PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 activating transcription factor 6 Homo sapiens 54-58 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 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 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 84-86 activating transcription factor 6 Homo sapiens 305-309 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 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 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 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 30336657-7 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 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 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 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 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 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 69-71 activating transcription factor 6 Homo sapiens 116-120 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 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 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 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 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 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 activating transcription factor 6 Homo sapiens 217-221 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 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 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 activating transcription factor 6 Homo sapiens 105-109 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 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 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