PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32973403-13 2020 Conclusion: In summary, these results demonstrate that ER stress plays a crucial role in CENPF expression, and XBP1 may up-regulate DNA-binding affinities after TG treatment to the promoter of CENPF. Thapsigargin 161-163 X-box binding protein 1 Homo sapiens 111-115 34917610-7 2021 Gly supplementation could reduce the ER stress induced by TG by significantly improving the ER levels and significantly downregulating the expression of genes related to ER stress (Xbp1, ATF4, and ATF6). Thapsigargin 58-60 X-box binding protein 1 Homo sapiens 181-185 34035477-10 2021 PMDD LCLs had a 1.36-fold decrease in Tg-induced XBP1 splicing response compared to controls, and a 1.62-fold decreased response (p = 0.005), with a diagnosis x treatment interaction (F(3,33)=3.51, p = 0.026) in the E2-exposed condition. Thapsigargin 38-40 X-box binding protein 1 Homo sapiens 49-53 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. Thapsigargin 100-112 X-box binding protein 1 Homo sapiens 193-197 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). Thapsigargin 297-309 X-box binding protein 1 Homo sapiens 32-36 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. Thapsigargin 213-225 X-box binding protein 1 Homo sapiens 53-57 32376153-7 2020 Low dose Tg induced the IRE1alpha-XBP1 pathway and strengthened TJ barrier. Thapsigargin 9-11 X-box binding protein 1 Homo sapiens 34-38 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). Thapsigargin 49-61 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). Thapsigargin 63-65 X-box binding protein 1 Homo sapiens 365-388 31540861-8 2019 ER stress induced by thapsigargin increased spliced X-box binding protein-1 (XBP-1, transcription factor that increases the transcription of UPR target genes) levels in a time-dependent manner followed by autophagy and resulted to cell apoptosis. Thapsigargin 21-33 X-box binding protein 1 Homo sapiens 52-75 31540861-8 2019 ER stress induced by thapsigargin increased spliced X-box binding protein-1 (XBP-1, transcription factor that increases the transcription of UPR target genes) levels in a time-dependent manner followed by autophagy and resulted to cell apoptosis. Thapsigargin 21-33 X-box binding protein 1 Homo sapiens 77-82 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. Thapsigargin 45-57 X-box binding protein 1 Homo sapiens 128-133 27556805-9 2016 RESULTS: Proof of principle came in our results by the fact that the 26 nt non-conventional splice site in Xbp1 was detected as the top hit by our new RSR algorithm in heterozygote (Het) samples from both Thapsigargin (Tg) and Dithiothreitol (Dtt) treated experiments but absent in the negative control Ire1alpha knock-out (KO) samples. Thapsigargin 205-217 X-box binding protein 1 Homo sapiens 107-111 29916547-8 2018 Once XBP1 was activated by Thapsigargin, AXL expression was restored. Thapsigargin 27-39 X-box binding protein 1 Homo sapiens 5-9 29142472-7 2017 PGE1 enhanced the TG-induced expression of C/EBP homologous protein (CHOP), glucose-regulated protein (GRP) 78 and spliced X box-binding protein 1 at 6 h. However, it attenuated their expressions after 24 h. PGE1 alone induced protein and mRNA expressions of GRP78; PGE1 also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phospho-eukaryotic initiation factor 2alpha and CHOP. Thapsigargin 18-20 X-box binding protein 1 Homo sapiens 123-146 31416082-14 2019 CSE treatment significantly increased the expression of GRP78, IRE1, XBP-1 and ATF6 at the protein level at 48 h. Pretreatment with TG enhanced, whereas pretreatment with 4-PBA inhibited, the CSE-induced expression of alpha-SMA, GRP78 and XBP-1. Thapsigargin 132-134 X-box binding protein 1 Homo sapiens 69-74 31416082-14 2019 CSE treatment significantly increased the expression of GRP78, IRE1, XBP-1 and ATF6 at the protein level at 48 h. Pretreatment with TG enhanced, whereas pretreatment with 4-PBA inhibited, the CSE-induced expression of alpha-SMA, GRP78 and XBP-1. Thapsigargin 132-134 X-box binding protein 1 Homo sapiens 239-244 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. Thapsigargin 52-64 X-box binding protein 1 Homo sapiens 145-149 27928013-6 2017 Ectopic expression of UL41 decreased the expression of XBP1 and blocked XBP1 splicing activation induced by the ER stress inducer thapsigargin. Thapsigargin 130-142 X-box binding protein 1 Homo sapiens 72-76 27928013-7 2017 Wild-type (WT) HSV-1, but not the UL41-null mutant HSV-1 (R2621), decreased XBP1 mRNA induced by thapsigargin. Thapsigargin 97-109 X-box binding protein 1 Homo sapiens 76-80 27556805-9 2016 RESULTS: Proof of principle came in our results by the fact that the 26 nt non-conventional splice site in Xbp1 was detected as the top hit by our new RSR algorithm in heterozygote (Het) samples from both Thapsigargin (Tg) and Dithiothreitol (Dtt) treated experiments but absent in the negative control Ire1alpha knock-out (KO) samples. Thapsigargin 219-221 X-box binding protein 1 Homo sapiens 107-111 18771604-4 2009 Induction of the spliced form of XBP1 as well as total XBP1 by thapsigargin was significantly attenuated in patients with BD. Thapsigargin 63-75 X-box binding protein 1 Homo sapiens 33-37 24362465-7 2014 Furthermore, IRE1, XBP-1, or Grp78 knockdown significantly increased thapsigargin lethality, as observed with CDK1/5 inhibition/knockdown. Thapsigargin 69-81 X-box binding protein 1 Homo sapiens 19-24 23026561-9 2013 Similarly, the increase in GRP78 and XBP-1 protein levels was shown to be higher in neurons treated with Abeta or thapsigargin in the presence of KCN in comparison with levels determined in neurons treated with the neurotoxins alone. Thapsigargin 114-126 X-box binding protein 1 Homo sapiens 37-42 23335849-4 2013 XBP1 mRNA splicing and expression of endoplasmic reticulum stress response genes were determined in cells exposed to thapsigargin in the presence or absence of quinotrierixin. Thapsigargin 117-129 X-box binding protein 1 Homo sapiens 0-4 23335849-7 2013 In cells exposed to thapsigargin, quinotrierixin inhibited XBP1 mRNA splicing and PKR-like endoplasmic reticulum kinase activation, and reduced cellular and nuclear levels of spliced XBP1 and C/EBP homologous protein. Thapsigargin 20-32 X-box binding protein 1 Homo sapiens 59-63 23335849-7 2013 In cells exposed to thapsigargin, quinotrierixin inhibited XBP1 mRNA splicing and PKR-like endoplasmic reticulum kinase activation, and reduced cellular and nuclear levels of spliced XBP1 and C/EBP homologous protein. Thapsigargin 20-32 X-box binding protein 1 Homo sapiens 183-187 23711492-7 2013 Conversely, knockdown of Klotho in HEK 293 cells using siRNA caused further thapsigargin-induced increases in pIRE-1, XBP-1s, and BiP. Thapsigargin 76-88 X-box binding protein 1 Homo sapiens 118-123 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. Thapsigargin 34-46 X-box binding protein 1 Homo sapiens 89-93 21199669-3 2011 In both, a human line of fetal thyroid cells (TAD-2 cells) and primary cultures of human thyroid cells, thapsigargin and tunicamicin triggered ER stress evaluated by BiP mRNA levels and XBP-1 splicing. Thapsigargin 104-116 X-box binding protein 1 Homo sapiens 186-191 18771604-4 2009 Induction of the spliced form of XBP1 as well as total XBP1 by thapsigargin was significantly attenuated in patients with BD. Thapsigargin 63-75 X-box binding protein 1 Homo sapiens 55-59 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. Thapsigargin 21-33 X-box binding protein 1 Homo sapiens 195-199 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. Thapsigargin 142-154 X-box binding protein 1 Homo sapiens 22-45 18653996-3 2008 Quinotrierixin inhibited thapsigargin-induced XBP1 activation in HeLa cells with an IC50 of 0.067 microM. Thapsigargin 25-37 X-box binding protein 1 Homo sapiens 46-50 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. Thapsigargin 15-27 X-box binding protein 1 Homo sapiens 119-123 17917237-6 2007 The molecular formula of trierixin is C(37)H(52)N(2)O(8)S. Trierixin inhibited thapsigargin-induced XBP1-luciferase activation in HeLa/XBP1-luc cells and endogenous XBP1 splicing in HeLa cells with an IC(50) of 14 ng/ml and 19 ng/ml, respectively. Thapsigargin 79-91 X-box binding protein 1 Homo sapiens 100-104 17917237-6 2007 The molecular formula of trierixin is C(37)H(52)N(2)O(8)S. Trierixin inhibited thapsigargin-induced XBP1-luciferase activation in HeLa/XBP1-luc cells and endogenous XBP1 splicing in HeLa cells with an IC(50) of 14 ng/ml and 19 ng/ml, respectively. Thapsigargin 79-91 X-box binding protein 1 Homo sapiens 135-139 17917237-6 2007 The molecular formula of trierixin is C(37)H(52)N(2)O(8)S. Trierixin inhibited thapsigargin-induced XBP1-luciferase activation in HeLa/XBP1-luc cells and endogenous XBP1 splicing in HeLa cells with an IC(50) of 14 ng/ml and 19 ng/ml, respectively. Thapsigargin 79-91 X-box binding protein 1 Homo sapiens 135-139 16899390-5 2006 Interestingly, nitric oxide induced the processing of the activating transcription factor 6alpha of the unfolded protein response, while thapsigargin also induced the activation of the transcription factor X-box Binding Protein 1. Thapsigargin 137-149 X-box binding protein 1 Homo sapiens 206-229 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. Thapsigargin 41-53 X-box binding protein 1 Homo sapiens 92-96 16364319-4 2006 Our findings demonstrate that at least 18 genes are specifically upregulated by ATF6alpha, while another UPR mediator, XBP1 or ER-stress inducer, thapsigargin could partially stimulate or even repress some of them in HCC cells. Thapsigargin 146-158 X-box binding protein 1 Homo sapiens 119-123