrin Homo sapiens 215-222 11914074-2 2002 We found that the alpha(1B)-AR undergoes N-linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation. Tunicamycin 140-151 adrenoceptor alpha 1B Homo sapiens 28-30 11952786-10 2002 Tunicamycin inhibited N-linked glycosylation of Ac45 and interfered with the cleavage process, suggesting that Ac45 needs proper folding for the cleavage to occur. Tunicamycin 0-11 ATPase H+ transporting accessory protein 1 Homo sapiens 48-52 11952786-10 2002 Tunicamycin inhibited N-linked glycosylation of Ac45 and interfered with the cleavage process, suggesting that Ac45 needs proper folding for the cleavage to occur. Tunicamycin 0-11 ATPase H+ transporting accessory protein 1 Homo sapiens 111-115 11867635-7 2002 M2BP-1,2 expressed in tunicamycin-treated cells contained no glycosyl residues, indicating that O-glycosylation is not occurring. Tunicamycin 22-33 galectin 3 binding protein Homo sapiens 0-4 11961028-6 2002 It was further shown that this glycosylation process is highly sensitive to inhibition by tunicamycin, which is a naturally occurring antibiotic, leading to retention of nonglycosylated nephrin molecules in the endoplasmic reticulum. Tunicamycin 90-101 NPHS1 adhesion molecule, nephrin Homo sapiens 186-193 11791712-7 2001 The spf1 disruptant also showed increased expression of Kar2p and sensitivity to tunicamycin. Tunicamycin 81-92 ion-transporting P-type ATPase SPF1 Saccharomyces cerevisiae S288C 4-8 11595658-2 2001 Cells expressing CRFR1 were treated with tunicamycin to block receptor glycosylation. Tunicamycin 41-52 corticotropin releasing hormone receptor 1 Homo sapiens 17-22 11837675-1 2001 The expression of the ischemia-responsive protein (irp94) was enhanced by endoplasmic reticulum (ER) stress inducing drugs such as brefeldin A (BFA), calcium ionophor A23187, dithiothreitol (DTT) and tunicamycin in fisher rat thyroid epithelial cell line (FRTL-5 cells). Tunicamycin 200-211 heat shock protein family A (Hsp70) member 4 Rattus norvegicus 51-56 11837675-2 2001 In particular, irp94 mRNA expression was increased dose dependently by tunicamycin, and there was increased irp94 expression when the cells were incubated with the thyroid-stimulating hormone (TSH) together. Tunicamycin 71-82 heat shock protein family A (Hsp70) member 4 Rattus norvegicus 15-20 11557602-3 2001 Wound repair stimulated by epidermal growth factor was substantially attenuated by 10(-7) M tunicamycin (TM), an N-glycosylation inhibitor, but not by the inhibitors deoxymannojirimycin or castanospermine. Tunicamycin 92-103 epidermal growth factor Homo sapiens 27-50 11557602-3 2001 Wound repair stimulated by epidermal growth factor was substantially attenuated by 10(-7) M tunicamycin (TM), an N-glycosylation inhibitor, but not by the inhibitors deoxymannojirimycin or castanospermine. Tunicamycin 105-107 epidermal growth factor Homo sapiens 27-50 11606310-10 2001 (b) Inhibiting receptor glycosylation in HEK293 cells with tunicamycin enabled tryptase-mediated PAR(2) activation. Tunicamycin 59-70 tryptase alpha/beta 1 Rattus norvegicus 79-87 11606310-10 2001 (b) Inhibiting receptor glycosylation in HEK293 cells with tunicamycin enabled tryptase-mediated PAR(2) activation. Tunicamycin 59-70 F2R like trypsin receptor 1 Homo sapiens 97-103 11590221-5 2001 Tunicamycin significantly reduced cell-associated PAF-AH activity and inhibited enzyme secretion; but it did not alter the ratio of secreted to cell-associated enzyme (1.8 at 6 h and 3.1 at 24 h), suggesting that glycosylation is not essential for PAF-AH secretion. Tunicamycin 0-11 phospholipase A2 group VII Homo sapiens 50-56 11544325-5 2001 Although these mutants were expressed on the cell surface and maintained its ability to associate with human TLR4, these mutations or tunicamycin treatment substantially impaired the ability of MD-2 to complement TLR4-mediated activation of NF-kappaB by LPS. Tunicamycin 134-145 lymphocyte antigen 96 Homo sapiens 194-198 11544325-5 2001 Although these mutants were expressed on the cell surface and maintained its ability to associate with human TLR4, these mutations or tunicamycin treatment substantially impaired the ability of MD-2 to complement TLR4-mediated activation of NF-kappaB by LPS. Tunicamycin 134-145 toll like receptor 4 Homo sapiens 213-217 11544325-5 2001 Although these mutants were expressed on the cell surface and maintained its ability to associate with human TLR4, these mutations or tunicamycin treatment substantially impaired the ability of MD-2 to complement TLR4-mediated activation of NF-kappaB by LPS. Tunicamycin 134-145 interferon regulatory factor 6 Homo sapiens 254-257 11451447-14 2001 In contrast, nonglycosylated PAC1 receptors produced by tunicamycin treatment of the transfected COS-7 cells showed a 30-fold lower affinity for PACAP-27 and were capable of signal transduction with 30--50-fold lower potency as compared with the glycosylated PAC1 receptors. Tunicamycin 56-67 adenylate cyclase activating polypeptide 1 Rattus norvegicus 145-150 11509666-5 2001 The results also demonstrate that induction of ER stress with calcium ionophore A23187, brefeldin A, or tunicamycin is associated with translocation of ER-associated c-Abl to mitochondria. Tunicamycin 104-115 ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens 166-171 11389975-2 2001 RAMP proteins modify the glycosylation status of CRLR and determine their receptor specificity; when treated with tunicamycin, a glycosylation inhibitor, CHO-K1 cells constitutively expressing both RAMP2 and CRLR lost the capacity to bind adrenomedullin. Tunicamycin 114-125 calcitonin receptor like receptor Homo sapiens 49-53 11478581-1 2001 Using flow cytometry or immunoprecipitation analysis in cells chronically infected with HIV-1 IIIB Supt-1, we noticed an additive effect of tunicamycin and low molecular weight dextran (LMDS) on the binding of the G3-4 monoclonal antibody to monomeric and oligomeric forms of glycoprotein 120 (gp120). Tunicamycin 140-151 Envelope surface glycoprotein gp160, precursor Human immunodeficiency virus 1 294-299 11478581-2 2001 The inhibition of glycosylation by tunicamycin reduced the number of monomeric and oligomeric forms of gp120. Tunicamycin 35-46 inter-alpha-trypsin inhibitor heavy chain 4 Homo sapiens 103-108 11389975-2 2001 RAMP proteins modify the glycosylation status of CRLR and determine their receptor specificity; when treated with tunicamycin, a glycosylation inhibitor, CHO-K1 cells constitutively expressing both RAMP2 and CRLR lost the capacity to bind adrenomedullin. Tunicamycin 114-125 receptor activity-modifying protein 2 Cricetulus griseus 198-203 11389975-2 2001 RAMP proteins modify the glycosylation status of CRLR and determine their receptor specificity; when treated with tunicamycin, a glycosylation inhibitor, CHO-K1 cells constitutively expressing both RAMP2 and CRLR lost the capacity to bind adrenomedullin. Tunicamycin 114-125 calcitonin receptor like receptor Homo sapiens 208-212 11389975-4 2001 Whichever RAMP protein was co-expressing with CRLR, the ligand binding was sensitive to tunicamycin. Tunicamycin 88-99 calcitonin receptor like receptor Homo sapiens 46-50 11162531-5 2001 In a murine hepatocellular carcinoma cell line, Sdf2l1 was strongly induced by tunicamycin and a calcium ionophore, A23187, and weakly induced by heat stress but was not induced by cycloheximide. Tunicamycin 79-90 stromal cell-derived factor 2-like 1 Mus musculus 48-54 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 nuclear factor kappa B subunit 1 Homo sapiens 36-45 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 11360202-5 2001 Moreover, p65-/- fibroblasts were killed more efficiently by calcium ionopore and tunicamycin but not hydrogen peroxide compared to wild type fibroblasts. Tunicamycin 82-93 RELA proto-oncogene, NF-kB subunit Homo sapiens 10-13 11360202-6 2001 We also show that parthenolide, a NF-kappaB inhibitor, sensitizes breast cancer cells to tunicamycin. Tunicamycin 89-100 nuclear factor kappa B subunit 1 Homo sapiens 34-43 11328816-7 2001 In the ceramidase overexpressing HEK293 cells, 133-kDa (Golgi-form) and 113-kDa (endoplasmic reticulum-form) Myc-tagged ceramidases were detected, whereas these two proteins were converted to a 87-kDa protein concomitantly with loss of activity when expressed in the presence of tunicamycin, indicating that the N-glycosylation process is indispensable for the expression of the enzyme activity. Tunicamycin 279-290 MYC proto-oncogene, bHLH transcription factor Homo sapiens 109-112 11261789-8 2001 Furthermore, inhibition of glycosylation of these Tf-1beta2 cells by tunicamycin treatment yields a standard 39-kDa molecule recognized on western blot with anti-gamma c antibody, as seen for the standard 64-kDa isoform of gamma c. Tunicamycin 69-80 interleukin 2 receptor subunit gamma Homo sapiens 162-169 11261789-8 2001 Furthermore, inhibition of glycosylation of these Tf-1beta2 cells by tunicamycin treatment yields a standard 39-kDa molecule recognized on western blot with anti-gamma c antibody, as seen for the standard 64-kDa isoform of gamma c. Tunicamycin 69-80 interleukin 2 receptor subunit gamma Homo sapiens 223-230 11181082-4 2001 Inhibition of glycosylation by tunicamycin also abolished cathepsin K maturation. Tunicamycin 31-42 cathepsin K Homo sapiens 58-69 11226227-8 2001 Characteristic aspects of the cyt1 phenotype, including radial swelling and accumulation of callose, can be mimicked with the inhibitor of N-glycosylation, tunicamycin. Tunicamycin 156-167 Glucose-1-phosphate adenylyltransferase family protein Arabidopsis thaliana 30-34 11171045-0 2001 Tunicamycin induces ubiquitination and degradation of apolipoprotein B in HepG2 cells. Tunicamycin 0-11 apolipoprotein B Homo sapiens 54-70 11171045-4 2001 The present study was undertaken to address the question of whether the inhibition of N-linked glycosylation with tunicamycin would interfere with apoB-100 production. Tunicamycin 114-125 apolipoprotein B Homo sapiens 147-155 11171045-5 2001 We demonstrated that the treatment of HepG2 cells with tunicamycin decreased the net production of apoB-100 by enhancing co-translational degradation of the protein. Tunicamycin 55-66 apolipoprotein B Homo sapiens 99-107 11171045-7 2001 Because lactacystin only partly reversed the effects of tunicamycin on apoB biogenesis, tunicamycin seemed also to induce apoB co-translational degradation in HepG2 cells by one or more non-proteasomal pathways. Tunicamycin 88-99 apolipoprotein B Homo sapiens 122-126 11171045-8 2001 Furthermore, tunicamycin increased apoB ubiquitination approx. Tunicamycin 13-24 apolipoprotein B Homo sapiens 35-39 11171045-11 2001 Thus the tunicamycin-mediated inhibition of N-linked glycosylation interferes with the production of apoB-100 that is mediated by both proteasomal and non-proteasomal pathways. Tunicamycin 9-20 apolipoprotein B Homo sapiens 101-109 11345535-7 2001 In addition, 7D5 immunoprecipitated the approximately 58 kDa unglycosylated gp91phox protein from solubilized membrane fractions of tunicamycin-treated PLB-985 granulocytes, indicating that glycans were not required for 7D5 binding. Tunicamycin 132-143 cytochrome b-245 beta chain Homo sapiens 76-84 11024053-8 2001 Treatment with tunicamycin abolished any differences in beta-catenin phosphorylation for the mock vis a vis the GnT-lll transfectants. Tunicamycin 15-26 catenin (cadherin associated protein), beta 1 Mus musculus 56-68 11024053-8 2001 Treatment with tunicamycin abolished any differences in beta-catenin phosphorylation for the mock vis a vis the GnT-lll transfectants. Tunicamycin 15-26 glucosaminyl (N-acetyl) transferase family member 7 Mus musculus 112-115 11010973-8 2000 Pretreatment of NIH 3T3 cells with UVC markedly attenuates the subsequent induction of CHOP mRNA by the cellular stress activators methylmethane sulfate, tunicamycin, glucose deprivation, and methionine deprivation for as long as at least 16 h. This inhibitory effect of UVC on CHOP expression in response to stress is independent of the presence or absence of p53 and does not involve mRNA degradation as opposed to the UVC effect that inhibits p21 expression seen only in the absence of p53. Tunicamycin 154-165 DNA-damage inducible transcript 3 Mus musculus 87-91 11134314-2 2001 The results reveal that in this cell system, the precursor is efficiently cleaved and the resulting G1 and G2 glycoproteins are transported from the endoplasmic reticulum (ER) to the Golgi complex, where they are retained, a process that could be blocked by tunicamycin. Tunicamycin 258-269 proline rich protein BstNI subfamily 3 Homo sapiens 100-109 11089547-13 2000 Likewise, a decrease in glucose consumption (-50%) after treatment of cells with tunicamycin was accompanied by a decrease (-70% vs. control) in the membrane expression of a 50-kDa form of Glut-1 and an increase in its unglycosylated 41-kDa form. Tunicamycin 81-92 solute carrier family 2 member 1 Rattus norvegicus 189-195 11104692-6 2000 Palmitoylation of LPC was found to be sensitive to the protein palmitoyltransferase inhibitor tunicamycin but not cerulenin. Tunicamycin 94-105 proprotein convertase subtilisin/kexin type 7 Homo sapiens 18-21 11119727-3 2000 Tunicamycin dose-dependently inhibited the glycosylation of a myc-tagged hCRLR and in parallel specific [(125)I]CGRP and -ADM binding. Tunicamycin 0-11 calcitonin receptor like receptor Homo sapiens 73-78 11119727-3 2000 Tunicamycin dose-dependently inhibited the glycosylation of a myc-tagged hCRLR and in parallel specific [(125)I]CGRP and -ADM binding. Tunicamycin 0-11 calcitonin related polypeptide alpha Homo sapiens 112-116 11119727-3 2000 Tunicamycin dose-dependently inhibited the glycosylation of a myc-tagged hCRLR and in parallel specific [(125)I]CGRP and -ADM binding. Tunicamycin 0-11 adrenomedullin Homo sapiens 122-125 11046064-7 2000 The expressed CCR2B was found to be N:-glycosylated, as N:-glycosidase F treatment of the receptor or growth of the cells in tunicamycin reduced the receptor size to the same level, from 50 to 45 kDa. Tunicamycin 125-136 C-C motif chemokine receptor 2 Homo sapiens 14-19 11105962-0 2000 Axonal and neuronal amyloid precursor protein immunoreactivity in the brains of guinea pigs given tunicamycin. Tunicamycin 98-109 amyloid-beta A4 protein Cavia porcellus 20-45 11105962-1 2000 Amyloid precursor protein (APP) immunocytochemistry was used to study axonal and neuronal changes in guinea pig brains exposed to tunicamycin. Tunicamycin 130-141 amyloid-beta A4 protein Cavia porcellus 0-25 10922362-4 2000 mRNA expression of Herp was strongly up-regulated by inducers of ER stress, including mercaptoethanol, tunicamycin, A23187, and thapsigargin. Tunicamycin 103-114 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 19-23 11041857-6 2000 Activity measurements of CD39L4 isolated from tunicamycin-treated, transiently transfected COS-7 cells indicate that glycosylation is not required for full ADPase activity. Tunicamycin 46-57 ectonucleoside triphosphate diphosphohydrolase 5 (inactive) Homo sapiens 25-31 10801872-6 2000 Treatment with tunicamycin and N-glycosidase F led to a BACE derivative with a molecular weight corresponding to an unmodified version. Tunicamycin 15-26 beta-secretase 1 Homo sapiens 56-60 11027576-2 2000 It has a mutation in the DAD1 gene and enters apoptosis at the restrictive temperature of 39 degrees C. The defect of Dad1p causes a loss of N-linked glycosylation; therefore, it was thought that an inhibition of N-linked glycosylation induced apoptosis.However, tunicamycin, a potent inhibitor of N-linked glycosylation, had not caused apoptosis in wild-type BHK21 cells. Tunicamycin 263-274 dolichyl-diphosphooligosaccharide--protein glycosyltransferase subunit DAD1 Mesocricetus auratus 25-29 11027576-2 2000 It has a mutation in the DAD1 gene and enters apoptosis at the restrictive temperature of 39 degrees C. The defect of Dad1p causes a loss of N-linked glycosylation; therefore, it was thought that an inhibition of N-linked glycosylation induced apoptosis.However, tunicamycin, a potent inhibitor of N-linked glycosylation, had not caused apoptosis in wild-type BHK21 cells. Tunicamycin 263-274 dolichyl-diphosphooligosaccharide--protein glycosyltransferase subunit DAD1 Mesocricetus auratus 118-123 10993946-2 2000 In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice. Tunicamycin 20-31 prion protein Mus musculus 59-65 10993946-2 2000 In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice. Tunicamycin 20-31 sodium channel, voltage-gated, type II, alpha Mus musculus 107-112 10993946-2 2000 In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice. Tunicamycin 20-31 prion protein Mus musculus 186-193 10993946-2 2000 In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice. Tunicamycin 20-31 prion protein Mus musculus 207-213 10993946-2 2000 In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice. Tunicamycin 20-31 prion protein Mus musculus 59-62 10971580-3 2000 HumHtrA2 is upregulated in mammalian cells in response to stress induced by both heat shock and tunicamycin treatment. Tunicamycin 96-107 HtrA serine peptidase 2 Homo sapiens 0-8 11000257-2 2000 These viruses use the related sodium-phosphate symporters Pit1 and Pit2, respectively, as receptors in nonhamster cells, and evidence has suggested that the corresponding transporters of CHO cells may be masked by tunicamycin-sensitive secreted inhibitors. Tunicamycin 214-225 sodium-dependent phosphate transporter 2 Cricetulus griseus 67-71 11000257-4 2000 Moreover, expression of E36 Pit2 in CHO cells conferred tunicamycin-independent susceptibilities to both viruses. Tunicamycin 56-67 sodium-dependent phosphate transporter 2 Cricetulus griseus 28-32 10973810-2 2000 When J774.1 cells were pretreated with tunicamycin, their granulocytin-dependent TNF-alpha production was greatly reduced. Tunicamycin 39-50 tumor necrosis factor Mus musculus 81-90 10988254-4 2000 Tunicamycin treatment completely abolished hFucTIII enzyme activity while castanospermine treatment diminished hFucTIII enzyme activity to approximately 40% of the activity of the native enzyme. Tunicamycin 0-11 fucosyltransferase 3 (Lewis blood group) Homo sapiens 43-51 10933718-9 2000 Thus, we infer that the tunicamycin-dependent infection of mouse cells by RD114 and type D retroviruses is caused by deglycosylation of mASCT1, which unmasks previously buried sites for viral interactions. Tunicamycin 24-35 solute carrier family 1 (glutamate/neutral amino acid transporter), member 4 Mus musculus 136-142 10971580-7 2000 HumHtrA2 cleaves beta-casein with an inhibitor profile similar to that previously described for E. coli HtrA, in addition to an increase in beta-casein turnover when the assay temperature is raised from 37 to 45 degrees C. The biochemical and sequence similarities between humHtrA2 and its bacterial homologues, in conjunction with its nuclear location and upregulation in response to tunicamycin and heat shock suggest that it is involved in mammalian stress response pathways. Tunicamycin 385-396 HtrA serine peptidase 2 Homo sapiens 0-8 10971580-7 2000 HumHtrA2 cleaves beta-casein with an inhibitor profile similar to that previously described for E. coli HtrA, in addition to an increase in beta-casein turnover when the assay temperature is raised from 37 to 45 degrees C. The biochemical and sequence similarities between humHtrA2 and its bacterial homologues, in conjunction with its nuclear location and upregulation in response to tunicamycin and heat shock suggest that it is involved in mammalian stress response pathways. Tunicamycin 385-396 HtrA serine peptidase 1 Homo sapiens 3-7 10799532-2 2000 In fact, the glycosylation inhibitor tunicamycin induces dephosphorylation of mammalian BiP. Tunicamycin 37-48 heat shock protein family A (Hsp70) member 5 Homo sapiens 88-91 11069764-8 2000 In the presence of tunicamycin, NPP3 was not N-glycosylated. Tunicamycin 19-30 ectonucleotide pyrophosphatase/phosphodiesterase 3 Homo sapiens 32-36 10799532-5 2000 In contrast to tunicamycin treatment, water stress condition stimulated phosphorylation of BiP species in soybean cultured cells and stressed leaves. Tunicamycin 15-26 ER-binding immunoglobulin protein BIP2 Glycine max 91-94 10799532-7 2000 We also compared the induction of the soybean BiP gene family, which consists of at least four members designated soyBiPA, soyBiPB, soyBiPC, and soyBiPD, by tunicamycin and osmotic stress. Tunicamycin 157-168 ER-binding immunoglobulin protein BIP2 Glycine max 46-49 10799532-8 2000 Although all soybean BiP genes were induced by tunicamycin, just the soyBiPA RNA was up-regulated by osmotic stress. Tunicamycin 47-58 ER-binding immunoglobulin protein BIP2 Glycine max 21-24 10788525-5 2000 Moreover, p22(phox) coprecipitated with unglycosylated gp91(phox) primary translation product made in the presence of tunicamycin, suggesting that heterodimer formation does not require glycosylation. Tunicamycin 118-129 calcineurin like EF-hand protein 1 Homo sapiens 10-13 10771098-3 2000 In Sf21 insect cells, overexpression of canine GRP94 led to the appearance of a multiplet of three or more molecular-mass isoforms which was reduced to a single mobility form following treatment of cells with tunicamycin, suggesting stable accumulations of consecutively modified protein. Tunicamycin 209-220 heat shock protein 90 beta family member 1 Canis lupus familiaris 47-52 10753675-7 2000 Tunicamycin reversed the polarity of secretion of CgA to the basolateral side. Tunicamycin 0-11 chromogranin A Bos taurus 50-53 10725401-4 2000 Tunicamycin inhibition experiments showed that the apical polarity of VEGF(165) was independent of N-glycosylation. Tunicamycin 0-11 vascular endothelial growth factor A Homo sapiens 70-74 10760948-3 2000 This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, calcium ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Tunicamycin 188-199 heat shock protein family A (Hsp70) member 5 Homo sapiens 77-82 10760948-3 2000 This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, calcium ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells. Tunicamycin 201-203 heat shock protein family A (Hsp70) member 5 Homo sapiens 77-82 10727211-7 2000 Treating the transfected cells with tunicamycin inhibited the secretion and LAO activity of the recombinant apoxin I. Tunicamycin 36-47 interleukin 4 induced 1 Homo sapiens 76-79 10708769-5 2000 Treatment with the glycosylation inhibitor tunicamycin both enhances the synthesis of Mif1 mRNA and protein. Tunicamycin 43-54 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 86-90 10692464-4 2000 Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1. Tunicamycin 61-72 tumor necrosis factor Bos taurus 79-106 10692464-4 2000 Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1. Tunicamycin 61-72 oxidized low density lipoprotein receptor 1 Bos taurus 191-196 10692464-4 2000 Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1. Tunicamycin 61-72 oxidized low density lipoprotein receptor 1 Bos taurus 198-204 10692464-4 2000 Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1. Tunicamycin 61-72 oxidized low density lipoprotein receptor 1 Bos taurus 199-204 10708769-6 2000 The Mif1 5" flanking region contains a functional ER stress-responsive element which is sufficient for induction by tunicamycin. Tunicamycin 116-127 homocysteine inducible ER protein with ubiquitin like domain 1 Homo sapiens 4-8 10721463-2 2000 We observed that the inhibition of glycosylation by high concentrations of tunicamycin results in the reduction of an oligomeric gp120 on the surface of infected MoIT 4 cells as well as the decrease in the concentration of a monomeric form in the cytoplasm. Tunicamycin 75-86 inter-alpha-trypsin inhibitor heavy chain 4 Homo sapiens 129-134 11201795-4 2000 Pretreatment of this stable clones with tunicamycin, a potent inhibitor of N-glycosylation, caused the appearance of unglycosylated Trk core protein. Tunicamycin 40-51 neurotrophic receptor tyrosine kinase 1 Rattus norvegicus 132-135 10808272-6 2000 The pIgR molecule (molecular mass 100 kDa) after complete deglycosylation by tunicamycin treatment was still able to bind to pIgA, indicating that N-glycosylation of pIgR is not necessary for pIgA-pIgR binding. Tunicamycin 77-88 polymeric immunoglobulin receptor Mus musculus 4-8 10761711-3 2000 Immunoprecipitation studies of human tumor cell lines revealed that FU-MK-1 recognizes a monomeric membrane glycoprotein with two forms, 40 kDa (major form) and 42 kDa (minor form), and with a molecular mass of 35 kDa following treatment with the N-glycosylation inhibitor tunicamycin. Tunicamycin 273-284 epithelial cell adhesion molecule Homo sapiens 71-75 10888037-4 2000 In this study we show that inhibition of N-linked glycosylation using tunicamycin or the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin resulted in down-regulation of IGF-1R at the cell surface in Ewing"s sarcoma cell lines (RD-ES and ES-1 cells). Tunicamycin 70-81 insulin like growth factor 1 receptor Homo sapiens 199-205 10949666-9 2000 Accumulation of an immunopositive cell specific asparagine-linked (N-linked) glycoprotein, Factor VIII:C in the absence of Glc3Man9GlcNAc2-PP-Dol in tunicamycin treated cells has been proposed as an apoptotic triggering mechanism under the current experimental conditions. Tunicamycin 149-160 coagulation factor VIII Bos taurus 91-102 10714394-8 2000 Similarly, under suboptimal conditions, a synergistic effect was obtained with tunicamycin and PMA: each one alone was ineffective but in combination they induced the acquisition of HA binding by the lymphoma cells, while their CD44 expression was not enhanced. Tunicamycin 79-90 CD44 molecule (Indian blood group) Homo sapiens 228-232 10517826-1 1999 The cytotoxic drug tunicamycin kills cells because it is a specific inhibitor of UDP-N-acetylglucosamine:dolichol phosphate N-acetylglucosamine-1-P transferase (GPT), an enzyme that catalyzes the initial step of the biosynthesis of dolichol-linked oligosaccharides. Tunicamycin 19-30 UDP-glcnac-adolichol phosphate glcnac-1-p-transferase Arabidopsis thaliana 161-164 10561463-5 1999 Furthermore sThy-1 lacking glycosylation could be produced with the inhibitor tunicamycin but in contrast cell surface expression of unglycosylated GPI anchored Thy-1 could not be obtained. Tunicamycin 78-89 thy-1 membrane glycoprotein Cricetulus griseus 13-18 10542372-3 1999 When mouse blastocysts were exposed to the alkylating agent MMS, the metabolic inhibitor sodium arsenite or an inhibitor of protein glycosylation tunicamycin, levels of the CHOP-10 mRNA were increased by two- to threefold relative to the mRNA for beta-actin. Tunicamycin 146-157 DNA-damage inducible transcript 3 Mus musculus 173-180 10542372-9 1999 The results suggest that there is a link between the extent of glycoprotein synthesis and the sensitivity of CHOP-10 to tunicamycin. Tunicamycin 120-131 DNA-damage inducible transcript 3 Mus musculus 109-116 10537138-3 1999 Through functional analysis of the hSR-transfected cells cultured in the presence of various glycosylation inhibitors, it was found that tunicamycin and castanospermine were able to significantly reduce the secretin-stimulated cAMP response. Tunicamycin 137-148 HSR Homo sapiens 35-38 10537138-3 1999 Through functional analysis of the hSR-transfected cells cultured in the presence of various glycosylation inhibitors, it was found that tunicamycin and castanospermine were able to significantly reduce the secretin-stimulated cAMP response. Tunicamycin 137-148 secretin Homo sapiens 207-215 10536042-5 1999 In exploring structure-function relationships among N-glycans, and since tunicamycin has various reported biochemical activities; we have generated a germline deletion in the mouse GPT gene. Tunicamycin 73-84 glutamic pyruvic transaminase, soluble Mus musculus 181-184 10517826-4 1999 Cells that are treated with tunicamycin normally experience an unfolded protein response and induce genes that encode endoplasmic reticulum chaperones such as the binding protein (BiP). Tunicamycin 28-39 binding protein Arabidopsis thaliana 180-183 10517826-9 1999 These observations suggest that excess GPT activity obviates the normal unfolded protein response that cells experience when exposed to tunicamycin. Tunicamycin 136-147 UDP-glcnac-adolichol phosphate glcnac-1-p-transferase Arabidopsis thaliana 39-42 10574586-7 1999 By expressing chimeric rFII/hFII constructs in tunicamycin-treated HEK293 cells, it was shown that the kringle 2 structure of prothrombin was responsible for this difference. Tunicamycin 47-58 coagulation factor II, thrombin Homo sapiens 126-137 10569245-10 1999 The tunicamycin sensitivity of (delta)ire1 cells was also suppressed by extra expression of KAR2, suggesting that BiP plays a principal role in protecting cell growth against misfolded proteins accumulated in the ER. Tunicamycin 4-15 bifunctional endoribonuclease/protein kinase IRE1 Saccharomyces cerevisiae S288C 38-42 10569245-10 1999 The tunicamycin sensitivity of (delta)ire1 cells was also suppressed by extra expression of KAR2, suggesting that BiP plays a principal role in protecting cell growth against misfolded proteins accumulated in the ER. Tunicamycin 4-15 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 92-96 10517826-4 1999 Cells that are treated with tunicamycin normally experience an unfolded protein response and induce genes that encode endoplasmic reticulum chaperones such as the binding protein (BiP). Tunicamycin 28-39 binding protein Arabidopsis thaliana 163-178 10484609-6 1999 Inhibition of N-linked glycosylation with tunicamycin (TM) prevented secretion of HL enzyme activity and protein mass. Tunicamycin 42-53 lipase C, hepatic type Homo sapiens 82-84 10482549-4 1999 (i) The U(L)3 proteins forming all six bands were present in lysates of cells infected with wild-type virus and treated with tunicamycin or monensin or in cells infected with the mutant lacking the gene encoding the U(S)3 protein kinase. Tunicamycin 125-136 nuclear protein UL3 Human alphaherpesvirus 1 8-13 10514258-7 1999 When the N-glycosylation was completely blocked with the addition of tunicamycin to the culture, the secretion of hG-CSF and hGH was decreased to a negligible level although the other host-derived proteins were well secreted to the culture broth regardless of the presence of tunicamycin. Tunicamycin 69-80 colony stimulating factor 3 Homo sapiens 114-120 10514258-7 1999 When the N-glycosylation was completely blocked with the addition of tunicamycin to the culture, the secretion of hG-CSF and hGH was decreased to a negligible level although the other host-derived proteins were well secreted to the culture broth regardless of the presence of tunicamycin. Tunicamycin 276-287 colony stimulating factor 3 Homo sapiens 114-120 10415113-6 1999 In HA-1 cells, adapt78 mRNA was induced by the calcium ionophore A23187, 2-deoxyglucose, brefeldin A, tunicamycin, thapsigargin, and cyclopiazonic acid, with thapsigargin being the most potent inducer (7.3-fold). Tunicamycin 102-113 regulator of calcineurin 1 Homo sapiens 15-22 10417322-10 1999 Treatment with tunicamycin (TUN) diminished the binding of MUC2 to CRT, suggesting a requirement for initial N-glycan addition during this process. Tunicamycin 15-26 mucin 2, oligomeric mucus/gel-forming Homo sapiens 59-63 10417322-10 1999 Treatment with tunicamycin (TUN) diminished the binding of MUC2 to CRT, suggesting a requirement for initial N-glycan addition during this process. Tunicamycin 15-26 calreticulin Homo sapiens 67-70 10503534-5 1999 The T. reesei pdi1 promoter has two possible unfolded protein response (UPR) elements and it was shown by treatments with dithiothreitol and tunicamycin that the gene is under the control of the UPR pathway. Tunicamycin 141-152 protein disulfide isomerase PDI1 Saccharomyces cerevisiae S288C 14-18 10419504-4 1999 Tunicamycin treatment resulted in a 140-kDa protein, the deduced size of NPC1, suggesting that NPC1 is N-glycosylated. Tunicamycin 0-11 NPC intracellular cholesterol transporter 1 Cricetulus griseus 73-77 10398368-7 1999 Bacteriophage displaying CTLA-4 with somatostatin in CDR3 (CTLA-4R-Som3) specifically bound somatostatin receptors on transfected CHO-K1 cells pre-incubated with 1 microg/ml tunicamycin to remove receptor glycosylation. Tunicamycin 174-185 cytotoxic T-lymphocyte associated protein 4 Homo sapiens 25-31 10398368-7 1999 Bacteriophage displaying CTLA-4 with somatostatin in CDR3 (CTLA-4R-Som3) specifically bound somatostatin receptors on transfected CHO-K1 cells pre-incubated with 1 microg/ml tunicamycin to remove receptor glycosylation. Tunicamycin 174-185 CDR3 Homo sapiens 53-57 10411905-3 1999 Cyclin D1 protein synthesis was rapidly inhibited by tunicamycin treatment. Tunicamycin 53-64 cyclin D1 Homo sapiens 0-9 10411905-6 1999 Enforced overexpression of cyclin D1 in tunicamycin-treated cells maintained cyclin D- and E-dependent kinase activities and kept cells in cycle in the face of a fully activated UPR. Tunicamycin 40-51 cyclin D1 Homo sapiens 27-36 10419504-4 1999 Tunicamycin treatment resulted in a 140-kDa protein, the deduced size of NPC1, suggesting that NPC1 is N-glycosylated. Tunicamycin 0-11 NPC intracellular cholesterol transporter 1 Cricetulus griseus 95-99 10395686-4 1999 Pulse-chase experiments and treatment of cells with brefeldin A and/or tunicamycin showed that IL-16 is secreted despite the absence of a signal peptide, but with a signal peptide IL-16 is processed through the endoplasmic reticulum-golgi pathway and is glycosylated. Tunicamycin 71-82 interleukin 16 Homo sapiens 95-100 10222064-5 1999 Cycloheximide (protein synthesis inhibitor), tunicamycin (N-linked glycosylation inhibitor), and beta-d-xyloside (chondroitin sulfation inhibitor) all inhibited IL-4-mediated downregulation of TNFalpha-induced monocyte HA binding. Tunicamycin 45-56 interleukin 4 Homo sapiens 161-165 10222064-5 1999 Cycloheximide (protein synthesis inhibitor), tunicamycin (N-linked glycosylation inhibitor), and beta-d-xyloside (chondroitin sulfation inhibitor) all inhibited IL-4-mediated downregulation of TNFalpha-induced monocyte HA binding. Tunicamycin 45-56 tumor necrosis factor Homo sapiens 193-201 10229326-1 1999 To elucidate the role of N-glycosylation in the functional activity of the universal glucose transporter, Glut-1, we investigated effects of the N-glycosylation inhibitor, tunicamycin, on glucose transport by human leukemic cell lines K562, U937 and HL60. Tunicamycin 172-183 solute carrier family 2 member 1 Homo sapiens 106-112 10208935-7 1999 An important shift in the relative mobility of gp250 in SDS-PAGE was observed after tunicamycin treatment of infected cells labeled with [3H]glucosamine, confirming the presence of N-linked sugars on gp250. Tunicamycin 84-95 sortilin related receptor 1 Homo sapiens 47-52 10328552-4 1999 The MBL binding to Colo205 cells was more strongly reduced by the pretreatment of the cells with an O-linked glycosylation inhibitor, benzyl-2-acetamide-2-deoxy-alpha-galactopyranoside (Bz-alpha-GalNAc), rather than an N-linked glycosylation inhibitor, tunicamycin. Tunicamycin 253-264 mannose binding lectin 2 Homo sapiens 4-7 10024536-15 1999 RA-treated P19 cells were about 4-fold more resistant to tunicamycin, a fungal antibiotic which inhibits GPT, than were control cells. Tunicamycin 57-68 glutamic pyruvic transaminase, soluble Mus musculus 105-108 10424404-6 1999 Interestingly, while the majority of the breast cancer cell lines can respond to tunicamycin- and thapsigargin-induced stress by increasing the steady state levels of grp94 and grp78 transcripts, the induction at the GRP protein level is variable and does not always correspond with the transcript level. Tunicamycin 81-92 heat shock protein 90 beta family member 1 Homo sapiens 167-172 10424404-6 1999 Interestingly, while the majority of the breast cancer cell lines can respond to tunicamycin- and thapsigargin-induced stress by increasing the steady state levels of grp94 and grp78 transcripts, the induction at the GRP protein level is variable and does not always correspond with the transcript level. Tunicamycin 81-92 heat shock protein family A (Hsp70) member 5 Homo sapiens 177-182 10424404-6 1999 Interestingly, while the majority of the breast cancer cell lines can respond to tunicamycin- and thapsigargin-induced stress by increasing the steady state levels of grp94 and grp78 transcripts, the induction at the GRP protein level is variable and does not always correspond with the transcript level. Tunicamycin 81-92 gastrin releasing peptide Homo sapiens 217-220 10024536-17 1999 4-fold increased resistance to tunicamycin compared with activity in membranes from untreated control cells, demonstrating that resistance to tunicamycin is correlated with induced GPT activity. Tunicamycin 31-42 glutamic pyruvic transaminase, soluble Mus musculus 181-184 10024536-17 1999 4-fold increased resistance to tunicamycin compared with activity in membranes from untreated control cells, demonstrating that resistance to tunicamycin is correlated with induced GPT activity. Tunicamycin 142-153 glutamic pyruvic transaminase, soluble Mus musculus 181-184 10225275-3 1999 Inhibition of N-linked glycosylation by tunicamycin revealed that NS1 synthesised in MVE-infected C6/36 cells was derived from two polypeptide backbones of 39 kDa (NS1(o)) and 47 kDa (NS1"). Tunicamycin 40-51 influenza virus NS1A binding protein Homo sapiens 66-69 9925876-7 1999 Tunicamycin, an inhibitor of N-linked glycosylation, blocked normal surface membrane expression of a HERG-green fluorescent protein (GFP) fusion protein (HERGGFP) transiently expressed in human embryonic kidney (HEK 293) cells imaged with confocal microscopy. Tunicamycin 0-11 potassium voltage-gated channel subfamily H member 2 Homo sapiens 101-105 9880569-6 1999 In contrast, inhibition of glycosylation of P69, by tunicamycin treatment of the insect cells, produced an enzymatically inactive protein. Tunicamycin 52-63 islet cell autoantigen 1 Homo sapiens 44-47 9931016-4 1999 The ecto-apyrase was also expressed in the presence of tunicamycin, which completely prevented N-linked glycosylation, resulting in a nonglycosylated core protein devoid of ATP and ADP hydrolyzing activity. Tunicamycin 55-66 ectonucleoside triphosphate diphosphohydrolase 1 Homo sapiens 4-16 9931016-7 1999 The glycosylated ecto-apyrase exists as a homodimer in situ as assessed by both size-exclusion chromatography of detergent-solubilized ecto-apyrase and cross-linking of membrane-bound ecto-apyrase, in contrast to the enzymatically deglycosylated ecto-apyrase and the tunicamycin-treated ecto-apyrase. Tunicamycin 267-278 ectonucleoside triphosphate diphosphohydrolase 1 Homo sapiens 17-29 10073711-4 1999 The inclusion of tunicamycin during these time-course experiments suggested that EGT is glycosylated. Tunicamycin 17-28 ecdysteroid UDP-glucosyl transferase Autographa californica nucleopolyhedrovirus 81-84 9854035-4 1999 Secretion of alpha1-antitrypsin, an unrelated N-glycoprotein, was also inhibited by monensin, BFA and tunicamycin, but not by CCCP, castanospermine or N-methyldeoxynojirimycin. Tunicamycin 102-113 serpin family A member 1 Homo sapiens 13-31 9878696-6 1999 The antibiotic tunicamycin completely inhibited GPT activity at a concentration of 100-200 ng ml(-1) and an IC50 of 40 ng ml(-1), but had little effect on the other two enzymes. Tunicamycin 15-26 glutamic--pyruvic transaminase Homo sapiens 48-51 10025674-8 1999 Tunicamycin prevented calcium toxicity; gel electrophoresis studies showed that this protection was likely due to degradation of the NR1 subunit. Tunicamycin 0-11 glutamate ionotropic receptor NMDA type subunit 1 Homo sapiens 133-136 10367750-4 1999 METHODS: We generated the GRP-inducing culture conditions by exposing cells to 2-deoxyglucose (2DG), calcium ionophore A23187 and tunicamycin, and examined cellular sensitivity to cisplatin and carboplatin under these conditions. Tunicamycin 130-141 gastrin releasing peptide Homo sapiens 26-29 10402670-5 1999 Tunicamycin and A23187, the calcium ionophore, enhanced BiP mRNA accumulation first at the neurula stage, while heat shock induced BiP mRNA accumulation first at the gastrula stage. Tunicamycin 0-11 heat shock 70 kDa protein 5b Xenopus laevis 56-59 9922157-11 1998 Finally, a comparison of cleavage site selection in the presence and absence of tunicamycin treatment showed that N-glycosylation of certain mutant forms of CSF-1(256) sterically interfered with protease accessibility, which in turn had an effect on the selection of the site used for cleavage. Tunicamycin 80-91 colony stimulating factor 1 Homo sapiens 157-162 10461108-3 1999 MDCK cells (2 x 10(6) cells/well) were cultured to a confluent state, and the binding of OPN to the cellular surface was then inhibited by adding one of the following 4 substances: human OPN polyclonal antibody, thrombin, cyclic Arg-Gly-Asp (RGD) peptides and tunicamycin. Tunicamycin 260-271 secreted phosphoprotein 1 Canis lupus familiaris 89-92 9727361-7 1998 Immunoblot analyses revealed that in WT10 cells, 34% of AQP2 is glycosylated, which was reduced to 2% after tunicamycin treatment. Tunicamycin 108-119 aquaporin 2 Canis lupus familiaris 56-60 9837919-4 1998 Inhibition of acquisition of N-linked oligosaccharides by tunicamycin treatment in CHO cells stably expressing TSHR produced nonglycosylated TSHR, which was totally nonfunctional. Tunicamycin 58-69 thyrotropin receptor Cricetulus griseus 111-115 9837919-4 1998 Inhibition of acquisition of N-linked oligosaccharides by tunicamycin treatment in CHO cells stably expressing TSHR produced nonglycosylated TSHR, which was totally nonfunctional. Tunicamycin 58-69 thyrotropin receptor Cricetulus griseus 141-145 9832151-2 1998 The glycosylation inhibitor tunicamycin induced a dose-dependent decrease in the rVMAT1-mediated uptake of [3H]serotonin. Tunicamycin 28-39 solute carrier family 18 member A1 Rattus norvegicus 81-87 10049651-10 1998 Northern blot analysis revealed that RTP mRNA expression was induced in HUVECs treated with not only homocysteine but also 2-mercaptoethanol and tunicamycin, both of which are known to induce ER stress. Tunicamycin 145-156 N-myc downstream regulated 1 Homo sapiens 37-40 9820151-7 1998 Sp1 is O-glycosylated while PEF-1 appears to have a novel type of glycosylation, as shown by the interaction with pokeweed lectin and by the inhibition of this interaction by tunicamycin. Tunicamycin 175-186 penta-EF-hand domain containing 1 Homo sapiens 28-33 9778359-6 1998 In this study, we focused on the consequences of removing N-linked glycosylation from the P2X2 receptor by using two different approaches, tunicamycin treatment or site-directed mutagenesis. Tunicamycin 139-150 purinergic receptor P2X 2 Homo sapiens 90-94 9778359-9 1998 Cell surface labeling with biotin or indirect immunofluorescence revealed that the expression of the nonglycosylated receptors produced by either tunicamycin or site-directed mutagenesis is greatly reduced at the cell surface, indicating that the nonglycosylated P2X2 receptors are retained inside the cell. Tunicamycin 146-157 purinergic receptor P2X 2 Homo sapiens 263-267 9767079-2 1998 Treatment of cells expressing wild-type RFC with tunicamycin (0-3 microg) resulted in a progressive shift of the approximately 85 kDa RFC on western blots to 65 kDa. Tunicamycin 49-60 solute carrier family 19 member 1 Homo sapiens 40-43 9767079-2 1998 Treatment of cells expressing wild-type RFC with tunicamycin (0-3 microg) resulted in a progressive shift of the approximately 85 kDa RFC on western blots to 65 kDa. Tunicamycin 49-60 solute carrier family 19 member 1 Homo sapiens 134-137 9767079-3 1998 At 3 microg/ml tunicamycin, the nearly complete loss of glycosylated RFC was accompanied by a approximately 25% decreased rate of methotrexate uptake. Tunicamycin 15-26 solute carrier family 19 member 1 Homo sapiens 69-72 10100886-0 1998 Effect of cycloheximide and tunicamycin on the gonadotrophin-releasing hormone stimulated distal glycosylation of luteinizing hormone by rat pituitary cells. Tunicamycin 28-39 gonadotropin releasing hormone 1 Homo sapiens 47-78 10100886-2 1998 In the present report, we have further examined the GnRH-induced [3H]Gal-LH synthesis and release by treating anterior pituitary cells with polypeptide synthesis and glycosylation inhibitors (cycloheximide and tunicamycin, respectively). Tunicamycin 210-221 gonadotropin releasing hormone 1 Homo sapiens 52-56 10100886-8 1998 Addition of tunicamycin to the pituitary cells inhibited the rates of synthesis and release of [3H]Man-LH which had been induced by GnRH, without altering those of [14C]Leu-LH. Tunicamycin 12-23 gonadotropin releasing hormone 1 Homo sapiens 132-136 9751510-10 1998 Complete inhibition of hTPO N-glycosylation with tunicamycin led to a 95% decrease in hTPO at the plasma membrane and, thus, to a decrease in enzymatic activity at the cell surface, emphasizing the role of N-glycans in the intracellular trafficking of hTPO. Tunicamycin 49-60 thyroid peroxidase Homo sapiens 23-27 9751510-10 1998 Complete inhibition of hTPO N-glycosylation with tunicamycin led to a 95% decrease in hTPO at the plasma membrane and, thus, to a decrease in enzymatic activity at the cell surface, emphasizing the role of N-glycans in the intracellular trafficking of hTPO. Tunicamycin 49-60 thyroid peroxidase Homo sapiens 86-90 9751510-10 1998 Complete inhibition of hTPO N-glycosylation with tunicamycin led to a 95% decrease in hTPO at the plasma membrane and, thus, to a decrease in enzymatic activity at the cell surface, emphasizing the role of N-glycans in the intracellular trafficking of hTPO. Tunicamycin 49-60 thyroid peroxidase Homo sapiens 86-90 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 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 47-51 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 76-81 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 82-85 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 9835451-2 1998 Inhibition of N-linked glycosylation by tunicamycin, which has previously been shown to block the translocation of IGF-1R to the cell surface, blocked cell growth and/or induced cell death in these cell lines. Tunicamycin 40-51 insulin like growth factor 1 receptor Homo sapiens 115-121 10049651-9 1998 It encoded a novel protein with 394 amino acids, which was termed RTP (reducing agent and tunicamycin-responsive protein). Tunicamycin 90-101 N-myc downstream regulated 1 Homo sapiens 66-69 9727361-10 1998 However, in tunicamycin-treated WT10 cells, all AQP2 in the apical membrane was unglycosylated, whereas in untreated cells 30% of AQP2 in the apical membrane was glycosylated. Tunicamycin 12-23 aquaporin 2 Canis lupus familiaris 48-52 9727361-10 1998 However, in tunicamycin-treated WT10 cells, all AQP2 in the apical membrane was unglycosylated, whereas in untreated cells 30% of AQP2 in the apical membrane was glycosylated. Tunicamycin 12-23 aquaporin 2 Canis lupus familiaris 130-134 9692865-7 1998 Moreover, tunicamycin treatment revealed the core form of pIgR had a molecular mass of approximately 100 kDa. Tunicamycin 10-21 polymeric immunoglobulin receptor Mus musculus 58-62 9660831-6 1998 The study of the secretion of HBe derived from C-terminal-truncated precursors demonstrates that the tunicamycin-sensitive secretion absolutely requires a part of the C-terminal region that is removed to form mature HBe, indicating that the cellular tunicamycin-sensitive protein increases the efficiency of the intracellular transport of P22. Tunicamycin 101-112 calcineurin like EF-hand protein 1 Homo sapiens 339-342 9660831-6 1998 The study of the secretion of HBe derived from C-terminal-truncated precursors demonstrates that the tunicamycin-sensitive secretion absolutely requires a part of the C-terminal region that is removed to form mature HBe, indicating that the cellular tunicamycin-sensitive protein increases the efficiency of the intracellular transport of P22. Tunicamycin 250-261 calcineurin like EF-hand protein 1 Homo sapiens 339-342 9654121-3 1998 First, stable K562 transfectants expressing human B7-1 were treated with the N-glycosylation inhibitor tunicamycin. Tunicamycin 103-114 CD80 molecule Homo sapiens 50-54 9654121-5 1998 Significantly, the non-glycosylated cell surface-associated B7-1 on tunicamycin-treated cells retained the capacity to bind CTLA-4 x Ig, a soluble derivative of the CTLA-4(CD152) counter-receptor. Tunicamycin 68-79 CD80 molecule Homo sapiens 60-64 9654121-5 1998 Significantly, the non-glycosylated cell surface-associated B7-1 on tunicamycin-treated cells retained the capacity to bind CTLA-4 x Ig, a soluble derivative of the CTLA-4(CD152) counter-receptor. Tunicamycin 68-79 cytotoxic T-lymphocyte associated protein 4 Homo sapiens 124-130 9654121-5 1998 Significantly, the non-glycosylated cell surface-associated B7-1 on tunicamycin-treated cells retained the capacity to bind CTLA-4 x Ig, a soluble derivative of the CTLA-4(CD152) counter-receptor. Tunicamycin 68-79 cytotoxic T-lymphocyte associated protein 4 Homo sapiens 165-171 9654121-5 1998 Significantly, the non-glycosylated cell surface-associated B7-1 on tunicamycin-treated cells retained the capacity to bind CTLA-4 x Ig, a soluble derivative of the CTLA-4(CD152) counter-receptor. Tunicamycin 68-79 cytotoxic T-lymphocyte associated protein 4 Homo sapiens 172-177 9492298-2 1998 ERp29 was induced to high levels in the rat hepatoma cells under metabolic stress conditions known to cause an aberrant accumulation of proteins in the ER [(e.g. culture in presence of the Ca2+ ionophore A23187, inhibitors of Ca2+-ATPase (thapsigargin), intracellular protein transport (brefeldin A), or protein N-glycosylation (tunicamycin)]. Tunicamycin 329-340 endoplasmic reticulum protein 29 Rattus norvegicus 0-5 9557657-7 1998 Treatment of AGMK and cr5 cells with tunicamycin reduced binding of protective monoclonal Ab (MAb) 190/4, which suggested that N-glycans are required for binding of MAb 190/4 to havcr-1. Tunicamycin 37-48 hepatitis A virus cellular receptor 1 Homo sapiens 178-185 9545520-5 1998 The expression of grp78 is constitutive and can be enhanced by starvation, treatment with tunicamycin, the calcium ionophore A23187 or elevated temperatures (40 degrees C). Tunicamycin 90-101 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 18-23 9531536-6 1998 It entailed exposing mice with defined chop genotypes to a single sublethal intraperitoneal injection of tunicamycin and resulted in a severe illness characterized by transient renal insufficiency. Tunicamycin 105-116 DNA-damage inducible transcript 3 Mus musculus 39-43 9507013-12 1998 rPLD1 bound to concanavalin A-Sepharose beads, and its electrophoretic mobility was altered by treatment with endoglycosidase F. The amount of PLD bound to the beads was decreased in a concentration-dependent manner when tunicamycin was added to the Sf9 expression system. Tunicamycin 221-232 phospholipase D1 Rattus norvegicus 0-5 9507013-12 1998 rPLD1 bound to concanavalin A-Sepharose beads, and its electrophoretic mobility was altered by treatment with endoglycosidase F. The amount of PLD bound to the beads was decreased in a concentration-dependent manner when tunicamycin was added to the Sf9 expression system. Tunicamycin 221-232 glycosylphosphatidylinositol specific phospholipase D1 Homo sapiens 1-4 9507013-13 1998 Tunicamycin also decreased membrane localization of rPLD1. Tunicamycin 0-11 phospholipase D1 Rattus norvegicus 52-57 9668061-4 1998 Inhibition of N-glycosylation with tunicamycin treatment slowed down the rate of dimerization and introduced further oligomerization of the MUC2 apomucin in the endoplasmic reticulum. Tunicamycin 35-46 mucin 2, oligomeric mucus/gel-forming Homo sapiens 140-144 9668061-6 1998 The non-N-glycosylated species of the MUC2 mucin were retained in the endoplasmic reticulum because no O-glycosylated species were precipitated after inhibition by tunicamycin. Tunicamycin 164-175 mucin 2, oligomeric mucus/gel-forming Homo sapiens 38-42 9668061-6 1998 The non-N-glycosylated species of the MUC2 mucin were retained in the endoplasmic reticulum because no O-glycosylated species were precipitated after inhibition by tunicamycin. Tunicamycin 164-175 LOC100508689 Homo sapiens 43-48 9422791-5 1998 The aglycosylated fragment CCP2-ap-SPag was also expressed by using tunicamycin. Tunicamycin 68-79 AGBL carboxypeptidase 2 Homo sapiens 27-31 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 endoplasmic reticulum protein 29 Rattus norvegicus 22-27 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 9701462-12 1998 RTP mRNA was also observed in unstimulated cells and induced by not only homocysteine but also 2-mercaptoethanol and tunicamycin. Tunicamycin 117-128 N-myc downstream regulated 1 Homo sapiens 0-3 10353723-5 1998 ER stress induced calreticulin expression in response to either thapsigargin or tunicamycin was equivalent in these cells to that seen in control, nontransfected cells, leading us to conclude that calreticulin is unlikely be involved in its own induction. Tunicamycin 80-91 calreticulin Homo sapiens 18-30 10353723-6 1998 Levels of the mRNA encoding the fusion protein were also increased by tunicamycin, but not thapsigargin, suggesting that, in agreement with our previous observations, inhibition of N-linked glycosylation may increase the stability of calreticulin mRNA. Tunicamycin 70-81 calreticulin Homo sapiens 234-246 9388239-10 1997 Altered glycosylation generated the new beta1 integrin form since integrin core beta1-chain proteins of the same molecular weight were yielded in Ki-ras, Ha-ras, and control transfectants after removal of sugar residues with endoglycosidase F or following tunicamycin treatment to inhibit glycosylation. Tunicamycin 256-267 integrin subunit beta 1 Homo sapiens 40-54 9415709-5 1997 Moreover, both chemical depalmitoylation by hydroxylamine and inhibition of palmitoyl-CoA transferase in vivo by tunicamycin treatment incresed the reconstitutive activity of detergent extracts and eliminated the differences between native and opioid-dependent cells, indicating that the increase in stimulatory activity is due to depalmitoylation of Gs alpha. Tunicamycin 113-124 GNAS complex locus Homo sapiens 351-359 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 9409285-7 1997 Alterations in apoB conformation and their impact on degradation were also investigated by using DTT and by inhibiting N-linked glycosylation with tunicamycin. Tunicamycin 147-158 apolipoprotein B Homo sapiens 15-19 9409741-5 1997 The grp78-K8/18 association is induced by culturing cells in the presence of tunicamycin or after glucose starvation. Tunicamycin 77-88 heat shock protein family A (Hsp70) member 5 Homo sapiens 4-9 9409741-5 1997 The grp78-K8/18 association is induced by culturing cells in the presence of tunicamycin or after glucose starvation. Tunicamycin 77-88 keratin 8 Homo sapiens 10-15 9367877-6 1997 Both thapsigargin, and tunicamycin, increased calreticulin secretion from the cells, although this might be due to more than simply saturation of KDEL receptor binding. Tunicamycin 23-34 calreticulin Homo sapiens 46-58 9367877-6 1997 Both thapsigargin, and tunicamycin, increased calreticulin secretion from the cells, although this might be due to more than simply saturation of KDEL receptor binding. Tunicamycin 23-34 KDEL endoplasmic reticulum protein retention receptor 1 Homo sapiens 146-159 9409285-11 1997 In tunicamycin-treated cells, DTT further accelerated the degradation of unglycosylated apoB. Tunicamycin 3-14 apolipoprotein B Homo sapiens 88-92 9376679-3 1997 To study the roles of N-glycosylation in the GnT-III function, rat GnT-III was expressed in COS-1 cells under tunicamycin or castanospermine treatment. Tunicamycin 110-121 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Rattus norvegicus 67-74 9388233-6 1997 The latter results were obtained also when BiP was overexpressed not via transfection but as a response to ER stress by tunicamycin. Tunicamycin 120-131 heat shock protein family A (Hsp70) member 5 Homo sapiens 43-46 18982490-6 1997 The expressed UDPGT was a glycoprotein as indicated by electrophoretic mobility shift in Mr approximately 3,000-4,000 when expressed in the presence of tunicamycin. Tunicamycin 152-163 UDP glucuronosyltransferase family 1 member A4 Homo sapiens 14-19 9376679-4 1997 The tunicamycin-treated GnT-III, which was not N-glycosylated, had almost no activity. Tunicamycin 4-15 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 24-31 9376679-10 1997 The null glycosylation mutant had no activity, corresponding to the case of tunicamycin-treated wild-type GnT-III. Tunicamycin 76-87 beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase Homo sapiens 106-113 9089636-4 1997 Using a temperature-sensitive RNA polymerase II mutant, we demonstrate that increased stability was the primary determinant of higher ALG7 mRNA abundance in response to glucose limitation or treatment with tunicamycin. Tunicamycin 206-217 UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase Saccharomyces cerevisiae S288C 134-138 9268304-6 1997 Prior heat shock did not protect cells from IDAM but pretreatment with trans-4,5-dihydroxy-1,2-dithiane (DTTox), thapsigargin, or tunicamycin enhanced expression of the endoplasmic reticulum (ER) chaperones GRP78 and GRP94 and rendered cells tolerant to IDAM. Tunicamycin 130-141 heat shock protein family A (Hsp70) member 5 Sus scrofa 207-212 9268304-6 1997 Prior heat shock did not protect cells from IDAM but pretreatment with trans-4,5-dihydroxy-1,2-dithiane (DTTox), thapsigargin, or tunicamycin enhanced expression of the endoplasmic reticulum (ER) chaperones GRP78 and GRP94 and rendered cells tolerant to IDAM. Tunicamycin 130-141 heat shock protein 90 beta family member 1 Sus scrofa 217-222 9261166-5 1997 We report that PrP molecules mutated at Thr182 alone or at both Thr182 and Thr198 [corrected] fail to reach the cell surface after synthesis, but that those mutated at Thr198 [corrected] or synthesized in the presence of tunicamycin can be detected on the plasma membrane. Tunicamycin 221-232 prion protein Mus musculus 15-18 9271078-6 1997 Cells that were Ca2+ depleted for 2 h slowly secreted an abnormal slightly smaller complex oligosaccharide form of alpha1-antitrypsin at approximately the same rate as the non-glycosylated protein generated by treatment with tunicamycin. Tunicamycin 225-236 serpin family A member 1 Homo sapiens 115-133 9102228-11 1997 Inhibition of N-linked glycosylation with tunicamycin resulted in decreased HA binding of cells bearing an active CD44 receptor. Tunicamycin 42-53 CD44 molecule (Indian blood group) Homo sapiens 114-118 9145315-5 1997 Inhibition of the N-glycosylation pathway by tunicamycin resulted in a decreased ETSA-B21 signal on the cell membrane. Tunicamycin 45-56 cytohesin 1 Homo sapiens 86-89 9237560-9 1997 There were a number of precursor TNF isoforms that were unchanged upon tunicamycin treatment and these presumably reflect protein modifications other than glycosylation. Tunicamycin 71-82 tumor necrosis factor Mus musculus 33-36 9241531-4 1997 Here, by means of cytofluorimetric analysis evidence is provided, that the induction of APN surface expression is partially resistent to the action of the inhibitors of protein biosynthesis, puromycin and cycloheximide, and is not prevented by tunicamycin, an inhibitor of glycosylation. Tunicamycin 244-255 alanyl aminopeptidase, membrane Homo sapiens 88-91 9149128-2 1997 Here we report that MDR cells are hypersensitive to the N-linked glycosylation inhibitor tunicamycin, which induces partial inhibition of GLUT-1 glycosylation and diminishes GLUT-1-mediated transport. Tunicamycin 89-100 solute carrier family 2 member 1 Homo sapiens 138-144 9149128-2 1997 Here we report that MDR cells are hypersensitive to the N-linked glycosylation inhibitor tunicamycin, which induces partial inhibition of GLUT-1 glycosylation and diminishes GLUT-1-mediated transport. Tunicamycin 89-100 solute carrier family 2 member 1 Homo sapiens 174-180 9112387-6 1997 Flow cytometric analysis showed decreased expression of the hCaR on the cell membrane in tunicamycin-treated cells. Tunicamycin 89-100 CXADR Ig-like cell adhesion molecule Homo sapiens 60-64 9112387-8 1997 Tunicamycin treatment of cells, transfected with a mutant hCaR complementary DNA containing a nonsense codon at position 599 preceding the 1st transmembrane domain, blocked the secretion of a 95-kDa protein, representing the amino-terminal extracellular domain, into the medium. Tunicamycin 0-11 CXADR Ig-like cell adhesion molecule Homo sapiens 58-62 9139799-7 1997 In addition, tunicamycin-derived, nonglycosylated LHRs were present at the cell surface and exhibited a phenotype consistent with mature receptors due to their capability to mediate hCG-stimulated cAMP production as well as bind oLH with high affinity. Tunicamycin 13-24 hypertrichosis 2 (generalised, congenital) Homo sapiens 182-185 9038234-4 1997 However, grp78/grp94 transcription was induced by the glycosylation inhibitor tunicamycin, suggesting that there are at least two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in response to glycosylation inhibition, which is operable in WEHI7.2 cells. Tunicamycin 78-89 heat shock protein 5 Mus musculus 9-14 9038234-4 1997 However, grp78/grp94 transcription was induced by the glycosylation inhibitor tunicamycin, suggesting that there are at least two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in response to glycosylation inhibition, which is operable in WEHI7.2 cells. Tunicamycin 78-89 heat shock protein 90, beta (Grp94), member 1 Mus musculus 15-20 9038234-4 1997 However, grp78/grp94 transcription was induced by the glycosylation inhibitor tunicamycin, suggesting that there are at least two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in response to glycosylation inhibition, which is operable in WEHI7.2 cells. Tunicamycin 78-89 heat shock protein 5 Mus musculus 130-135 9038234-4 1997 However, grp78/grp94 transcription was induced by the glycosylation inhibitor tunicamycin, suggesting that there are at least two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in response to glycosylation inhibition, which is operable in WEHI7.2 cells. Tunicamycin 78-89 heat shock protein 90, beta (Grp94), member 1 Mus musculus 136-141 9030589-7 1997 Interestingly, even nonglycosylated GM2AP is delivered to the lysosome, as shown by tunicamycin treatment and subcellular fractionation. Tunicamycin 84-95 ganglioside GM2 activator Homo sapiens 36-41 9159886-5 1997 Northern hybridization analysis demonstrated that BiP mRNA was present constitutively in the Xenopus A6 kidney epithelial cell line and that BiP mRNA levels could be enhanced by treatment of the cells with galactose-free media, 2-deoxyglucose, 2-deoxygalactose, glucosamine, tunicamycin, heat shock, dithiothreitol, and the calcium ionophore, A23187. Tunicamycin 275-286 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 50-53 9159886-5 1997 Northern hybridization analysis demonstrated that BiP mRNA was present constitutively in the Xenopus A6 kidney epithelial cell line and that BiP mRNA levels could be enhanced by treatment of the cells with galactose-free media, 2-deoxyglucose, 2-deoxygalactose, glucosamine, tunicamycin, heat shock, dithiothreitol, and the calcium ionophore, A23187. Tunicamycin 275-286 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 141-144 8995369-9 1997 Furthermore, expression of gp65 and gp55 cDNAs in human 293 cells treated with tunicamycin results in the production of unglycosylated core proteins of identical size to deglycosylated gp65 and gp55. Tunicamycin 79-90 neuroplastin Homo sapiens 185-189 9006956-6 1997 The same complex of the four putative chaperones with Tg was observed in cells treated with tunicamycin, indicating that these four ER chaperones stably associate with Tg when it is misfolded/misassembled due to inhibition of its glycosylation. Tunicamycin 92-103 thyroglobulin Rattus norvegicus 54-56 9006956-6 1997 The same complex of the four putative chaperones with Tg was observed in cells treated with tunicamycin, indicating that these four ER chaperones stably associate with Tg when it is misfolded/misassembled due to inhibition of its glycosylation. Tunicamycin 92-103 thyroglobulin Rattus norvegicus 168-170 8995369-9 1997 Furthermore, expression of gp65 and gp55 cDNAs in human 293 cells treated with tunicamycin results in the production of unglycosylated core proteins of identical size to deglycosylated gp65 and gp55. Tunicamycin 79-90 neuroplastin Homo sapiens 194-198 9020069-5 1997 Northern blot analysis revealed that induction of ORP150 in U373 cells was not limited to hypoxia but also observed by 2-deoxyglucose or tunicamycin treatment. Tunicamycin 137-148 hypoxia up-regulated 1 Homo sapiens 50-56 9110380-6 1997 Tunicamycin elicited a 2.4- and 2.7-fold increase in IAPP mRNA levels in the low and high glucose media, respectively; however, it did not change insulin mRNA. Tunicamycin 0-11 islet amyloid polypeptide Homo sapiens 53-57 9111868-15 1997 In many, but not in all cases, CD44 does not bind HA unless it is stimulated by phorbol esters, activated by agonistic anti-CD44 antibody, or deglycosylated (e.g., by tunicamycin). Tunicamycin 167-178 CD44 molecule (Indian blood group) Homo sapiens 31-35 8972186-7 1997 The Y-box proteins can repress the inducibility of the grp78 core element mediated by treatment of cells with A23187, thapsigargin, and tunicamycin. Tunicamycin 136-147 heat shock protein family A (Hsp70) member 5 Homo sapiens 55-60 9473774-4 1997 Nonrestricted CD45 epitopes were not affected by the sialyl acid cleavage with sodium metaperiodate or neuraminidase, but were sensitive to both, tunicamycin, the N-glycosylation inhibitor and monensin, an inhibitor of protein transport through the Golgi compartment. Tunicamycin 146-157 protein tyrosine phosphatase receptor type C Homo sapiens 14-18 8961954-6 1996 Inhibition of N-glycosylation with an optimized concentration of tunicamycin yielded completely nonglycosylated hPTH/PTHrP receptor (approximately 60 kDa). Tunicamycin 65-76 parathyroid hormone Homo sapiens 112-116 8961954-6 1996 Inhibition of N-glycosylation with an optimized concentration of tunicamycin yielded completely nonglycosylated hPTH/PTHrP receptor (approximately 60 kDa). Tunicamycin 65-76 parathyroid hormone like hormone Homo sapiens 117-122 8961954-10 1996 The molecular weight (approximately 60000) of the band representing the photo-cross-linked, nonglycosylated receptor (obtained from the tunicamycin-treated HEK-293/C-21 cells) was similar to that of the deglycosylated photo-cross-linked receptor (obtained by enzymatic treatment with Endoglycosidase-F/N-glycosidase-F). Tunicamycin 136-147 TBL1X/Y related 1 Homo sapiens 164-168 8939898-13 1996 RTP mRNA was also observed in unstimulated cells and induced by not only homocysteine but also 2-mercaptoethanol and tunicamycin. Tunicamycin 117-128 N-myc downstream regulated 1 Homo sapiens 0-3 8973632-7 1996 Inhibition of N-glycosylation by tunicamycin dramatically reduced the expression of IFN-gamma, but did not block its secretion. Tunicamycin 33-44 interferon gamma Homo sapiens 84-93 8887673-8 1996 Like KAR2, SSI1 is induced both in the presence of tunicamycin and in a kar2-159 mutant strain, conditions which lead to an accumulation of unfolded proteins in the ER. Tunicamycin 51-62 Hsp70 family chaperone LHS1 Saccharomyces cerevisiae S288C 11-15 8922392-18 1996 Tunicamycin treatment inhibits HA binding by CD44v and at the same time destroys oligomerization. Tunicamycin 0-11 CD44 molecule (Indian blood group) Rattus norvegicus 45-50 8932376-1 1996 The Saccharomyces cerevisiae IRE1 gene, encoding a putative receptor-type protein kinase, is known to be required for inositol prototrophy and for the induction of a chaperon molecule, BiP, encoded by KAR2, under stress conditions such as tunicamycin addition. Tunicamycin 239-250 bifunctional endoribonuclease/protein kinase IRE1 Saccharomyces cerevisiae S288C 29-33 8918549-7 1996 Complete inhibition of the binding of these glycoprotein precursors to calnexin by tunicamycin or castanospermine indicates the importance of partially trimmed N-linked oligosaccharides for their association. Tunicamycin 83-94 calnexin Homo sapiens 71-79 8794367-5 1996 Tunicamycin treatment, which inhibits N-glycosylation, increased the rate of migration of the UL37 protein to 68 kDa, verifying its modification by N-glycosylation in HCMV-infected cells. Tunicamycin 0-11 envelope glycoprotein UL37 Human betaherpesvirus 5 94-98 8995369-9 1997 Furthermore, expression of gp65 and gp55 cDNAs in human 293 cells treated with tunicamycin results in the production of unglycosylated core proteins of identical size to deglycosylated gp65 and gp55. Tunicamycin 79-90 neuroplastin Homo sapiens 27-31 8995369-9 1997 Furthermore, expression of gp65 and gp55 cDNAs in human 293 cells treated with tunicamycin results in the production of unglycosylated core proteins of identical size to deglycosylated gp65 and gp55. Tunicamycin 79-90 neuroplastin Homo sapiens 36-40 8987625-4 1996 Synthesis of the recombinant proteins in the absence and presence of tunicamycin revealed that both E1 and E2 were glycosylated with apparent molecular weights of 52 kDa and 37 kDa, respectively. Tunicamycin 69-80 small nucleolar RNA, H/ACA box 73A Homo sapiens 100-109 8888624-2 1996 In Arabidopsis seedlings, accumulation of transcripts for BiP was induced not only by inhibition of the N-glycosylation of proteins by tunicamycin but also by inhibition of the processing of N-linked glycans by castanospermine. Tunicamycin 135-146 Heat shock protein 70 (Hsp 70) family protein Arabidopsis thaliana 58-61 8837730-0 1996 Inhibition by tunicamycin of mucin synthesis, not morphological changes, in epidermis during retinol-induced mucous metaplasia of chick embryonic cultured skin. Tunicamycin 14-25 mucin 2, oligomeric mucus/gel-forming Gallus gallus 29-34 8837730-4 1996 RESULTS: Tunicamycin, which prevents the formation of N-glycans and inhibits maturation or morphological organization of various epithelial cells, irreversibly inhibited the synthesis of sulfated glycoproteins (O-glycans, mucin) in the epidermis only when applied to retinol-pretreated skin. Tunicamycin 9-20 mucin 2, oligomeric mucus/gel-forming Gallus gallus 222-227 8837730-7 1996 CONCLUSION: These results suggest that tunicamycin did not prevent morphological changes induced by retinol but inhibited mucin synthesis by a direct action on the epidermis of retinol-pretreated skin. Tunicamycin 39-50 mucin 2, oligomeric mucus/gel-forming Gallus gallus 122-127 8837730-8 1996 Because in some cell-line mucin precursors contain high mannose N-linked oligosaccharides side chains, tunicamycin may have inhibited mucin synthesis. Tunicamycin 103-114 mucin 2, oligomeric mucus/gel-forming Gallus gallus 26-31 8837730-8 1996 Because in some cell-line mucin precursors contain high mannose N-linked oligosaccharides side chains, tunicamycin may have inhibited mucin synthesis. Tunicamycin 103-114 mucin 2, oligomeric mucus/gel-forming Gallus gallus 134-139 8932376-1 1996 The Saccharomyces cerevisiae IRE1 gene, encoding a putative receptor-type protein kinase, is known to be required for inositol prototrophy and for the induction of a chaperon molecule, BiP, encoded by KAR2, under stress conditions such as tunicamycin addition. Tunicamycin 239-250 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 201-205 8932376-4 1996 Introduction of IRE2/HAC1 into the ire1 mutant clearly restored the expression of KAR2 upon tunicamycin treatment. Tunicamycin 92-103 transcription factor HAC1 Saccharomyces cerevisiae S288C 21-25 8932376-4 1996 Introduction of IRE2/HAC1 into the ire1 mutant clearly restored the expression of KAR2 upon tunicamycin treatment. Tunicamycin 92-103 bifunctional endoribonuclease/protein kinase IRE1 Saccharomyces cerevisiae S288C 35-39 8932376-4 1996 Introduction of IRE2/HAC1 into the ire1 mutant clearly restored the expression of KAR2 upon tunicamycin treatment. Tunicamycin 92-103 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 82-86 8932376-5 1996 ire2/hac1-disrupted yeast cells showed not only the inositol auxotrophic phenotype but also the tunicamycin sensitivity, and failed to induce the expression of KAR2. Tunicamycin 96-107 transcription factor HAC1 Saccharomyces cerevisiae S288C 5-9 8654361-4 1996 Our studies indicate that LHS1 is regulated by the unfolded protein response pathway, as evidenced by its transcriptional induction in cells treated with tunicamycin, and in various mutants defective in precursor processing (sec11-7, sec53-6 and sec59-1). Tunicamycin 154-165 Hsp70 family chaperone LHS1 Saccharomyces cerevisiae S288C 26-30 8700133-2 1996 The use of hNET-specific antibodies and the membrane-impermeant biotinylating reagent sulfosuccinimidobiotin establishes that treatment of stably transfected LLC-PK1 cells with tunicamycin depletes surface membranes of mature hNET glycoproteins, which is consistent with a failure of less stable, nonglycosylated subunits to replenish surface compartments. Tunicamycin 177-188 solute carrier family 6 member 2 Homo sapiens 11-15 8700133-2 1996 The use of hNET-specific antibodies and the membrane-impermeant biotinylating reagent sulfosuccinimidobiotin establishes that treatment of stably transfected LLC-PK1 cells with tunicamycin depletes surface membranes of mature hNET glycoproteins, which is consistent with a failure of less stable, nonglycosylated subunits to replenish surface compartments. Tunicamycin 177-188 solute carrier family 6 member 2 Homo sapiens 226-230 8645293-4 1996 Other stress inducers, tunicamycin, A23187, and heat shock, which caused an accumulation of unfolded proteins, also induced the PDI mRNA, indicating that the unfolded protein accumulation response induces PDI gene expression. Tunicamycin 23-34 prolyl 4-hydroxylase subunit beta Homo sapiens 128-131 8828806-4 1996 Tunicamycin (0.01 ng/ml) when added to the incubation media together with glucose prevented the decrease in Ca2+ATPase activity. Tunicamycin 0-11 carbonic anhydrase 2 Homo sapiens 108-118 8648261-5 1996 Northern hybridization of poly(A)+ RNA from LLC-PK1 cells illustrated that in tunicamycin-treated cells, NHE-3 mRNA expression increased threefold over control cells. Tunicamycin 78-89 solute carrier family 9 member A3 Sus scrofa 105-110 8648261-8 1996 NHE-3 immunoblots of whole cell extract from tunicamycin-treated cells showed that in addition to the 95 kd protein, an 87 kd band was also detected. Tunicamycin 45-56 solute carrier family 9 member A3 Sus scrofa 0-5 8846915-7 1996 Tunicamycin treatment experiments, biochemical fractionation and extraction experiments, and proteinase K protection experiments collectively indicate that Axl2p is an integral membrane glycoprotein at the plasma membrane. Tunicamycin 0-11 Axl2p Saccharomyces cerevisiae S288C 156-161 8837227-7 1996 Analysis of GPC synthesis in the presence of tunicamycin revealed that the unglycosylated GPC appeared as two polypeptides of 43 and 46 kDa. Tunicamycin 45-56 glycophorin C (Gerbich blood group) Homo sapiens 90-93 8645293-4 1996 Other stress inducers, tunicamycin, A23187, and heat shock, which caused an accumulation of unfolded proteins, also induced the PDI mRNA, indicating that the unfolded protein accumulation response induces PDI gene expression. Tunicamycin 23-34 prolyl 4-hydroxylase subunit beta Homo sapiens 205-208 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 gastrin releasing peptide Rattus norvegicus 45-48 8593668-7 1996 Using quantitative electron-microscopic immunocytochemistry, the lysosomal contents of SGP-1 were shown to increase significantly after the administration of tunicamycin in vivo. Tunicamycin 158-169 prosaposin Rattus norvegicus 87-92 8601595-3 1996 Our results show that treatment of a panel of human cell lines which constitutively express CD44 with the inhibitor of N-linked glycosylation tunicamycin results in the loss of attachment of these cells to hyaluronate-coated substrate. Tunicamycin 142-153 CD44 molecule (Indian blood group) Homo sapiens 92-96 8635486-5 1996 The PDGF-induced IGF-1R expression was suppressed in the presence of tunicamycin, an inhibitor of N-linked glycosylation. Tunicamycin 69-80 insulin like growth factor 1 receptor Homo sapiens 17-23 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 7492303-8 1995 Tunicamycin or treatment with endoglucosidase H reduced the molecular mass of hypertonicity-induced Cox-2 by 5 kDa. Tunicamycin 0-11 cytochrome c oxidase II, mitochondrial Rattus norvegicus 100-105 8636209-8 1996 In contrast, treatment of T cells with tunicamycin suggested that N-linked glycosylation of CD3 delta is required for TCR assembly. Tunicamycin 39-50 CD3 delta subunit of T-cell receptor complex Homo sapiens 92-101 8636209-8 1996 In contrast, treatment of T cells with tunicamycin suggested that N-linked glycosylation of CD3 delta is required for TCR assembly. Tunicamycin 39-50 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 118-121 8546698-3 1996 Photoaffinity labelling of cell-surface AT2 receptors revealed that PC-12 cells grown in the presence of tunicamycin expressed, in addition to the previously described 140 kDa receptor, lower-molecular-mass receptors of 63 kDa, 47 kDa and 32 kDa. Tunicamycin 105-116 angiotensin II receptor, type 2 Rattus norvegicus 40-43 8546698-6 1996 Both receptor forms exhibited a high affinity for angiotensin II, although a slight decrease (of about 2-fold) was consistently observed on tunicamycin-treated cells as compared with control cells. Tunicamycin 140-151 angiotensinogen Rattus norvegicus 50-64 8546698-9 1996 In conclusion, the stepwise action of tunicamycin suggests the presence of at least three N-linked oligosaccharide side chains on the AT2 receptor of PC-12 cells. Tunicamycin 38-49 angiotensin II receptor, type 2 Rattus norvegicus 134-137 8818631-8 1996 Exposure of cell monolayers to tunicamycin, an inhibitor of protein glycosylation, mimicked the effect of NO2 exposure on expression of GRP-78. Tunicamycin 31-42 heat shock protein family A (Hsp70) member 5 Homo sapiens 136-142 12232600-0 1996 The Effect of Tunicamycin on the Interaction of Fibronectin and HT1080 Cells. Tunicamycin 14-25 fibronectin 1 Homo sapiens 48-59 7500048-5 1995 To examine this issue, we have directly explored the binding of calnexin to both Ii truncation mutants lacking the typical sites of N-glycosylation or Ii produced in cells treated with tunicamycin to prevent glycan addition. Tunicamycin 185-196 calnexin Mus musculus 64-72 7492299-5 1995 SDS/PAGE of rhLF expressed in the presence of tunicamycin revealed a protein with the same M(r) as that of enzymically deglycosylated natural hLF. Tunicamycin 46-57 HLF transcription factor, PAR bZIP family member Homo sapiens 13-16 7592880-3 1995 Tunicamycin also induced biochemical changes in Cx43 protein; the level increased, and a considerable fraction became phosphorylated and Triton X-100 insoluble, in contrast to untreated cells where Cx43 was non-phosphorylated and Triton X-100 soluble. Tunicamycin 0-11 gap junction protein alpha 1 Homo sapiens 48-52 7592677-3 1995 Tunicamycin, an N-glycosylation inhibitor, markedly inhibited GM-CSF binding, GM-CSF-induced deoxyglucose uptake, and protein tyrosine phosphorylation in HL-60(eos) cells but did not affect cell surface expression of the alpha subunit as detected by an anti-alpha subunit monoclonal antibody. Tunicamycin 0-11 colony stimulating factor 2 Homo sapiens 62-68 8750891-9 1995 The 5-HT2C receptor cell line (3T3/2C) was grown in the presence of tunicamycin to metabolically inhibit N-linked glycosylation. Tunicamycin 68-79 5-hydroxytryptamine receptor 2C Rattus norvegicus 4-10 7592677-3 1995 Tunicamycin, an N-glycosylation inhibitor, markedly inhibited GM-CSF binding, GM-CSF-induced deoxyglucose uptake, and protein tyrosine phosphorylation in HL-60(eos) cells but did not affect cell surface expression of the alpha subunit as detected by an anti-alpha subunit monoclonal antibody. Tunicamycin 0-11 colony stimulating factor 2 Homo sapiens 78-84 7666502-3 1995 Treatment with the N glycosylation inhibitor tunicamycin converted the two SPI-3 proteins to a single 40-kDa protein, close to the size of 42 kDa predicted from the DNA sequence, suggesting that the SPI-3 protein, unlike the other two orthopoxvirus serpins, is a glycoprotein. Tunicamycin 45-56 serpin family B member 6 Homo sapiens 75-80 7666502-3 1995 Treatment with the N glycosylation inhibitor tunicamycin converted the two SPI-3 proteins to a single 40-kDa protein, close to the size of 42 kDa predicted from the DNA sequence, suggesting that the SPI-3 protein, unlike the other two orthopoxvirus serpins, is a glycoprotein. Tunicamycin 45-56 serpin family B member 6 Homo sapiens 199-204 7665231-6 1995 Incubation of NCI-H1688 cells with tunicamycin or cleavage of carbohydrate residues of NCI-H1688 or MCF-7/AdrVp membrane proteins with PNGase F leads to the appearance of a sharp 35-kDa band reactive with anti-P-95 antisera. Tunicamycin 35-46 nibrin Homo sapiens 210-214 7543137-5 1995 Treatment of the nonbinding clone with tunicamycin reduced the size of the protein and allowed the cells to recognize HA via CD44. Tunicamycin 39-50 CD44 antigen Cricetulus griseus 125-129 7665923-11 1995 Pulse-chase experiments revealed that gp80 is synthesized from a 55-kD precursor molecule, the maturation of which was prevented by treating cells with tunicamycin. Tunicamycin 152-163 interleukin 6 receptor Homo sapiens 38-42 7543138-9 1995 Furthermore, culture in tunicamycin for 2-3 d converted parental and inducible cell lines into cells showing constitutive CD44-mediated HA binding. Tunicamycin 24-35 CD44 antigen Mus musculus 122-126 7619064-7 1995 Pretreatment of the cells with tunicamycin to inhibit the first step of N-glycosylation led to intracellular accumulation of immature rLCAT (approximately 46-48 kDa) and a marked reduction in enzyme secreted. Tunicamycin 31-42 lecithin cholesterol acyltransferase Rattus norvegicus 134-139 12242382-7 1995 Treating plants with tunicamycin, a drug that blocks N-glycosylation in the ER, or with cold shock, known to block secretory protein transport, led to a marked accumulation of aERD2 and aSAR1 transcripts. Tunicamycin 21-32 ER lumen protein retaining receptor family protein Arabidopsis thaliana 176-181 12242382-7 1995 Treating plants with tunicamycin, a drug that blocks N-glycosylation in the ER, or with cold shock, known to block secretory protein transport, led to a marked accumulation of aERD2 and aSAR1 transcripts. Tunicamycin 21-32 secretion-associated RAS super family 2 Arabidopsis thaliana 186-191 7663166-5 1995 Tunicamycin treatment of infected cells resulted in a mobility shift of OSF-2 (approximately 90-kDa band) on Western blots. Tunicamycin 0-11 periostin, osteoblast specific factor Mus musculus 72-77 7744857-3 1995 On the basis of tunicamycin sensitivity, both GLUT1 species arose from a common protein migrating at 36 kDa. Tunicamycin 16-27 solute carrier family 2 (facilitated glucose transporter), member 1 Mus musculus 46-51 7658166-10 1995 Treatment of COS1 cells with tunicamycin for 24 h had the same effect on wild type hLPL processing and edoplasmic reticulum distribution. Tunicamycin 29-40 lipoprotein lipase Homo sapiens 83-87 7721836-6 1995 Tunicamycin treatment of transfected COS-7 cells as well as peptide-N-glycosidase F digestion of the transporter converted the 58-kDa species to a 50-kDa form, indicating that the latter represents the hNET core protein. Tunicamycin 0-11 solute carrier family 6 member 2 Homo sapiens 202-206 7867726-9 1995 These bands likely represent differently glycosylated forms of the two RET primary products (117 and 122 kDa) detected in tunicamycin-treated cells. Tunicamycin 122-133 ret proto-oncogene Homo sapiens 71-74 7710927-0 1995 Inhibition of N-linked glycosylation of P-glycoprotein by tunicamycin results in a reduced multidrug resistance phenotype. Tunicamycin 58-69 ATP binding cassette subfamily B member 1 Homo sapiens 40-54 7710927-3 1995 Incubation of clone A cells with tunicamycin for different periods resulted in a time-dependent increase in daunorubicin accumulation, reflecting a reduction in P-gp function. Tunicamycin 33-44 ATP binding cassette subfamily B member 1 Homo sapiens 161-165 7710927-5 1995 Reduction in surface-associated P-gp following exposure to tunicamycin was established by FACS analysis, Western blot analysis and immunoprecipitation of surface-iodinated P-gp. Tunicamycin 59-70 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 7710927-5 1995 Reduction in surface-associated P-gp following exposure to tunicamycin was established by FACS analysis, Western blot analysis and immunoprecipitation of surface-iodinated P-gp. Tunicamycin 59-70 ATP binding cassette subfamily B member 1 Homo sapiens 172-176 7710927-6 1995 In addition, immunoprecipitation of P-gp from 32P-orthophosphate-labelled cells demonstrated reduced phosphorylation of P-gp associated with tunicamycin exposure. Tunicamycin 141-152 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 7710927-6 1995 In addition, immunoprecipitation of P-gp from 32P-orthophosphate-labelled cells demonstrated reduced phosphorylation of P-gp associated with tunicamycin exposure. Tunicamycin 141-152 ATP binding cassette subfamily B member 1 Homo sapiens 120-124 7776966-12 1995 Similarly, when cells expressing the wild type FSHR were treated with tunicamycin to prevent N-linked glycosylation, the resulting nonglycosylated FSHR was not able to bind FSH. Tunicamycin 70-81 follicle stimulating hormone receptor Homo sapiens 47-51 7776966-12 1995 Similarly, when cells expressing the wild type FSHR were treated with tunicamycin to prevent N-linked glycosylation, the resulting nonglycosylated FSHR was not able to bind FSH. Tunicamycin 70-81 follicle stimulating hormone receptor Homo sapiens 147-151 7720792-0 1995 Tunicamycin potently inhibits tumor necrosis factor-induced hepatocyte apoptosis. Tunicamycin 0-11 tumor necrosis factor Mus musculus 30-51 7832797-0 1995 Tunicamycin inhibits the expression of functional thrombin receptors on human T-lymphoblastoid cells. Tunicamycin 0-11 coagulation factor II, thrombin Homo sapiens 50-58 7832797-2 1995 In the present report we investigated the effect of tunicamycin, a specific inhibitor of N-linked glycosylation, on the expression and function of the thrombin receptor on human T-lymphoblastoid cells. Tunicamycin 52-63 coagulation factor II, thrombin Homo sapiens 151-159 7832797-3 1995 We found that tunicamycin selectively inhibited thrombin-induced Ca2+ mobilization in a dose-dependent manner while the same response triggered by anti-CD3 antibody was unchanged in these cells. Tunicamycin 14-25 coagulation factor II, thrombin Homo sapiens 48-56 7832797-4 1995 Surface expression of the thrombin receptor, as assessed by immunofluorescence staining using two different antibodies, was strongly decreased in the presence of tunicamycin. Tunicamycin 162-173 coagulation factor II, thrombin Homo sapiens 26-34 7720792-1 1995 The protein glycosylation inhibitor tunicamycin protected male BALB/c mice from tumor necrosis factor alpha-induced liver failure. Tunicamycin 36-47 tumor necrosis factor Mus musculus 80-101 7720792-2 1995 Tunicamycin also inhibited tumor necrosis factor-induced cell death in primary hepatocyte cultures with a median inhibitory concentration of 8 nM, but not in the tumor cell line WEHI 164 clone 13. Tunicamycin 0-11 tumor necrosis factor Mus musculus 27-48 7811745-4 1995 LPL in cells treated with tunicamycin, preventing the transfer of N-linked oligosaccharide chain, was unglycosylated (51 kDa) and inactive. Tunicamycin 26-37 lipoprotein lipase Homo sapiens 0-3 7876241-2 1995 Most proteins that calnexin binds are N-glycosylated, and treatment of cells with tunicamycin or inhibitors of initial glucose trimming steps interferes with calnexin binding. Tunicamycin 82-93 calnexin Homo sapiens 19-27 7876241-2 1995 Most proteins that calnexin binds are N-glycosylated, and treatment of cells with tunicamycin or inhibitors of initial glucose trimming steps interferes with calnexin binding. Tunicamycin 82-93 calnexin Homo sapiens 158-166 7876246-5 1995 Nonglycosylated MPO precursors synthesized in the presence of tunicamycin did not interact with CRT. Tunicamycin 62-73 myeloperoxidase Homo sapiens 16-19 8548206-6 1995 Tunicamycin diminished the formation of leukocyte IFN, but the decrease in titre of this IFN is due to the inhibition of protein synthesis. Tunicamycin 0-11 interferon alpha 1 Homo sapiens 50-53 8548206-6 1995 Tunicamycin diminished the formation of leukocyte IFN, but the decrease in titre of this IFN is due to the inhibition of protein synthesis. Tunicamycin 0-11 interferon alpha 1 Homo sapiens 89-92 7873794-3 1994 This study was undertaken to investigate the internalization of Sertoli-derived SGP-2 and synthesis of an endogenous efferent duct form of SGP-2 by nonciliated cells targeted to their secondary lysosomes on animals whose efferent ducts were ligated and/or received injections of tunicamycin. Tunicamycin 279-290 clusterin Homo sapiens 139-144 7875740-5 1994 Treatment of CD4+ cell lines with tunicamycin resulted in the appearance of a 47,000 MW band for both allelic forms indicating that the difference in M(r) is due to glycosylation. Tunicamycin 34-45 CD4 molecule Bos taurus 13-16 7526846-1 1994 In order to determine whether the endoplasmic reticulum (ER) luminal FK506-binding protein, FKBP13, shares properties of ER molecular chaperones, MDCK cells were treated with either tunicamycin or Ca2+ ionophores. Tunicamycin 182-193 FKBP prolyl isomerase 2 Homo sapiens 92-98 7895167-3 1994 Treatment of H-2Dd+ target cells with tunicamycin prevents their binding to Ly-49A+ cells and renders them susceptible to lysis by Ly-49A+ NK cells. Tunicamycin 38-49 killer cell lectin-like receptor, subfamily A, member 1 Mus musculus 76-82 7895167-3 1994 Treatment of H-2Dd+ target cells with tunicamycin prevents their binding to Ly-49A+ cells and renders them susceptible to lysis by Ly-49A+ NK cells. Tunicamycin 38-49 killer cell lectin-like receptor, subfamily A, member 1 Mus musculus 131-137 7877727-0 1994 Tunicamycin inhibits prostaglandin F2 alpha receptor-mediated phosphoinositide hydrolysis in cultured rat astrocytes. Tunicamycin 0-11 prostaglandin F receptor Rattus norvegicus 21-52 7999029-5 1994 Both the mature and non-mature forms of the G-CSFR appear to be N-glycosylated, as determined by glycanase digestion and inhibition of glycosylation by tunicamycin. Tunicamycin 152-163 colony stimulating factor 3 receptor (granulocyte) Mus musculus 44-50 7526846-2 1994 By Northern-blot analysis, tunicamycin resulted in a 2-fold rise in FKBP13 mRNA, whereas ionophores (A23187 and ionomycin) caused a more impressive rise in FKBP13 mRNA (up to 5-fold with ionomycin). Tunicamycin 27-38 FKBP prolyl isomerase 2 Homo sapiens 68-74 7523405-10 1994 The expression of the serotonin transporter in tunicamycin-treated Sf9 cells resulted in low levels of ligand binding activity (0.2 pmol/mg) but unchanged Kd. Tunicamycin 47-58 solute carrier family 6 member 4 Rattus norvegicus 22-43 7808470-1 1994 A gene which overexpresses a 36-kDa protein (p36) in tunicamycin-resistant Leishmania was mapped by transfection and overexpression to the upstream region of the drug maker in the extrachromosomal amplicon. Tunicamycin 53-64 annexin A2 Homo sapiens 45-48 8044801-10 1994 Treatment of DCC-expressing cells with tunicamycin decreased the apparent molecular weight of the immunoreactive proteins, establishing that DCC is a glycoprotein. Tunicamycin 39-50 DCC netrin 1 receptor Homo sapiens 13-16 8044801-10 1994 Treatment of DCC-expressing cells with tunicamycin decreased the apparent molecular weight of the immunoreactive proteins, establishing that DCC is a glycoprotein. Tunicamycin 39-50 DCC netrin 1 receptor Homo sapiens 141-144 8038169-6 1994 Its levels were correlated with RCK1 current amplitudes (IRCK1) and upon incubation of the cRNA-injected oocytes with tunicamycin, its molecular weight was decreased and at the same time IRCK1 was reduced. Tunicamycin 118-129 potassium voltage-gated channel subfamily A member 1 Rattus norvegicus 32-36 7972488-4 1994 The signal peptide is cleaved at the same position as in maize and the mature protein undergoes tunicamycin-sensitive glycosylation, yielding a product with the same mobility on SDS-PAGE as authentic maize ABP1. Tunicamycin 96-107 auxin-binding protein 1 Zea mays 206-210 8006041-5 1994 Monensin or tunicamycin treatment resulted in a shift of the 27-29-kDa human CR-1 protein to 24 kDa and 20 kDa, respectively. Tunicamycin 12-23 teratocarcinoma-derived growth factor 1 Mus musculus 77-81 8089706-2 1994 Under conditions which block the addition of opsin to outer segments, various lipids continue to be synthesized and transported to the outer segment in the presence of monensin, puromycin, brefeldin A, tunicamycin and several general metabolic inhibitors. Tunicamycin 202-213 rhodopsin, gene2 L homeolog Xenopus laevis 45-50 7515860-6 1994 Expression of sLe(a) and sLe(x) antigens and binding to E-selectin were reduced by pre-treatment of SW1990 cells with the O-linked glycosylation inhibitor benzyl-alpha-GalNAc but not with the N-linked glycosylation inhibitor tunicamycin. Tunicamycin 225-236 selectin E Homo sapiens 56-66 7515913-5 1994 Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction. Tunicamycin 0-11 complement C3d receptor 2 Homo sapiens 25-29 7515913-5 1994 Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction. Tunicamycin 0-11 Fc epsilon receptor II Homo sapiens 87-91 7515913-5 1994 Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction. Tunicamycin 0-11 Fc epsilon receptor II Homo sapiens 181-185 7515913-5 1994 Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction. Tunicamycin 0-11 complement C3d receptor 2 Homo sapiens 186-190 8188375-7 1994 The effects on grp78 expression of heat shock and tunicamycin treatment, the latter of which specifically stimulates mammalian grp78, were investigated. Tunicamycin 50-61 heat shock protein family A (Hsp70) member 5 Homo sapiens 15-20 8188375-8 1994 While the level of the grp78 protein remained constant under all circumstances, grp78 mRNA was unaffected by heat shock but induced fivefold by tunicamycin. Tunicamycin 144-155 heat shock protein family A (Hsp70) member 5 Homo sapiens 80-85 7994083-9 1994 Growth of cells in the presence of tunicamycin demonstrates that both P190 and P70 are glycosylated, with the deglycosylated forms migrating in polyacrylamide gels as proteins of 165 kDa and 45 kDa, respectively. Tunicamycin 35-46 annexin A6 Homo sapiens 79-82 8163533-7 1994 PNGase F digestion of extracts prepared from LLC-NET- and hNET-transfected HeLa cells convert all immunoreactive species to a 46-kDa form, equivalent to that observed following incubation of whole cells with the glycosylation inhibitor tunicamycin. Tunicamycin 236-247 solute carrier family 6 member 2 Homo sapiens 58-62 8163533-9 1994 On the other hand, NE transport and antagonist ([125I]RTI-55) binding assays on whole LLC-NET cells treated with tunicamycin reveal a pronounced reduction in NE transport activity and hNET membrane density paralleled by an inability of NET proteins to replenish the higher M(r) hNET pool. Tunicamycin 113-124 solute carrier family 6 member 2 Homo sapiens 90-93 8163533-9 1994 On the other hand, NE transport and antagonist ([125I]RTI-55) binding assays on whole LLC-NET cells treated with tunicamycin reveal a pronounced reduction in NE transport activity and hNET membrane density paralleled by an inability of NET proteins to replenish the higher M(r) hNET pool. Tunicamycin 113-124 solute carrier family 6 member 2 Homo sapiens 184-188 8163533-9 1994 On the other hand, NE transport and antagonist ([125I]RTI-55) binding assays on whole LLC-NET cells treated with tunicamycin reveal a pronounced reduction in NE transport activity and hNET membrane density paralleled by an inability of NET proteins to replenish the higher M(r) hNET pool. Tunicamycin 113-124 solute carrier family 6 member 2 Homo sapiens 185-188 8163533-9 1994 On the other hand, NE transport and antagonist ([125I]RTI-55) binding assays on whole LLC-NET cells treated with tunicamycin reveal a pronounced reduction in NE transport activity and hNET membrane density paralleled by an inability of NET proteins to replenish the higher M(r) hNET pool. Tunicamycin 113-124 solute carrier family 6 member 2 Homo sapiens 278-282 7909499-3 1994 Prevention of post-translational addition of N-linked oligosaccharides by treatment of the resistant cells with tunicamycin resulted in a dramatic enhancement in LAK cell cytotoxicity which was partially inhibited by antibodies against LFA-1 and ICAM-1. Tunicamycin 112-123 alpha kinase 1 Homo sapiens 162-165 7909499-3 1994 Prevention of post-translational addition of N-linked oligosaccharides by treatment of the resistant cells with tunicamycin resulted in a dramatic enhancement in LAK cell cytotoxicity which was partially inhibited by antibodies against LFA-1 and ICAM-1. Tunicamycin 112-123 integrin subunit alpha L Homo sapiens 236-241 7909499-3 1994 Prevention of post-translational addition of N-linked oligosaccharides by treatment of the resistant cells with tunicamycin resulted in a dramatic enhancement in LAK cell cytotoxicity which was partially inhibited by antibodies against LFA-1 and ICAM-1. Tunicamycin 112-123 intercellular adhesion molecule 1 Homo sapiens 246-252 7909499-5 1994 Tunicamycin treatment caused a decrease in the molecular weight of ICAM-1 from approximately 95,000 to 50,000 Da. Tunicamycin 0-11 intercellular adhesion molecule 1 Homo sapiens 67-73 8155721-2 1994 43% of 35S-labeled LPL subunits in tunicamycin (TUN)-treated cells did not bind to a heparin-Sepharose column and 46% was eluted with 0.6 M NaCl. Tunicamycin 35-46 lipoprotein lipase Homo sapiens 19-22 8138587-3 1994 Sensitivity to tunicamycin indicated that N-linked post-translational modifications to this 43 kDa core species generated the full complement of 50 kDa (intermediate) and 52 kDa (mature) p52(PAI-1) glycosylated isoforms. Tunicamycin 15-26 similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52) Rattus norvegicus 187-190 8138587-3 1994 Sensitivity to tunicamycin indicated that N-linked post-translational modifications to this 43 kDa core species generated the full complement of 50 kDa (intermediate) and 52 kDa (mature) p52(PAI-1) glycosylated isoforms. Tunicamycin 15-26 serpin family E member 1 Rattus norvegicus 191-196 8132654-13 1994 Interestingly, degradation of unglycosylated apoB, detected in tunicamycin-pretreated cells, occurred earlier, resulted in generation of additional fragments, and was largely uninhibited by ALLN. Tunicamycin 63-74 apolipoprotein B Homo sapiens 45-49 8027512-9 1994 The Golgi apparatus inhibitors monensin, swainsonine and tunicamycin enhanced ricin toxicity, as evidenced by shortened survival times. Tunicamycin 57-68 ricin Ricinus communis 78-83 8110797-7 1994 Inhibition of N-glycosylation by tunicamycin also increased the binding of monoclonal antibody LRB 200 to hepatocyte apoB. Tunicamycin 33-44 apolipoprotein B Rattus norvegicus 117-121 8110187-10 1994 The trypsin-resistant MUC2 fragment contained N-linked carbohydrate, as indicated by a decrease in size as a result of peptidyl N-glycosidase digestion or tunicamycin treatment of HM3 cells. Tunicamycin 155-166 mucin 2, oligomeric mucus/gel-forming Homo sapiens 22-26 8110187-10 1994 The trypsin-resistant MUC2 fragment contained N-linked carbohydrate, as indicated by a decrease in size as a result of peptidyl N-glycosidase digestion or tunicamycin treatment of HM3 cells. Tunicamycin 155-166 cholinergic receptor muscarinic 3 Homo sapiens 180-183 8114674-4 1994 Enzymatically active recombinant hPGHS-1 and hPGHS-2 were present as glycosylated proteins in the microsomal fraction prepared from infected cells, whereas recombinant hPGHS-1 and hPGHS-2 prepared from the microsomal fraction of cells treated with tunicamycin, an inhibitor of N-linked glycosylation, were enzymatically inactive. Tunicamycin 248-259 prostaglandin-endoperoxide synthase 1 Homo sapiens 33-40 7979996-4 1994 The recombinant E2 protein appeared to be glycosylated since it was susceptible to tunicamycin. Tunicamycin 83-94 ubiquitin conjugating enzyme E2 B Homo sapiens 16-26 8011427-3 1994 We show here that (1) in CHO-Y2 cells, basal endocytosis, like insulin-induced internalization, was markedly altered despite normal receptor turnover and (2) in both CHO-R and CHO-Y2 cells, basal receptor endocytosis was altered by tunicamycin, an inhibitor of protein N-glycosylation, whereas insulin-induced internalization was not. Tunicamycin 232-243 insulin Cricetulus griseus 63-70 8032172-3 1994 Stable transfection studies show that GRP78 transcription is also regulated by ethanol and that ethanol also potentiates GRP78 induction by classical inducing agents such as tunicamycin. Tunicamycin 174-185 heat shock protein 5 Mus musculus 121-126 7937345-3 1994 Tunicamycin pretreatment concentration-dependently decreased GLP-1 binding to RINm5F cells due to a decreased receptor number without change of receptor affinity. Tunicamycin 0-11 glucagon Rattus norvegicus 61-66 7516308-7 1993 Furthermore, isoproterenol stimulation of protein glycosylation by exogenous dolichyl monophosphate and its inhibition by tunicamycin (GlcNAc-1P transferase inhibitor) supported the concept that isoproterenol specifically stimulated protein N-glycosylation event(s) in the cell. Tunicamycin 122-133 dolichyl-phosphate N-acetylglucosaminephosphotransferase 1 Homo sapiens 135-156 7935356-11 1993 Tunicamycin, an inhibitor of co-translational transfer of core oligosaccharide, provoked rapid phosphorylation of eIF-2 alpha and inhibition of translational initiation whereas sugar analog inhibitors of glycoprotein processing did neither. Tunicamycin 0-11 eukaryotic translation initiation factor 2A Rattus norvegicus 114-125 7686870-2 1993 The recombinant NS1 protein (re-NS1) produced in infected insect cells was localized on the cell surface and was apparently glycosylated, because it was susceptible to treatment with both tunicamycin and N-glycanase. Tunicamycin 188-199 protein tyrosine phosphatase non-receptor type 11 Homo sapiens 16-19 8397508-6 1993 Inhibition of N-glycosylation with tunicamycin caused a dramatic intracellular degradation of these convertases within the endoplasmic reticulum, with the net effect of a reduction in the available activity of PC1 and PC2. Tunicamycin 35-46 proprotein convertase subtilisin/kexin type 1 Rattus norvegicus 210-213 8397508-6 1993 Inhibition of N-glycosylation with tunicamycin caused a dramatic intracellular degradation of these convertases within the endoplasmic reticulum, with the net effect of a reduction in the available activity of PC1 and PC2. Tunicamycin 35-46 proprotein convertase subtilisin/kexin type 2 Rattus norvegicus 218-221 8212855-10 1993 Moreover tunicamycin treatment of cells infected with the virus indicated that p32 was glycosylated. Tunicamycin 9-20 inhibitor of growth family member 2 Homo sapiens 79-82 8227155-5 1993 Immunoprecipitation with anti-flg antibody followed by electrophoresis produced a band of 90 Kd in tunicamycin-treated cells expressing the mutant as well as the wild-type receptors, indicating that the inhibition of binding was not due to defective expression of the protein. Tunicamycin 99-110 filaggrin Homo sapiens 30-33 7690438-7 1993 Inhibition of N-linked glycosylation by tunicamycin resulted in the production of identical-sized nascent L-selectin by normal and CLL cells. Tunicamycin 40-51 selectin L Homo sapiens 106-116 7686870-2 1993 The recombinant NS1 protein (re-NS1) produced in infected insect cells was localized on the cell surface and was apparently glycosylated, because it was susceptible to treatment with both tunicamycin and N-glycanase. Tunicamycin 188-199 polyglutamine binding protein 1 Homo sapiens 29-35 8337817-5 1993 Using myxoma virus and recombinant vaccinia virus constructs for experiments with tunicamycin and peptide N-glycosidase F, it is shown that the secreted SERP1 protein is modified by N-linked glycosylation. Tunicamycin 82-93 stress associated endoplasmic reticulum protein 1 Homo sapiens 153-158 8486673-9 1993 Rat CRP acquired the ability to bind to phosphorylcholine-Sepharose and to form the dimeric and oligomeric species prior to acquiring resistance to endo H. Studies using tunicamycin revealed that the N-linked oligosaccharide present in rat CRP was not required for formation of its dimeric component, oligomerization, ability to bind to phosphorylcholine, or secretion. Tunicamycin 170-181 C-reactive protein Rattus norvegicus 4-7 8222275-7 1993 Tunicamycin (0.3-3.0 micrograms/l) increased the percentage of Hex B in the medium, whereas an increased release of Hex was noted only after 48 h. Tunicamycin is known to enhance the secretion of N-linked oligosaccharide-free forms of lysosomal enzymes. Tunicamycin 0-11 O-GlcNAcase Homo sapiens 63-66 8222275-7 1993 Tunicamycin (0.3-3.0 micrograms/l) increased the percentage of Hex B in the medium, whereas an increased release of Hex was noted only after 48 h. Tunicamycin is known to enhance the secretion of N-linked oligosaccharide-free forms of lysosomal enzymes. Tunicamycin 147-158 O-GlcNAcase Homo sapiens 63-66 8222275-7 1993 Tunicamycin (0.3-3.0 micrograms/l) increased the percentage of Hex B in the medium, whereas an increased release of Hex was noted only after 48 h. Tunicamycin is known to enhance the secretion of N-linked oligosaccharide-free forms of lysosomal enzymes. Tunicamycin 147-158 O-GlcNAcase Homo sapiens 116-119 7685904-3 1993 FKB2 mRNA levels are elevated in cells blocked in N-glycosylation--i.e., in wild-type cells treated with tunicamycin and in the sec53-6 mutant grown at the nonpermissive temperature. Tunicamycin 105-116 peptidylprolyl isomerase family protein FPR2 Saccharomyces cerevisiae S288C 0-4 8099781-2 1993 (i) Tunicamycin completely inhibited mannose incorporation into Thy-1. Tunicamycin 4-15 Thy-1 cell surface antigen Rattus norvegicus 64-69 8223708-11 1993 Two inhibitors of MPR-mediated enzyme transport, tunicamycin and chloroquine, were used. Tunicamycin 49-60 progesterone receptor membrane component 1 Rattus norvegicus 18-21 8388383-8 1993 1) Tunicamycin treatment of wild type u-PAR-expressing cells. Tunicamycin 3-14 plasminogen activator, urokinase receptor Homo sapiens 38-43 8319938-3 1993 However, when the receptor was subjected to deglycosylation by treatment with tunicamycin, the receptors of the KMT-17 and MRK-49F cells gave the same molecular mass of 225K, indicating that the difference in molecular mass between two cell lines resulted from the different oligosaccharide sizes. Tunicamycin 78-89 ciliogenesis associated kinase 1 Rattus norvegicus 123-126 8315416-1 1993 Tunicamycin inhibits the dolichol pathway for N-linked glycosylation of proteins, including photoreceptor opsin, and causes a buildup of tubulo-vesicular profiles in the intersegmental space between photoreceptor rod inner and outer segments associated with disruption of new disc assembly. Tunicamycin 0-11 rhodopsin, gene2 L homeolog Xenopus laevis 106-111 8490167-0 1993 Effect of tunicamycin treatment on ligand binding to the erythropoietin receptor: conversion from two classes of binding sites to a single class. Tunicamycin 10-21 erythropoietin receptor Mesocricetus auratus 57-80 8490167-4 1993 Scatchard plots of baby hamster kidney (BHK) cells that had been engineered to express cloned mouse EPO-R were also biphasic and the plots of cells cultured with tunicamycin became a single phase with high-affinity sites. Tunicamycin 162-173 erythropoietin receptor Mus musculus 100-105 8490167-8 1993 BHK cells that expressed mutant EPO-R showed biphasic Scatchard plots that were converted to single-phase plots with only high-affinity sites by tunicamycin treatment. Tunicamycin 145-156 erythropoietin receptor Mesocricetus auratus 32-37 8477700-6 1993 In addition, inhibition of PiM and PiZ alpha 1-AT glycosylation and secretion by tunicamycin did not result in the accumulation of the protein, but instead in its rapid lag-free degradation. Tunicamycin 81-92 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 27-30 8477700-6 1993 In addition, inhibition of PiM and PiZ alpha 1-AT glycosylation and secretion by tunicamycin did not result in the accumulation of the protein, but instead in its rapid lag-free degradation. Tunicamycin 81-92 serpin family A member 1 Homo sapiens 39-49 8454000-3 1993 Treatment of the cells with tunicamycin caused a rapid decrease in GRP78 phosphorylation within 2 to 4 h in both cell types prior to GRP78 induction. Tunicamycin 28-39 heat shock protein family A (Hsp70) member 5 Homo sapiens 67-72 8454000-3 1993 Treatment of the cells with tunicamycin caused a rapid decrease in GRP78 phosphorylation within 2 to 4 h in both cell types prior to GRP78 induction. Tunicamycin 28-39 heat shock protein family A (Hsp70) member 5 Homo sapiens 133-138 8454000-4 1993 Following a longer period of tunicamycin treatment, GRP78 phosphorylation recovered gradually in parallel with the accumulation of newly synthesized GRP78. Tunicamycin 29-40 heat shock protein family A (Hsp70) member 5 Homo sapiens 52-57 8454000-4 1993 Following a longer period of tunicamycin treatment, GRP78 phosphorylation recovered gradually in parallel with the accumulation of newly synthesized GRP78. Tunicamycin 29-40 heat shock protein family A (Hsp70) member 5 Homo sapiens 149-154 8454000-5 1993 The half-life of GRP78 was over 24 h and similar in both normal and transformed cells either with or without tunicamycin treatment. Tunicamycin 109-120 heat shock protein family A (Hsp70) member 5 Homo sapiens 17-22 8454000-6 1993 In contrast, the half-life of phosphate groups incorporated into GRP78 was about 120 min in both types of cells in the absence of tunicamycin treatment. Tunicamycin 130-141 heat shock protein family A (Hsp70) member 5 Homo sapiens 65-70 7679747-9 1993 (iii) The UL10 protein in cells treated with tunicamycin formed a single band (apparent M(r) of 47,000) reactive with the anti-UL10 antibody, indicating that the 47,000-M(r) protein was a precursor of N-glycosylated, more slowly migrating forms of UL10. Tunicamycin 45-56 envelope glycoprotein M Human alphaherpesvirus 1 10-14 7679747-9 1993 (iii) The UL10 protein in cells treated with tunicamycin formed a single band (apparent M(r) of 47,000) reactive with the anti-UL10 antibody, indicating that the 47,000-M(r) protein was a precursor of N-glycosylated, more slowly migrating forms of UL10. Tunicamycin 45-56 envelope glycoprotein M Human alphaherpesvirus 1 127-131 7679747-9 1993 (iii) The UL10 protein in cells treated with tunicamycin formed a single band (apparent M(r) of 47,000) reactive with the anti-UL10 antibody, indicating that the 47,000-M(r) protein was a precursor of N-glycosylated, more slowly migrating forms of UL10. Tunicamycin 45-56 envelope glycoprotein M Human alphaherpesvirus 1 127-131 8484745-1 1993 By culturing with tunicamycin A1, an inhibitor of N-glycosylation, or by sialidase digestion, mouse monocytic cells P388D1 were induced to carry out Fc receptor-mediated phagocytosis of IgG-coated sheep red blood cells. Tunicamycin 18-29 Fc receptor Mus musculus 149-160 8464905-3 1993 Tunicamycin and pulse-chase experiments revealed that the mature protein was processed by N-linked glycosylation of a 145-kDa erbB-3 core polypeptide. Tunicamycin 0-11 erb-b2 receptor tyrosine kinase 3 Homo sapiens 126-132 8431454-6 1993 Adding tunicamycin or deoxymannojirimycin to the TGF-beta 1-treated and untreated cells caused these 55 and 65 kDa glucose transporters to migrate as one band at 40-43 kDa. Tunicamycin 7-18 transforming growth factor, beta 1 Mus musculus 49-59 8093618-7 1993 The addition of high concentrations of tunicamycin to 293-GC-C cells also reduced the M(r) to 120,000, indicating that GC-C is an N-linked glycoprotein. Tunicamycin 39-50 guanylate cyclase 2C Homo sapiens 58-62 8093618-7 1993 The addition of high concentrations of tunicamycin to 293-GC-C cells also reduced the M(r) to 120,000, indicating that GC-C is an N-linked glycoprotein. Tunicamycin 39-50 guanylate cyclase 2C Homo sapiens 119-123 8430814-7 1993 Treatment of fetal rabbit lung explants with inhibitors of oligosaccharide addition (tunicamycin) and processing (castanospermine), which act within the endoplasmic reticulum, significantly reduced the rate of transport of newly synthesized SP-A to lamellar bodies. Tunicamycin 85-96 pulmonary surfactant-associated protein A Oryctolagus cuniculus 241-245 1450177-9 1992 Inhibition of LPL secretion by tunicamycin in both peritoneal macrophages and J774.1 cells prevented a hypertriglyceridemic very low density lipoprotein-induced triglyceride accumulation, an effect that was counteracted by addition of exogenous LPL. Tunicamycin 31-42 lipoprotein lipase Mus musculus 14-17 8476209-6 1993 Upon addition of tunicamycin, to cycling cells the progression through G1 was blocked in a similar way to that following HMG CoA reductase inhibition. Tunicamycin 17-28 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 121-138 1450177-9 1992 Inhibition of LPL secretion by tunicamycin in both peritoneal macrophages and J774.1 cells prevented a hypertriglyceridemic very low density lipoprotein-induced triglyceride accumulation, an effect that was counteracted by addition of exogenous LPL. Tunicamycin 31-42 lipoprotein lipase Mus musculus 245-248 1505923-7 1992 By inhibition of the N-glycosylation using tunicamycin, rat C1-esterase inhibitor was identified as a glycoprotein. Tunicamycin 43-54 complement C1s Rattus norvegicus 60-71 8416385-3 1993 Nonglycosylated forms of gp120 generated either by deletion of the signal sequence of HIV-1 gp120 or by synthesis in the presence of tunicamycin failed to bind to CD4. Tunicamycin 133-144 Envelope surface glycoprotein gp160, precursor Human immunodeficiency virus 1 25-30 1479287-4 1992 LPL catalytic activity from the heparin-releasable fraction of adipocytes was inhibited by more than 70%, with similar decreases in LPL mass, when cells were cultured for 24 h in the presence of either tunicamycin or castanospermine. Tunicamycin 202-213 lipoprotein lipase Rattus norvegicus 0-3 1479287-7 1992 The appearance of 35S-labeled LPL in the medium was blocked by treatment of cells with tunicamycin and castanospermine, whereas secretion was not affected by DMJ or swainsonine. Tunicamycin 87-98 lipoprotein lipase Rattus norvegicus 30-33 1479287-9 1992 The unglycosylated [35S]LPL that was synthesized in the presence of tunicamycin demonstrated essentially no intracellular degradation. Tunicamycin 68-79 lipoprotein lipase Rattus norvegicus 24-27 1359965-10 1992 By contrast, inhibition of N-glycosylation with tunicamycin resulted into rapid degradation of non-N-glycosylated DPP IV molecules in both cell types. Tunicamycin 48-59 dipeptidylpeptidase 4 Rattus norvegicus 114-120 1425427-2 1992 Proenkephalin is synthesized in both N-glycosylated and unglycosylated forms, as demonstrated by treatment with tunicamycin. Tunicamycin 112-123 proenkephalin Rattus norvegicus 0-13 24178389-7 1992 Treatment of cells with tunicamycin, which inhibits N-glycosylation, and digestion of the (35)S-labelled processing intermediates with endoglycosidase H indicate that beta-1,3-glucanase has a single N-glycan attached to the C-terminal extension. Tunicamycin 24-35 glucan endo-1,3-beta-glucosidase, acidic-like Nicotiana tabacum 167-185 8141920-4 1993 The spot for transferrin shifted to the more basic isoforms by treatment for 3 hr with monensin or tunicamycin. Tunicamycin 99-110 transferrin Rattus norvegicus 13-24 1420307-7 1992 Glycosylation of the intrinsic factor was demonstrated by lectin binding to the recombinant protein separated on SDS-PAGE, and by a shift in apparent molecular mass from 47 kDa to 43 kDa following treatment of Sf9 cells with tunicamycin. Tunicamycin 225-236 cobalamin binding intrinsic factor Homo sapiens 21-37 1387671-7 1992 Treatment of AcMCP 1-infected Sf-21 cells with tunicamycin resulted in reduced production of the 21- and 23-kDa proteins and an increase in 16- to 18-kDa products, the predicted size range of uncleaved and nonglycosylated rat MCP 1. Tunicamycin 47-58 C-C motif chemokine ligand 2 Rattus norvegicus 15-20 1325440-2 1992 Overproduction of BiP/Kar2 protein was achieved by the cloning of the KAR2 gene on multicopy plasmids and the treatment of cells harboring the cloned KAR2 gene with tunicamycin. Tunicamycin 165-176 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 22-26 1325440-2 1992 Overproduction of BiP/Kar2 protein was achieved by the cloning of the KAR2 gene on multicopy plasmids and the treatment of cells harboring the cloned KAR2 gene with tunicamycin. Tunicamycin 165-176 Hsp70 family ATPase KAR2 Saccharomyces cerevisiae S288C 150-154 1506413-2 1992 Expression of the glucose regulated proteins (GRP78 and GRP94) is greatly increased after cells are exposed to stress agents (including A23187 and tunicamycin) which inhibit ER function. Tunicamycin 147-158 heat shock protein family A (Hsp70) member 5 Homo sapiens 46-51 1506413-2 1992 Expression of the glucose regulated proteins (GRP78 and GRP94) is greatly increased after cells are exposed to stress agents (including A23187 and tunicamycin) which inhibit ER function. Tunicamycin 147-158 heat shock protein 90 beta family member 1 Homo sapiens 56-61 1506413-6 1992 The increased accumulation of GRP78 mRNA after exposure of cells to either thapsigargin, brefeldin A, AIF4-, A23187, or tunicamycin can be blocked by pre-incubation in cycloheximide. Tunicamycin 120-131 heat shock protein family A (Hsp70) member 5 Homo sapiens 30-35 1386872-4 1992 Moreover, tunicamycin treatment of a CD23-binding cell line, RPMI 8226, significantly reduced the binding of CD23 incorporated into fluorescent liposomes, and a sugar, fucose-1-phosphate, was found to inhibit CD23-liposome binding to RPMI 8226 cells, suggesting the contribution of sugar structures on the CD23 ligand. Tunicamycin 10-21 Fc epsilon receptor II Homo sapiens 37-41 1398755-3 1992 In this study we show that tunicamycin-treated cells release small CD23 fragments with a MW of 16,000. Tunicamycin 27-38 Fc epsilon receptor II Homo sapiens 67-71 1386872-4 1992 Moreover, tunicamycin treatment of a CD23-binding cell line, RPMI 8226, significantly reduced the binding of CD23 incorporated into fluorescent liposomes, and a sugar, fucose-1-phosphate, was found to inhibit CD23-liposome binding to RPMI 8226 cells, suggesting the contribution of sugar structures on the CD23 ligand. Tunicamycin 10-21 Fc epsilon receptor II Homo sapiens 109-113 1386872-4 1992 Moreover, tunicamycin treatment of a CD23-binding cell line, RPMI 8226, significantly reduced the binding of CD23 incorporated into fluorescent liposomes, and a sugar, fucose-1-phosphate, was found to inhibit CD23-liposome binding to RPMI 8226 cells, suggesting the contribution of sugar structures on the CD23 ligand. Tunicamycin 10-21 Fc epsilon receptor II Homo sapiens 109-113 1386872-4 1992 Moreover, tunicamycin treatment of a CD23-binding cell line, RPMI 8226, significantly reduced the binding of CD23 incorporated into fluorescent liposomes, and a sugar, fucose-1-phosphate, was found to inhibit CD23-liposome binding to RPMI 8226 cells, suggesting the contribution of sugar structures on the CD23 ligand. Tunicamycin 10-21 Fc epsilon receptor II Homo sapiens 109-113 1344885-0 1992 Bean homologs of the mammalian glucose-regulated proteins: induction by tunicamycin and interaction with newly synthesized seed storage proteins in the endoplasmic reticulum. Tunicamycin 72-83 brain expressed associated with NEDD4 1 Homo sapiens 0-4 1515555-7 1992 Production of TNF but not F2 was inhibited when the cells were cultured with tunicamycin and PDB. Tunicamycin 77-88 tumor necrosis factor Homo sapiens 14-17 1318394-9 1992 Nonglycosylated core MHVR proteins were made in Vac-MHVR-infected BHK-21 cells in the presence of tunicamycin by in vitro translation of MHVR mRNA in a rabbit reticulocyte cell-free system in the absence of microsomal membranes and by expression of an N-terminal deletion clone of MHVR lacking its signal peptide. Tunicamycin 98-109 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 21-25 1318394-9 1992 Nonglycosylated core MHVR proteins were made in Vac-MHVR-infected BHK-21 cells in the presence of tunicamycin by in vitro translation of MHVR mRNA in a rabbit reticulocyte cell-free system in the absence of microsomal membranes and by expression of an N-terminal deletion clone of MHVR lacking its signal peptide. Tunicamycin 98-109 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 52-56 1318394-9 1992 Nonglycosylated core MHVR proteins were made in Vac-MHVR-infected BHK-21 cells in the presence of tunicamycin by in vitro translation of MHVR mRNA in a rabbit reticulocyte cell-free system in the absence of microsomal membranes and by expression of an N-terminal deletion clone of MHVR lacking its signal peptide. Tunicamycin 98-109 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 52-56 1318394-9 1992 Nonglycosylated core MHVR proteins were made in Vac-MHVR-infected BHK-21 cells in the presence of tunicamycin by in vitro translation of MHVR mRNA in a rabbit reticulocyte cell-free system in the absence of microsomal membranes and by expression of an N-terminal deletion clone of MHVR lacking its signal peptide. Tunicamycin 98-109 carcinoembryonic antigen-related cell adhesion molecule 1 Mus musculus 52-56 1344885-1 1992 Treatment of developing bean cotyledons with the inhibitor of N-glycosylation tunicamycin enhanced the synthesis of at least two polypeptides with molecular mass 78 kDa and 97 kDa. Tunicamycin 78-89 brain expressed associated with NEDD4 1 Homo sapiens 24-28 1344885-5 1992 When newly synthesized storage glycoproteins phaseolin, phytohemagglutinin or alpha-amylase inhibitor were immunoprecipitated from an ER preparation of tunicamycin-treated tissue, the GRP78 homolog was always co-precipitated. Tunicamycin 152-163 heat shock protein family A (Hsp70) member 5 Homo sapiens 184-189 1356290-7 1992 In addition, ICAM-1 proteins expressed in the presence of tunicamycin also retained their virus binding capability. Tunicamycin 58-69 intercellular adhesion molecule 1 Homo sapiens 13-19 1596569-3 1992 Synthesis of this protein could also be induced by tunicamycin, suggesting that it might be the 78-Kd glucose-regulated protein (GRP78). Tunicamycin 51-62 heat shock protein 5 Mus musculus 129-134 1375936-9 1992 Growth of HL60 cells in tunicamycin inhibited the ability of these cells to support P-selectin-mediated binding and, to a lesser extent, E-selectin-mediated binding. Tunicamycin 24-35 selectin P Homo sapiens 84-94 1601876-6 1992 In vivo synthesis studies in the presence and absence of tunicamycin, an inhibitor of N-linked glycosylation, indicate that pro-P34 is 47 kDa. Tunicamycin 57-68 P34 probable thiol protease Glycine max 128-131 1583718-5 1992 Metabolic labelling of gp41 with [3H]GlcNAc occurred in the presence of tunicamycin. Tunicamycin 72-83 occlusion-derived virus glycoprotein Autographa californica nucleopolyhedrovirus 23-27 1371789-7 1992 In biosynthetic studies, all four anti-Fc alpha R antibodies and the IgA ligand bound a single 32-kDa core protein present in tunicamycin-treated cells, and the exceptional antibody again recognized molecules with relatively restricted glycosylation in the nontreated cells. Tunicamycin 126-137 Fc alpha receptor Homo sapiens 39-49 1315744-5 1992 It had been assumed that this cDNA, termed TRG for tunicamycin resistance gene, encoded GPT enzyme. Tunicamycin 51-62 UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase Cricetulus griseus 88-91 1521926-0 1992 Tunicamycin inhibits function and expression of the high-affinity IL-2 receptor in a murine IL-2-dependent cell line. Tunicamycin 0-11 interleukin 2 Mus musculus 66-70 1521926-0 1992 Tunicamycin inhibits function and expression of the high-affinity IL-2 receptor in a murine IL-2-dependent cell line. Tunicamycin 0-11 interleukin 2 Mus musculus 92-96 1521926-4 1992 Inhibition of proliferation by tunicamycin was accompanied by an inhibition of binding of 125I-IL-2 to its high-affinity receptor. Tunicamycin 31-42 interleukin 2 Mus musculus 95-99 1373378-5 1992 GRP78 overexpressing cells treated with tunicamycin or A23187 exhibited a reduced induction of endogenous GRP78 and GRP94 mRNAs compared to wild-type CHO cells. Tunicamycin 40-51 endoplasmic reticulum chaperone BiP Cricetulus griseus 0-5 1373378-5 1992 GRP78 overexpressing cells treated with tunicamycin or A23187 exhibited a reduced induction of endogenous GRP78 and GRP94 mRNAs compared to wild-type CHO cells. Tunicamycin 40-51 endoplasmic reticulum chaperone BiP Cricetulus griseus 106-111 1711069-2 1991 FMC46 detects an epitope of the leukocyte adhesion molecule-1 (LAM-1), a member of the selecting family (LAM-1, Endothelial Leukocyte Adhesion Molecular-1 (ELAM-1), and Granule Membrane Protein-140 (GMP-140), that is expressed on LAM-1-transfected cell lines, is a glycosylation epitope based on its loss after culture in tunicamycin, and is closely related to the LAM-1.2 epitope. Tunicamycin 322-333 selectin L Homo sapiens 32-61 1540178-5 1992 Preincubation of the transfected cells with the N-glycosylation inhibitor tunicamycin resulted in the conversion of the 47 kDa VEGF homodimer into a smaller, deglycosylated form of 42 kDa. Tunicamycin 74-85 vascular endothelial growth factor A Homo sapiens 127-131 1531639-2 1992 Cell treatment with the N-glycosylation inhibitor tunicamycin generated unglycosylated CD45 polypeptides of 130 and 140 kDa. Tunicamycin 50-61 protein tyrosine phosphatase receptor type C Homo sapiens 87-91 1531639-3 1992 Immunofluorescence flow cytometry and Scatchard techniques revealed that CD45 cell surface expression was decreased in a time- and dose-dependent manner upon tunicamycin incubation. Tunicamycin 158-169 protein tyrosine phosphatase receptor type C Homo sapiens 73-77 1531639-4 1992 Moreover, a remarkable decrease in CD45 phosphatase activity was detected in tunicamycin-treated cells, which correlated with the diminished CD45 cell surface expression. Tunicamycin 77-88 protein tyrosine phosphatase receptor type C Homo sapiens 35-39 1531639-4 1992 Moreover, a remarkable decrease in CD45 phosphatase activity was detected in tunicamycin-treated cells, which correlated with the diminished CD45 cell surface expression. Tunicamycin 77-88 protein tyrosine phosphatase receptor type C Homo sapiens 141-145 1576204-4 1992 Tunicamycin treatment, monitored by lectin-induced aggregation, drastically diminished cell adhesion to laminin and fibronectin, whereas cell binding to collagen IV was not affected. Tunicamycin 0-11 fibronectin 1 Homo sapiens 116-127 1660878-2 1991 In the presence of tunicamycin cathepsin D was synthesized as an unglycosylated 43-kDa proenzyme which was proteolytically processed via a 39-kDa intermediate to a 28-kDa mature form. Tunicamycin 19-30 cathepsin D Homo sapiens 31-42 1662699-4 1991 In tumour cells, U90 is located principally in the plasma membrane fraction and cannot be induced by heat shock, glucose starvation, or treatment with tunicamycin or calcium ionophore. Tunicamycin 151-162 small Cajal body-specific RNA 7 Homo sapiens 17-20 1723541-7 1991 Culture of RC-2A cells in the presence of tunicamycin (after removal of surface antigens by pronase) blocked re-expression of the epitopes recognised by all 3 mAb suggesting that they involve N-linked glycosylation. Tunicamycin 42-53 paired box 5 Homo sapiens 153-158 1656972-4 1991 Cells treated with tunicamycin (6.25 ng/ml) for 24 h lost approximately 35% of their high-affinity thrombin binding sites, yet binding of receptor monoclonal antibody TR-9 was not affected, indicating that the receptor was present in the membrane, but unable to bind thrombin. Tunicamycin 19-30 coagulation factor II Mus musculus 99-107 1656972-4 1991 Cells treated with tunicamycin (6.25 ng/ml) for 24 h lost approximately 35% of their high-affinity thrombin binding sites, yet binding of receptor monoclonal antibody TR-9 was not affected, indicating that the receptor was present in the membrane, but unable to bind thrombin. Tunicamycin 19-30 coagulation factor II Mus musculus 267-275 1924389-4 1991 By using N-glycosidase F, tunicamycin, and specific antibodies produced in both chicken and rabbit, we demonstrate that PlGF, derived from transfected COS-1 cells, is actually N-glycosylated and secreted into the medium. Tunicamycin 26-37 placental growth factor Homo sapiens 120-124 1937047-6 1991 The inhibition of the hGHR-ED secretion by treatment with tunicamycin suggests that glycosylation is important for secretion. Tunicamycin 58-69 growth hormone receptor Homo sapiens 22-26 1930196-6 1991 When glycosylation was prevented by tunicamycin, individual bands of nonglycosylated vascular permeability factor were also secreted at equivalent rates, but much more slowly (approximately 60 min) than native glycoprotein. Tunicamycin 36-47 vascular endothelial growth factor A Homo sapiens 85-113 1833390-4 1991 GP85 is then incorporated into the plasma membrane where its turnover rate is relatively slow, a t1/2 of approximately 8 h. Following tunicamycin treatment, we have detected two other precursor proteins: p42 which is unglycosylated and p58 which is O-glycosylated. Tunicamycin 134-145 erythrocyte membrane protein band 4.2 Homo sapiens 204-207 1833390-4 1991 GP85 is then incorporated into the plasma membrane where its turnover rate is relatively slow, a t1/2 of approximately 8 h. Following tunicamycin treatment, we have detected two other precursor proteins: p42 which is unglycosylated and p58 which is O-glycosylated. Tunicamycin 134-145 cyclin dependent kinase 11B Homo sapiens 236-239 1915351-10 1991 Adaptation of phosphate transport in NBL-1 cells to low-phosphate medium was abolished by tunicamycin, an inhibitor of protein glycosylation, indicating that the transporter in these cells, like that in bovine BBMV, is a glycoprotein. Tunicamycin 90-101 NBL1, DAN family BMP antagonist Canis lupus familiaris 37-42 1910317-7 1991 In the presence of inducers of Grp78 synthesis, such as ionomycin, tunicamycin, or 2-deoxyglucose, there was a large increase in the level of Grp78 in the cells but a decrease in the amount of phosphorylated protein. Tunicamycin 67-78 heat shock protein family A (Hsp70) member 5 Bos taurus 31-36 1910317-7 1991 In the presence of inducers of Grp78 synthesis, such as ionomycin, tunicamycin, or 2-deoxyglucose, there was a large increase in the level of Grp78 in the cells but a decrease in the amount of phosphorylated protein. Tunicamycin 67-78 heat shock protein family A (Hsp70) member 5 Bos taurus 142-147 1654885-3 1991 The most pronounced effects on VIP binding were obtained with tunicamycin and deoxymannojirimycin, which respectively caused 80% and 67% inhibition. Tunicamycin 62-73 vasoactive intestinal peptide Homo sapiens 31-34 1654885-6 1991 In contrast, tunicamycin and castanospermine caused decreases in the cell-surface number of functional VIP receptors without affecting affinity. Tunicamycin 13-24 vasoactive intestinal peptide Homo sapiens 103-106 1654885-8 1991 When compared with their counterpart synthesized in control cells, VIP-binding proteins produced by deoxymannojirimycin- or swainsonine-treated cells were smaller in size and exhibited the expected sensitivity to Endo H. No modification in the apparent molecular mass was observed in the presence of either castanospermine or tunicamycin. Tunicamycin 326-337 vasoactive intestinal peptide Homo sapiens 67-70 1908097-3 1991 In order to determine the relationship between active renin heterogeneity and differences in composition or attachment of oligosaccharides, two separate experiments were performed: (i) Tunicamycin, which interferes with normal glycosylation processing, increased the proportion of relatively basic renin forms secreted into the incubation media by rat renal cortical slices. Tunicamycin 185-196 renin Rattus norvegicus 298-303 1831351-7 1991 Complete blocking of the glycosylation of lipoprotein lipase with tunicamycin (1 microgram/ml) for 24 h resulted in synthesis of an inactive non-secretable form of lipase with a smaller subunit (Mr 51,000-52,000). Tunicamycin 66-77 lipoprotein lipase Mus musculus 42-60 1831351-7 1991 Complete blocking of the glycosylation of lipoprotein lipase with tunicamycin (1 microgram/ml) for 24 h resulted in synthesis of an inactive non-secretable form of lipase with a smaller subunit (Mr 51,000-52,000). Tunicamycin 66-77 lipase, endothelial Mus musculus 54-60 1831351-8 1991 Immunofluorescent studies showed that unglycosylated lipase in tunicamycin-treated cells was retained in the endoplasmic reticulum. Tunicamycin 63-74 lipase, endothelial Mus musculus 53-59 1713450-4 1991 When the transfected CHO cells are treated with tunicamycin a single 29 kDa hIGFBP-3 protein is observed. Tunicamycin 48-59 insulin like growth factor binding protein 3 Homo sapiens 76-84 2061316-10 1991 Inhibition of N-linked glycosylation by tunicamycin causes a complete block in intracellular Tg transport by inducing the formation of biologically irreversible aggregates, suggesting that glycosylation of Tg serves to prevent denaturation of the secretory protein within the ER lumen. Tunicamycin 40-51 thyroglobulin Homo sapiens 93-95 1423514-3 1992 Immunogold labelling of ultrathin sections from tunicamycin-treated rats revealed that, in about 5% of vasopressin neurones, the accretions could be immunogold-labelled for vasopressin and its associated neurophysin. Tunicamycin 48-59 arginine vasopressin Rattus norvegicus 103-114 1423514-3 1992 Immunogold labelling of ultrathin sections from tunicamycin-treated rats revealed that, in about 5% of vasopressin neurones, the accretions could be immunogold-labelled for vasopressin and its associated neurophysin. Tunicamycin 48-59 arginine vasopressin Rattus norvegicus 173-184 1735447-6 1992 When N-glycosylation was inhibited in prb1-Ala519 mutant cells by tunicamycin, a smaller molecule of about 71 kDa appeared consistent with single N-glycosylation and signal-sequence cleavage of the translocated mutant PrB molecule in the endoplasmic reticulum. Tunicamycin 66-77 proteinase B Saccharomyces cerevisiae S288C 38-42 1624059-2 1992 Tunicamycin-induced expression of the chimeric gene during Xenopus development was similar to the pattern of endogenous GRP78 protein synthesis, with expression first being detected at gastrula and increasing at least until the tailbud stage. Tunicamycin 0-11 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 120-125 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 1711069-2 1991 FMC46 detects an epitope of the leukocyte adhesion molecule-1 (LAM-1), a member of the selecting family (LAM-1, Endothelial Leukocyte Adhesion Molecular-1 (ELAM-1), and Granule Membrane Protein-140 (GMP-140), that is expressed on LAM-1-transfected cell lines, is a glycosylation epitope based on its loss after culture in tunicamycin, and is closely related to the LAM-1.2 epitope. Tunicamycin 322-333 selectin L Homo sapiens 63-68 1658176-8 1991 Tunicamycin treatment of cells resulted in an unglycosylated doublet comprised of one single chain and one cleaved form of apoJ. Tunicamycin 0-11 clusterin Homo sapiens 123-127 1710120-10 1991 ICAM-1 levels, as measured by surface labeling of C32 cells with FITC CD54 monoclonal antibody, were decreased in cells treated with tunicamycin. Tunicamycin 133-144 intercellular adhesion molecule 1 Homo sapiens 0-6 1710120-10 1991 ICAM-1 levels, as measured by surface labeling of C32 cells with FITC CD54 monoclonal antibody, were decreased in cells treated with tunicamycin. Tunicamycin 133-144 intercellular adhesion molecule 1 Homo sapiens 70-74 2025645-7 1991 GLUT1 protein, detected on immunoblots, accumulated 10- to 20-fold in response to all glycosylation inhibitors, with apparent molecular masses of 40 kDa after glucose deprivation, 42 kDa after 2-deoxyglucose and 38 kDa after glucosamine or tunicamycin treatments, compared to 45-50 kDa in glucose-fed cells. Tunicamycin 240-251 solute carrier family 2 member 1 Rattus norvegicus 0-5 1850937-5 1991 The inhibitory effect of tunicamycin on Ad5 DNA replication was much reduced in 293 cells which provide E1a gene products in trans. Tunicamycin 25-36 Alzheimer disease, familial, type 5 Homo sapiens 40-43 1850937-7 1991 These results suggest that tunicamycin inhibits a glycosylation event induced by the early gene products of Ad5 and SV40 viruses during the early phase of infection. Tunicamycin 27-38 Alzheimer disease, familial, type 5 Homo sapiens 108-111 2004604-4 1991 Forty-eight percent of recombinant proenkephalin was glycosylated; glycosylation could be entirely prevented by the addition of tunicamycin. Tunicamycin 128-139 proenkephalin Rattus norvegicus 35-48 1897978-2 1991 From the results of tunicamycin treatment and N-glycosidase F digestion, it was demonstrated that Namalwa-derived hGM-CSF was highly glycosylated at two potential N-glycosylation sites and several O-glycosylation sites as previously shown for naturally occurring hGM-CSF. Tunicamycin 20-31 colony stimulating factor 2 Homo sapiens 114-121 1840923-6 1991 In addition, both b-70 polypeptides can be induced in maize cell cultures with tunicamycin treatment. Tunicamycin 79-90 luminal-binding protein 2 Zea mays 18-22 1708210-7 1991 The SP-D translation product migrated faster than the major cellular form of SP-D but approximately 1 kDa slower than cellular SP-D synthesized in the presence of 2,2"-dipyridyl plus tunicamycin. Tunicamycin 183-194 surfactant protein D Rattus norvegicus 4-8 1916065-2 1991 The 78-kDa polypeptide was tentatively identified as glucose-regulated protein (GRP) 78 on the basis of molecular mass, pl (5.2), and tunicamycin inducibility, which took place upon treating embryos after the midblastula transition (MBT). Tunicamycin 134-145 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 53-87 1916065-5 1991 A comparison of tunicamycin-induced polypeptide synthesis in Xenopus embryos, A6 cell line, and white blood cells by 2D-PAGE and fluorography revealed three spots in the GRP78 region of the gel. Tunicamycin 16-27 heat shock protein family A (Hsp70) member 5 L homeolog Xenopus laevis 170-175 1850168-4 1991 Similarly, inhibition of N-linked glycosylation by tunicamycin during viral infection of cell monolayers altered their ability to induce IFN alpha. Tunicamycin 51-62 interferon alpha 1 Homo sapiens 137-146 1847926-8 1991 Nonglycosylated MPR 46 synthesized in the presence of tunicamycin, thus preserving the asparagine residues, had a normal stability and high affinity binding. Tunicamycin 54-65 mannose-6-phosphate receptor, cation dependent Homo sapiens 16-22 1706526-7 1991 This was tested by subjecting L8 myocytes and NIH 3T3 fibroblasts to glucose starvation or exposure to the calcium ionophore A23187, 2-mercaptoethanol, or tunicamycin, all known to increase GRP levels. Tunicamycin 155-166 gastrin releasing peptide Rattus norvegicus 190-193 1672608-7 1991 In the presence of tunicamycin, a 120 kDa form of P-gp was synthesized and this form was no longer processed. Tunicamycin 19-30 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 1672608-8 1991 Treating the 125 kDa precursor form with endo-beta-N-acetylglucosaminidase H (Endo H) and the 140 kDa mature form with N-glycanase diminished the molecular size of P-gp to that of the tunicamycin-treated form. Tunicamycin 184-195 ATP binding cassette subfamily B member 1 Homo sapiens 164-168 1705556-5 1991 The epitopes are protein and not carbohydrate as both monoclonals were able to precipitate deglycosylated CD13 from tunicamycin- and monensin-treated cells and o-glycanase-treated purified CD13. Tunicamycin 116-127 alanyl aminopeptidase, membrane Homo sapiens 106-110 1716973-10 1991 Tunicamycin blocked de novo glycosylation and led to reduced surface recognition of the CD22 antigen. Tunicamycin 0-11 CD22 molecule Homo sapiens 88-92 1705558-7 1991 The cDNA sequence is continuous across the junction between the 135- and 80-kD components, and a single 170-kD Ng-CAM polypeptide was isolated from tunicamycin-treated cells. Tunicamycin 148-159 L1 cell adhesion molecule Gallus gallus 111-117 1824944-8 1991 After treatment with tunicamycin, the transfectants secreted unglycosylated 18-kDa polypeptides which could also bind IgE. Tunicamycin 21-32 immunoglobulin heavy constant epsilon Homo sapiens 118-121 1645456-13 1991 In addition, affinity cross-linking experiments showed that [125I]IGF-II also bound to the unglycosylated receptor precursor that accumulated in the tunicamycin-treated cells, and the binding affinity of IGF-II for this species was indistinguishable from the binding affinity of IGF-II for the mature receptor. Tunicamycin 149-160 insulin like growth factor 2 Homo sapiens 66-72 1703479-4 1991 Ligand blotting using [125I]IGF-I revealed a major IGFBP of 40,000 mol wt, and treatment of the cells with tunicamycin reduced the mol wt of this protein to about 32,000. mRNA from Swiss 3T3 cells hybridized to a 32P-labeled oligonucleotide (50-mer) complementary to rat IGFBP-3. Tunicamycin 107-118 insulin-like growth factor binding protein 3 Rattus norvegicus 271-278 1645456-13 1991 In addition, affinity cross-linking experiments showed that [125I]IGF-II also bound to the unglycosylated receptor precursor that accumulated in the tunicamycin-treated cells, and the binding affinity of IGF-II for this species was indistinguishable from the binding affinity of IGF-II for the mature receptor. Tunicamycin 149-160 insulin like growth factor 2 Homo sapiens 204-210 1645456-13 1991 In addition, affinity cross-linking experiments showed that [125I]IGF-II also bound to the unglycosylated receptor precursor that accumulated in the tunicamycin-treated cells, and the binding affinity of IGF-II for this species was indistinguishable from the binding affinity of IGF-II for the mature receptor. Tunicamycin 149-160 insulin like growth factor 2 Homo sapiens 204-210 2000222-3 1991 When the neuroblastoma cells were treated with tunicamycin, a protein with an apparent molecular weight of 120 kd, which is consistent with that of the c-ret protein predicted from the cDNA sequence, appeared on immunoblots. Tunicamycin 47-58 ret proto-oncogene Homo sapiens 154-157 1985932-4 1991 Adipocytes cultured with Trans35S-label and tunicamycin produced an LPL species of 52,000 daltons, but tunicamycin abolished the incorporation of 35SO4 into LPL. Tunicamycin 44-55 lipoprotein lipase Gallus gallus 68-71 1985932-4 1991 Adipocytes cultured with Trans35S-label and tunicamycin produced an LPL species of 52,000 daltons, but tunicamycin abolished the incorporation of 35SO4 into LPL. Tunicamycin 103-114 lipoprotein lipase Gallus gallus 157-160 2017192-4 1991 Glc-fed cells that have been tunicamycin treated contain principally the 38,000 Mr GLUT-1 polypeptide, which is found predominantly in intracellular membrane fractions. Tunicamycin 29-40 solute carrier family 2 member 1 Rattus norvegicus 83-89 2265706-4 1990 The overexpressed pool of non-ADP-ribosylated GRP78 synthesized during tunicamycin treatment was available for ADP-ribosylation during subsequent amino acid starvation, especially in the absence of tunicamycin. Tunicamycin 198-209 heat shock protein 5 Mus musculus 46-51 2254345-6 1990 ERp72 mRNA and, to a lesser degree, PDI mRNA were induced by treatment of Chinese hamster ovary cells with tunicamycin or A23187. Tunicamycin 107-118 protein disulfide-isomerase Cricetulus griseus 36-39 2265706-4 1990 The overexpressed pool of non-ADP-ribosylated GRP78 synthesized during tunicamycin treatment was available for ADP-ribosylation during subsequent amino acid starvation, especially in the absence of tunicamycin. Tunicamycin 71-82 heat shock protein 5 Mus musculus 46-51 1702721-3 1990 Incubation of K-562 cells with the N-glycosylation inhibitor tunicamycin blocked carbohydrate processing during biosynthesis of CD45 proteins, generating unglycosylated polypeptides similar in size to those resulting from digestion of CD45 proteins with a mixture of both N- and O-glycanases. Tunicamycin 61-72 protein tyrosine phosphatase receptor type C Homo sapiens 128-132 1702721-3 1990 Incubation of K-562 cells with the N-glycosylation inhibitor tunicamycin blocked carbohydrate processing during biosynthesis of CD45 proteins, generating unglycosylated polypeptides similar in size to those resulting from digestion of CD45 proteins with a mixture of both N- and O-glycanases. Tunicamycin 61-72 protein tyrosine phosphatase receptor type C Homo sapiens 235-239 2258708-5 1990 Immunodepletion, biosynthetic labeling, and tunicamycin treatment confirm that the protein encoded by gene 37 in Qa-1b mice is Qa-1.2. Tunicamycin 44-55 histocompatibility 2, T region locus 23 Mus musculus 113-118 2258708-5 1990 Immunodepletion, biosynthetic labeling, and tunicamycin treatment confirm that the protein encoded by gene 37 in Qa-1b mice is Qa-1.2. Tunicamycin 44-55 histocompatibility 2, T region locus 23 Mus musculus 113-117 2318146-0 1990 Effects of tunicamycin on growth hormone binding in rat adipocytes. Tunicamycin 11-22 gonadotropin releasing hormone receptor Rattus norvegicus 26-40 2269328-3 1990 Furthermore, presentation of the insulin fragment as well as presentation of ovalbumin (OVA) was inhibited by treatment of APC with chloroquine, cerulenin or tunicamycin. Tunicamycin 158-169 insulin Homo sapiens 33-40 2173269-6 1990 A 16-kDa product was detected, while in cells infected in the presence of tunicamycin, the immunoprecipitated product had a mobility on SDS-polyacrylamide gels of approximately 6 kDa, indicating that the SFGF gene product is extensively post-transcriptionally modified. Tunicamycin 74-85 gp010L Rabbit fibroma virus 204-208 2171700-10 1990 Third, synthesis of 35S-labeled 46-Kd cell surface receptor protein was inhibited when the cells were grown in the presence of tunicamycin, while the synthesis of the 36-Kd species was unaffected. Tunicamycin 127-138 CD177 molecule Homo sapiens 38-59 2174119-4 1990 Aglycosylated anti-NIP IgG3 antibody has been produced by cell growth in the presence of the antibiotic tunicamycin. Tunicamycin 104-115 immunoglobulin heavy constant gamma 3 (G3m marker) Homo sapiens 23-27 2076345-10 1990 Nonglycosylated gp120 or gp160 delta proteins from tunicamycin-treated cultures did immunoprecipitate with anti-HIV-1 antiserum but did not interact with CD4. Tunicamycin 51-62 inter-alpha-trypsin inhibitor heavy chain 4 Homo sapiens 16-21 2076345-10 1990 Nonglycosylated gp120 or gp160 delta proteins from tunicamycin-treated cultures did immunoprecipitate with anti-HIV-1 antiserum but did not interact with CD4. Tunicamycin 51-62 glutamyl aminopeptidase Homo sapiens 25-30 2150412-3 1990 Secretion of hepatic lipase activity was abolished by tunicamycin, castanospermine, and N-methyldeoxynojirimycin. Tunicamycin 54-65 lipase C, hepatic type Rattus norvegicus 13-27 2168959-4 1990 Treatment of AcPVR-infected cells with tunicamycin revealed that the PVR is a glycoprotein containing N-glycosidic linkages and that carbohydrate accounts for nearly 50% of its molecular weight as estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Tunicamycin 39-50 PVR cell adhesion molecule Homo sapiens 15-18 2094823-3 1990 In the presence of tunicamycin, an antibiotic which inhibits protein glycosylation, the cellular amount of the hydrophobic DE 16S AChE is increased. Tunicamycin 19-30 acetylcholinesterase Rattus norvegicus 130-134 2386935-7 1990 The size distribution of O-linked oligosaccharides in ASGP-1 from tunicamycin-treated versus control MAT-B1 cells is indistinguishable, as determined by Bio-Gel P-4 chromatography following alkaline-borohydride treatment. Tunicamycin 66-77 mucin 4, cell surface associated Rattus norvegicus 54-60 2386935-9 1990 Tunicamycin-treated cells, consistent with the reduced expression of ASGP-1, are significantly more susceptible to natural killer cell-mediated lysis, when compared to untreated controls. Tunicamycin 0-11 mucin 4, cell surface associated Rattus norvegicus 69-75 1715769-3 1990 Oligosaccharide analysis of recombinant IL 6 utilizing tunicamycin and endoglycosidases revealed O- and N-linked glycosylation that is comparable to that of natural IL 6 derived from human monocytes and fibroblasts. Tunicamycin 55-66 interleukin 6 Homo sapiens 40-44 2386799-4 1990 6-d-old human monocytes have stores of mRNA for linear release of LPL up to 24 h. Enzyme activity in cells and in culture medium was almost completely inhibited by 24 h treatment with tunicamycin, an inhibitor of glycosylation. Tunicamycin 184-195 lipoprotein lipase Homo sapiens 66-69 2116966-4 1990 When human and Ren1 renins were expressed in oocytes treated with tunicamycin, both were secreted efficiently. Tunicamycin 66-77 renin 1 structural Mus musculus 15-19 2353452-5 1990 Endoglycosidase F treatment or labeling in the presence of tunicamycin suggests that YF prM and NS1 each have two N-linked oligosaccharides. Tunicamycin 59-70 influenza virus NS1A binding protein Homo sapiens 96-99 1700792-1 1990 We have isolated a portion of the uridine diphosphate N-acetyl-D-glucosamine:dolichol phosphate N-acetyl-glucosamine-1-phosphate transferase gene (GTR2) from the genome of a tunicamycin-resistant clonal Chinese hamster ovary cell line, 3E11. Tunicamycin 174-185 UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase Cricetulus griseus 147-151 2243109-2 1990 Biosynthetic experiments with articular chondrocytes in the presence of tunicamycin, an inhibitor of N-linked oligosaccharide synthesis, demonstrated a specific inhibition of [35S]SO4 incorporation into fibromodulin. Tunicamycin 72-83 fibromodulin Bos taurus 203-215 2246236-13 1990 The expression of functional vEGF receptors was inhibited when the cells were preincubated with tunicamycin, indicating that glycosylation of the receptor is important for the expression of functional vEGF receptors. Tunicamycin 96-107 vascular endothelial growth factor A Bos taurus 29-33 2246236-13 1990 The expression of functional vEGF receptors was inhibited when the cells were preincubated with tunicamycin, indicating that glycosylation of the receptor is important for the expression of functional vEGF receptors. Tunicamycin 96-107 vascular endothelial growth factor A Bos taurus 201-205 2111144-5 1990 Inhibition of de novo glycosylation by tunicamycin impaired the secretion of M-type alpha 1-antitrypsin by about 75% whereas inhibition of oligosaccharide processing by the mannosidase II inhibitor swainsonine did not alter the secretion of M-type alpha 1-antitrypsin. Tunicamycin 39-50 serpin family A member 1 Homo sapiens 84-103 2156003-8 1990 Experiments utilizing tunicamycin, endoglycosidase H and glycopeptidase F revealed that p130 and p40 exhibited properties characteristic of glycoproteins. Tunicamycin 22-33 nucleolar and coiled-body phosphoprotein 1 Homo sapiens 88-92 1690264-5 1990 In the presence of tunicamycin gp120 was no longer detectable and a non-glycosylated precursor of 75K was found instead. Tunicamycin 19-30 inter-alpha-trypsin inhibitor heavy chain 4 Homo sapiens 31-36 2111144-7 1990 Even unglycosylated alpha 1-antitrypsin secreted by human monocytes treated with tunicamycin formed a complex with elastase. Tunicamycin 81-92 serpin family A member 1 Homo sapiens 20-39 2303708-1 1990 Effect of tunicamycin on the glycosylation of IL-5 and the biologic activity of deglycosylated IL-5. Tunicamycin 10-21 interleukin 5 Mus musculus 46-50 2303708-9 1990 Furthermore, deglycosylated rIL-5 that had been translated in the presence of tunicamycin showed very limited heterogeneity by two-dimensional gel electrophoresis (first dimension, nonequilibrium pH gradient electrophoresis; second dimension, SDS-PAGE). Tunicamycin 78-89 interleukin 5 Rattus norvegicus 28-33 2303708-15 1990 Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions. Tunicamycin 49-60 interleukin 5 Rattus norvegicus 15-20 2303708-15 1990 Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions. Tunicamycin 49-60 interleukin 5 Mus musculus 16-20 2303708-15 1990 Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions. Tunicamycin 49-60 interleukin 5 Rattus norvegicus 91-95 2303708-15 1990 Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions. Tunicamycin 49-60 interleukin 5 Rattus norvegicus 203-208 2404451-8 1990 Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells. Tunicamycin 7-18 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 67-73 2404451-8 1990 Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells. Tunicamycin 7-18 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 235-241 2404451-8 1990 Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells. Tunicamycin 7-18 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 235-241 2404451-8 1990 Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells. Tunicamycin 264-275 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 67-73 2404451-8 1990 Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells. Tunicamycin 264-275 colony stimulating factor 2 (granulocyte-macrophage) Mus musculus 67-73 33798597-8 2021 In addition, we have found that treatment of SH-SY5Y cells with imipramine in combination of either thapsigargin or tunicamycin is associated with the alteration of ER stress-induced IRE1alpha-XBP1 signalling. Tunicamycin 116-127 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 183-192 2132545-9 1990 Tunicamycin, an inhibitor of glycosylation of proteins, reduced UVB light effect on the SS-A/Ro and SS-B/La antigen"s expression. Tunicamycin 0-11 tripartite motif containing 21 Homo sapiens 88-95 2132545-9 1990 Tunicamycin, an inhibitor of glycosylation of proteins, reduced UVB light effect on the SS-A/Ro and SS-B/La antigen"s expression. Tunicamycin 0-11 small RNA binding exonuclease protection factor La Homo sapiens 100-104 1694435-7 1990 This heterogeneity probably is a result of differences in glycosylation of LBP since pretreatment of the hepatocytes with tunicamycin results in accumulation of a single polypeptide with an apparent mass of 50 kD in SDS-PAGE. Tunicamycin 122-133 lipopolysaccharide-binding protein Oryctolagus cuniculus 75-78 2333387-3 1990 Furthermore, addition of 0.1 microgram mL-1 tunicamycin to the incubation medium virtually eliminated incorporation of glucose into the protein bands but had no effect on the pattern or rate of incorporation of labelled amino acids in parallel experiments. Tunicamycin 44-55 L1 cell adhesion molecule Mus musculus 39-43 657267-3 1978 Tunicamycin inhibited the incorporation of 3H-mannose into CSP by 92--98% and 14C-glucosamine by 84--96%, whereas total protein synthesis was decreased by only 15--45%. Tunicamycin 0-11 DnaJ heat shock protein family (Hsp40) member C5 Mus musculus 59-62 657267-4 1978 Tunicamycin treatment decreased total amounts of CSP by approximately 50--65%, with equal decreases in CSP occurring on the cell surface and in culture medium, whereas intracellular pools of CSP were not substantially affected. Tunicamycin 0-11 DnaJ heat shock protein family (Hsp40) member C5 Mus musculus 49-52 657267-4 1978 Tunicamycin treatment decreased total amounts of CSP by approximately 50--65%, with equal decreases in CSP occurring on the cell surface and in culture medium, whereas intracellular pools of CSP were not substantially affected. Tunicamycin 0-11 DnaJ heat shock protein family (Hsp40) member C5 Mus musculus 103-106 657267-4 1978 Tunicamycin treatment decreased total amounts of CSP by approximately 50--65%, with equal decreases in CSP occurring on the cell surface and in culture medium, whereas intracellular pools of CSP were not substantially affected. Tunicamycin 0-11 DnaJ heat shock protein family (Hsp40) member C5 Mus musculus 103-106 657267-8 1978 We examined the mechanism of the decrease in CSP after tunicamycin treatment. Tunicamycin 55-66 DnaJ heat shock protein family (Hsp40) member C5 Mus musculus 45-48 657267-10 1978 Tunicamycin had only a slight effect on the initial times and rates of CSP appearance on the cell surface; some apparent intracellular redistribution of CSP was detected by immunofluorescence. Tunicamycin 0-11 DnaJ heat shock protein family (Hsp40) member C5 Mus musculus 71-74 657267-11 1978 The major effect of tunicamycin treatment was to accelerate the rate of degradation of CSP 2--3 fold. Tunicamycin 20-31 DnaJ heat shock protein family (Hsp40) member C5 Mus musculus 87-90 33798597-9 2021 Despite potentiation of ER stress-induced XBP1 splicing, imipramine suppresses both thapsigargin- and tunicamycin-induced expression of Hrd1. Tunicamycin 102-113 synoviolin 1 Homo sapiens 136-140 33798597-8 2021 In addition, we have found that treatment of SH-SY5Y cells with imipramine in combination of either thapsigargin or tunicamycin is associated with the alteration of ER stress-induced IRE1alpha-XBP1 signalling. Tunicamycin 116-127 X-box binding protein 1 Homo sapiens 193-197 33803345-3 2021 On the other hand, treatment with tunicamycin (Tm) shifted the molecular weight of the full-length CREB3L2 protein downward but abolished CREB3 protein expression. Tunicamycin 34-45 cAMP responsive element binding protein 3 like 2 Homo sapiens 99-106 33822017-9 2021 In HT-29 cells, tunicamycin-induced ER stress triggered AGR2 intracellular expression and its secretion. Tunicamycin 16-27 anterior gradient 2, protein disulphide isomerase family member Homo sapiens 56-60 33235302-8 2020 ALA pre-treatment significantly reduced the expression of ER stress markers namely, GRP78, XBP1, sXBP1 and ATF4 in response to tunicamycin. Tunicamycin 127-138 heat shock protein family A (Hsp70) member 5 Homo sapiens 84-89 33235302-8 2020 ALA pre-treatment significantly reduced the expression of ER stress markers namely, GRP78, XBP1, sXBP1 and ATF4 in response to tunicamycin. Tunicamycin 127-138 X-box binding protein 1 Homo sapiens 91-95 33235302-8 2020 ALA pre-treatment significantly reduced the expression of ER stress markers namely, GRP78, XBP1, sXBP1 and ATF4 in response to tunicamycin. Tunicamycin 127-138 activating transcription factor 4 Homo sapiens 107-111 33235302-9 2020 In functional assays, ALA treatment abrogated significantly the tunicamycin-mediated transcriptional activation of ATF6 while it enhanced the insulin-stimulated glucose uptake and Glut4 translocation. Tunicamycin 64-75 activating transcription factor 6 Homo sapiens 115-119 33235302-10 2020 Silencing the expression of DNAJB3 but not HSP72 abolished the protective effect of ALA on tunicamycin-induced ER stress, suggesting thus that DNAJB3 is a key mediator of ALA-alleviated tunicamycin-induced ER stress. Tunicamycin 91-102 DnaJ heat shock protein family (Hsp40) member B3 Homo sapiens 28-34 33235302-10 2020 Silencing the expression of DNAJB3 but not HSP72 abolished the protective effect of ALA on tunicamycin-induced ER stress, suggesting thus that DNAJB3 is a key mediator of ALA-alleviated tunicamycin-induced ER stress. Tunicamycin 91-102 DnaJ heat shock protein family (Hsp40) member B3 Homo sapiens 143-149 33235302-10 2020 Silencing the expression of DNAJB3 but not HSP72 abolished the protective effect of ALA on tunicamycin-induced ER stress, suggesting thus that DNAJB3 is a key mediator of ALA-alleviated tunicamycin-induced ER stress. Tunicamycin 186-197 DnaJ heat shock protein family (Hsp40) member B3 Homo sapiens 28-34 33235302-10 2020 Silencing the expression of DNAJB3 but not HSP72 abolished the protective effect of ALA on tunicamycin-induced ER stress, suggesting thus that DNAJB3 is a key mediator of ALA-alleviated tunicamycin-induced ER stress. Tunicamycin 186-197 DnaJ heat shock protein family (Hsp40) member B3 Homo sapiens 143-149 33031913-4 2021 CHOP was induced in both strains after incubation with tunicamycin, indicating both strains have competent endoplasmic reticulum stress pathways. Tunicamycin 55-66 DNA-damage inducible transcript 3 Mus musculus 0-4 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 neurofilament light chain Rattus norvegicus 170-174 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 34973349-9 2022 In SIRT4-silenced cells, when treated with 2.5 mug/ml Tunicamycin for 16 hours, the increase in the expressions of ATF6, GRP78 and the ratio of spliced/unspliced XBP1 mRNA were reduced. Tunicamycin 54-65 X-box binding protein 1 Homo sapiens 162-166 34744019-5 2022 Tunicamycin treatment of S. cervi worms revealed that the expression of GRP94 is associated with ER stress. Tunicamycin 0-11 heat shock protein 90 beta family member 1 Bos taurus 72-77 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 65-93 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 heat shock protein family A (Hsp70) member 5 Homo sapiens 95-100 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 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 caspase 3 Homo sapiens 147-156 33803345-3 2021 On the other hand, treatment with tunicamycin (Tm) shifted the molecular weight of the full-length CREB3L2 protein downward but abolished CREB3 protein expression. Tunicamycin 34-45 cAMP responsive element binding protein 3 Homo sapiens 99-104 34979291-9 2021 Tunicamycin administration caused significant increase of the expression level of genes related to ER stress and UPR, such as CHOP, Grp78 and ATF6, but the berberine pre-treatment could significantly downregulate the expression level of these genes. Tunicamycin 0-11 DNA-damage inducible transcript 3 Mus musculus 126-130 34923100-6 2022 The total and nuclear NRF2 protein expression was also induced in porcine oocytes following H2O2 and tunicamycin (Tm) exposure. Tunicamycin 101-112 NFE2 like bZIP transcription factor 2 Homo sapiens 22-26 34923100-6 2022 The total and nuclear NRF2 protein expression was also induced in porcine oocytes following H2O2 and tunicamycin (Tm) exposure. Tunicamycin 114-116 NFE2 like bZIP transcription factor 2 Homo sapiens 22-26 34973349-9 2022 In SIRT4-silenced cells, when treated with 2.5 mug/ml Tunicamycin for 16 hours, the increase in the expressions of ATF6, GRP78 and the ratio of spliced/unspliced XBP1 mRNA were reduced. Tunicamycin 54-65 sirtuin 4 Homo sapiens 3-8 34973349-9 2022 In SIRT4-silenced cells, when treated with 2.5 mug/ml Tunicamycin for 16 hours, the increase in the expressions of ATF6, GRP78 and the ratio of spliced/unspliced XBP1 mRNA were reduced. Tunicamycin 54-65 activating transcription factor 6 Homo sapiens 115-119 34973349-9 2022 In SIRT4-silenced cells, when treated with 2.5 mug/ml Tunicamycin for 16 hours, the increase in the expressions of ATF6, GRP78 and the ratio of spliced/unspliced XBP1 mRNA were reduced. Tunicamycin 54-65 heat shock protein family A (Hsp70) member 5 Homo sapiens 121-126 34979291-9 2021 Tunicamycin administration caused significant increase of the expression level of genes related to ER stress and UPR, such as CHOP, Grp78 and ATF6, but the berberine pre-treatment could significantly downregulate the expression level of these genes. Tunicamycin 0-11 heat shock protein 5 Mus musculus 132-137 34979291-9 2021 Tunicamycin administration caused significant increase of the expression level of genes related to ER stress and UPR, such as CHOP, Grp78 and ATF6, but the berberine pre-treatment could significantly downregulate the expression level of these genes. Tunicamycin 0-11 activating transcription factor 6 Mus musculus 142-146 34937426-7 2022 Finally, we determined the effect of tunicamycin, a pharmacological inhibitor of N-linked glycosylation, and targeted mutations in Asn residues on SLC17A4 function. Tunicamycin 37-48 solute carrier family 17 member 4 Homo sapiens 147-154 34937426-12 2022 Immunoblot studies on lysates of transfected cells cultured in absence or presence of tunicamycin indicated that SLC17A4 is subject to N-linked glycosylation. Tunicamycin 86-97 solute carrier family 17 member 4 Homo sapiens 113-120 34636989-5 2021 We also verified the identified XBP1-dependent genes with specific silencing of this transcription factor during pharmacological ER stress induction with both an N-linked glycosylation inhibitor (tunicamycin) and a non-competitive inhibitor of the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) (thapsigargin). Tunicamycin 196-207 X-box binding protein 1 Homo sapiens 32-36 34832960-7 2021 IFN-beta expression induced by ER stress inducers, tunicamycin and thapsigargin, was abolished in RIG-I-deficient hepatocytes and macrophages, showing that RIG-I is required for ER stress-induced IFN-beta expression. Tunicamycin 51-62 interferon alpha Mus musculus 0-8 34832960-7 2021 IFN-beta expression induced by ER stress inducers, tunicamycin and thapsigargin, was abolished in RIG-I-deficient hepatocytes and macrophages, showing that RIG-I is required for ER stress-induced IFN-beta expression. Tunicamycin 51-62 DEAD/H box helicase 58 Mus musculus 156-161 34832960-7 2021 IFN-beta expression induced by ER stress inducers, tunicamycin and thapsigargin, was abolished in RIG-I-deficient hepatocytes and macrophages, showing that RIG-I is required for ER stress-induced IFN-beta expression. Tunicamycin 51-62 interferon alpha Mus musculus 196-204 34831215-4 2021 AIMS: The objective of this study was to investigate the effects of N-glycosylation inhibitors (tunicamycin or 2-deoxy-D-glucose) or the histone deacetylase inhibitor valproic acid (VPA) on FLT3-ITD localization and downstream activity. Tunicamycin 96-107 FMS-like tyrosine kinase 3 Mus musculus 190-194 34831215-10 2021 RESULTS: The susceptibility of FLT3-ITD-expressing cells to 17-AAG after pre-treatment with tunicamycin or 2-deoxy-D-glucose was demonstrated. Tunicamycin 92-103 fms related receptor tyrosine kinase 3 Homo sapiens 31-35 34831215-10 2021 RESULTS: The susceptibility of FLT3-ITD-expressing cells to 17-AAG after pre-treatment with tunicamycin or 2-deoxy-D-glucose was demonstrated. Tunicamycin 92-103 N-methylpurine DNA glycosylase Homo sapiens 63-66 34831215-11 2021 Importantly, in Ba/F3 cells that were stably expressing distinct FLT3-ITD variants that were located either in the juxtamembrane domain (JMD) or in the tyrosine kinase 1 domain (TKD1), response to the sequential treatments with tunicamycin and 17-AAG varied between individual FLT3-ITD motifs without dependence on the localization of the ITD. Tunicamycin 228-239 FMS-like tyrosine kinase 3 Mus musculus 65-69 34831215-12 2021 In all of the FLT3-ITD cell lines that were investigated, incubation with tunicamycin was accompanied by intracellular retention of FLT3-ITD due to the inhibition of glycosylation. Tunicamycin 74-85 FMS-like tyrosine kinase 3 Mus musculus 14-18 34831215-12 2021 In all of the FLT3-ITD cell lines that were investigated, incubation with tunicamycin was accompanied by intracellular retention of FLT3-ITD due to the inhibition of glycosylation. Tunicamycin 74-85 FMS-like tyrosine kinase 3 Mus musculus 132-136 34831215-14 2021 The allocation of FLT3 to different cellular compartments that was induced by tunicamycin, 2-deoxy-D-glucose, or VPA resulted in the activation of distinct downstream signaling pathways. Tunicamycin 78-89 FMS-like tyrosine kinase 3 Mus musculus 18-22 34968413-6 2022 AGB1 has previously been shown to control a distinct UPR pathway independently of IRE1 when treated with an ER stress inducer tunicamycin. Tunicamycin 126-137 GTP binding protein beta 1 Arabidopsis thaliana 0-4 34847196-11 2021 Expression of the pro-apoptotic protein CHOP was induced with TM, and not inhibited by vorinostat. Tunicamycin 62-64 DNA-damage inducible transcript 3 Mus musculus 40-44 34725321-7 2021 Using thapsigargin and tunicamycin to induce acute ER stress, we identified the transcription factor C/EBPdelta (CEBPD) as a mediator of PERK signaling to secretion of tumor promoting chemokines. Tunicamycin 23-34 CCAAT enhancer binding protein delta Homo sapiens 101-111 34725321-7 2021 Using thapsigargin and tunicamycin to induce acute ER stress, we identified the transcription factor C/EBPdelta (CEBPD) as a mediator of PERK signaling to secretion of tumor promoting chemokines. Tunicamycin 23-34 CCAAT enhancer binding protein delta Homo sapiens 113-118 34725321-7 2021 Using thapsigargin and tunicamycin to induce acute ER stress, we identified the transcription factor C/EBPdelta (CEBPD) as a mediator of PERK signaling to secretion of tumor promoting chemokines. Tunicamycin 23-34 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 137-141 34601014-12 2021 Also, tunicamycin blocked sevoflurane-induced downregulation of IRE1-JNK-beclin1 signaling pathway. Tunicamycin 6-17 mitogen-activated protein kinase 8 Rattus norvegicus 69-72 34601014-12 2021 Also, tunicamycin blocked sevoflurane-induced downregulation of IRE1-JNK-beclin1 signaling pathway. Tunicamycin 6-17 beclin 1 Rattus norvegicus 73-80 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 mitogen-activated protein kinase 14 Homo sapiens 73-76 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 mitogen-activated protein kinase 8 Homo sapiens 81-84 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 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 162-166 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 eukaryotic translation initiation factor 2A Homo sapiens 167-176 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 activating transcription factor 4 Homo sapiens 177-181 34494876-7 2021 The elimination of N-glycosylation by tunicamycin (TM) treatment, or mutagenesis, showed that N-glycosylation is critical for the proper cell surface expression of ACE2 but not for its carboxiprotease activity. Tunicamycin 38-49 angiotensin converting enzyme 2 Homo sapiens 164-168 34494876-7 2021 The elimination of N-glycosylation by tunicamycin (TM) treatment, or mutagenesis, showed that N-glycosylation is critical for the proper cell surface expression of ACE2 but not for its carboxiprotease activity. Tunicamycin 51-53 angiotensin converting enzyme 2 Homo sapiens 164-168 34716302-7 2021 PERK inhibitor ameliorated autophagy, fibrotic protein expression and apoptosis in TM-treated cells, indicating a role of the PERK/eIF2alpha pathway in autophagy activation during ER stress. Tunicamycin 83-85 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 0-4 34716302-7 2021 PERK inhibitor ameliorated autophagy, fibrotic protein expression and apoptosis in TM-treated cells, indicating a role of the PERK/eIF2alpha pathway in autophagy activation during ER stress. Tunicamycin 83-85 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 126-130 34716302-7 2021 PERK inhibitor ameliorated autophagy, fibrotic protein expression and apoptosis in TM-treated cells, indicating a role of the PERK/eIF2alpha pathway in autophagy activation during ER stress. Tunicamycin 83-85 eukaryotic translation initiation factor 2A Homo sapiens 131-140 34778390-11 2021 Moreover, treatment with the ER Stress inducer tunicamycin promoted VKORC1L1, but not VKORC1 expression. Tunicamycin 47-58 vitamin K epoxide reductase complex, subunit 1-like 1 Mus musculus 68-76 34700340-4 2022 For HBECs and A549 cells, atmospheric pressure cold plasma was able to alleviate tunicamycin-induced cell proliferation inhibition, inflammation and oxidant stress, and enhance nuclear factor-erythroid-2-related factor 2 (NRF2) pathway activation. Tunicamycin 81-92 NFE2 like bZIP transcription factor 2 Homo sapiens 177-220 34700340-4 2022 For HBECs and A549 cells, atmospheric pressure cold plasma was able to alleviate tunicamycin-induced cell proliferation inhibition, inflammation and oxidant stress, and enhance nuclear factor-erythroid-2-related factor 2 (NRF2) pathway activation. Tunicamycin 81-92 NFE2 like bZIP transcription factor 2 Homo sapiens 222-226 34700340-5 2022 Moreover, NRF2/ARE (anti-oxidant response elements) pathway was involved in the regulation of atmospheric pressure cold plasma on tunicamycin-induced oxidative stress. Tunicamycin 130-141 NFE2 like bZIP transcription factor 2 Homo sapiens 10-14 34759791-8 2021 Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels. Tunicamycin 14-16 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 58-62 34759791-8 2021 Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels. Tunicamycin 14-16 heat shock protein 5 Mus musculus 64-69 34759791-8 2021 Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels. Tunicamycin 14-16 activating transcription factor 6 Mus musculus 71-75 34759791-8 2021 Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels. Tunicamycin 14-16 X-box binding protein 1 Mus musculus 77-81 34759791-8 2021 Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels. Tunicamycin 14-16 DNA-damage inducible transcript 3 Mus musculus 87-91 34759791-9 2021 On the contrary, the expression of PERK, GRP78, XBP1, and CHOP was obviously reduced in TM-induced bEnd.3 cells after ESC treatment. Tunicamycin 88-90 eukaryotic translation initiation factor 2 alpha kinase 3 Mus musculus 35-39 34759791-9 2021 On the contrary, the expression of PERK, GRP78, XBP1, and CHOP was obviously reduced in TM-induced bEnd.3 cells after ESC treatment. Tunicamycin 88-90 heat shock protein 5 Mus musculus 41-46 34759791-9 2021 On the contrary, the expression of PERK, GRP78, XBP1, and CHOP was obviously reduced in TM-induced bEnd.3 cells after ESC treatment. Tunicamycin 88-90 X-box binding protein 1 Mus musculus 48-52 34759791-9 2021 On the contrary, the expression of PERK, GRP78, XBP1, and CHOP was obviously reduced in TM-induced bEnd.3 cells after ESC treatment. Tunicamycin 88-90 DNA-damage inducible transcript 3 Mus musculus 58-62 34681705-7 2021 Using qPCR to analyze the unfolded protein response genes, we observed that loss of S1R led to decreased levels of IRE1 and PERK-related effectors and increased over-expression of most of the effectors after a tunicamycin challenge. Tunicamycin 210-221 sigma non-opioid intracellular receptor 1 Danio rerio 84-87 34681705-8 2021 Finally, S1R deficiency led to alterations in mitochondria bioenergetics with decreased in basal, ATP-linked and non-mitochondrial respiration and following tunicamycin challenge. Tunicamycin 157-168 sigma non-opioid intracellular receptor 1 Danio rerio 9-12 34712218-8 2021 Furthermore, tunicamycin stimulation and PKR overexpression activated NF-kappaB and interferon response at the early stage of PRRSV infection, thus reinforcing the expression of type I interferons and proinflammatory cytokines and leading to inhibition of PRRSV. Tunicamycin 13-24 nuclear factor kappa B subunit 1 Homo sapiens 70-79 34671436-7 2021 The results of protein analysis showed that the levels of BIP, p-AMPK, and cleaved-caspase3 in the TM group increased significantly, while the levels decreased after ghrelin pretreatment. Tunicamycin 99-101 heat shock protein 5 Mus musculus 58-61 34153400-7 2021 Meanwhile, Lapatinib resistant HER2-positive breast cancer cells (LapR) display lower basal expression levels of UPR genes and enhanced tolerance to EnR stress with attenuated response to Brefeldin A and Tunicamycin. Tunicamycin 204-215 erb-b2 receptor tyrosine kinase 2 Homo sapiens 31-35 34618053-5 2021 Loss-of-function of NRP1 and NRP2 results in decreased tolerance to the ER stress inducer tunicamycin (TM), accelerating cell death. Tunicamycin 90-101 NAP1-related protein 1 Arabidopsis thaliana 20-24 34618053-5 2021 Loss-of-function of NRP1 and NRP2 results in decreased tolerance to the ER stress inducer tunicamycin (TM), accelerating cell death. Tunicamycin 90-101 NAP1-related protein 2 Arabidopsis thaliana 29-33 34837678-12 2021 The cells treated with 150 and 300 muM doses of TMAO for 24 hours showed a significant elevation in the protein and/or mRNA levels of TLR4 when compared to normal control or tunicamycin-treated cells. Tunicamycin 174-185 toll-like receptor 4 Mus musculus 134-138 34549824-3 2021 To this end, we generated Creld2-deficient mice and induced UPR by injection of tunicamycin. Tunicamycin 80-91 cysteine-rich with EGF-like domains 2 Mus musculus 26-32