PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 30475171-6 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 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 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 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 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 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 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 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 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 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 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 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 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 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 75-77 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 132-136 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 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 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 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 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 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 endoplasmic reticulum to nucleus signaling 1 Homo sapiens 203-212 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 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 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 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 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 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 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 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 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 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