PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 eukaryotic translation initiation factor 2 alpha kinase 3 Homo sapiens 198-202 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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