PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30194633-6 2018 At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux. Palmitic Acid 18-20 DNA damage inducible transcript 3 Homo sapiens 112-161 31518729-8 2020 PA affected cellular proliferation, apoptosis and endoplasmic reticulum stress markers along with reducing the phosphor-AKT/AKT levels and increasing the expression levels of caspase-3 and CHOP in GCs. Palmitic Acid 0-2 DNA damage inducible transcript 3 Homo sapiens 189-193 34179614-0 2021 Combination of Palmitic Acid and Methylseleninic Acid Induces Mitochondria-Dependent Apoptosis via Attenuation of the IRE1alpha Arm and Enhancement of CHOP in Hepatoma. Palmitic Acid 15-28 DNA damage inducible transcript 3 Homo sapiens 151-155 34179614-7 2021 The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells. Palmitic Acid 19-21 DNA damage inducible transcript 3 Homo sapiens 114-146 34179614-7 2021 The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells. Palmitic Acid 19-21 DNA damage inducible transcript 3 Homo sapiens 148-152 34179614-7 2021 The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells. Palmitic Acid 175-177 DNA damage inducible transcript 3 Homo sapiens 114-146 34179614-7 2021 The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells. Palmitic Acid 175-177 DNA damage inducible transcript 3 Homo sapiens 148-152 32736984-7 2020 CCAAT/enhancer-binding protein homologous protein (CHOP), an ER stress marker, was demonstrated to participate in PA-induced cytotoxicity. Palmitic Acid 114-116 DNA damage inducible transcript 3 Homo sapiens 0-49 32736984-7 2020 CCAAT/enhancer-binding protein homologous protein (CHOP), an ER stress marker, was demonstrated to participate in PA-induced cytotoxicity. Palmitic Acid 114-116 DNA damage inducible transcript 3 Homo sapiens 51-55 30194633-6 2018 At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux. Palmitic Acid 18-20 DNA damage inducible transcript 3 Homo sapiens 163-167 24368569-5 2013 Palmitic acid was the main compound responsible for this apoptotic effect by a ceramide-independent mechanism that involved endoplasmic reticulum (ER)-stress with upregulation of CCAAT/-enhancer-binding protein homologous protein (CHOP). Palmitic Acid 0-13 DNA damage inducible transcript 3 Homo sapiens 179-229 29234397-6 2017 ACE also protected HepG2 cells from PA- (300 muM-) induced endoplasmic reticulum (ER) stress and apoptosis and attenuated the related key molecules including GRP78, eIF2, and CHOP, respectively. Palmitic Acid 36-38 DNA damage inducible transcript 3 Homo sapiens 175-179 25841776-4 2015 In primary human hepatocytes, a lipotoxic concentration of PA triggered endoplasmic reticulum stress, induced the apoptotic transcription factor CHOP, and increased the percentage of apoptotic cells. Palmitic Acid 59-61 DNA damage inducible transcript 3 Homo sapiens 145-149 24446069-5 2014 PA treatment induced increased expression of PRKR-like endoplasmic reticulum kinase, inositol-requiring kinase 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and C/EBP homologous protein (CHOP) mRNA. Palmitic Acid 0-2 DNA damage inducible transcript 3 Homo sapiens 177-201 24446069-5 2014 PA treatment induced increased expression of PRKR-like endoplasmic reticulum kinase, inositol-requiring kinase 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and C/EBP homologous protein (CHOP) mRNA. Palmitic Acid 0-2 DNA damage inducible transcript 3 Homo sapiens 203-207 29046367-10 2017 Further, PA treatment significantly increased the expression of ERS markers, Ig heavy chain binding protein (Bip), and homologous proteins of CCAAT-enhancer binding proteins (CHOP). Palmitic Acid 9-11 DNA damage inducible transcript 3 Homo sapiens 175-179 25938832-6 2015 In addition, the palmitate sodium treatment also activated the PI3K/Akt pathway,induced expression of CHOP and Bax of the UPR and non-UPR signaling pathways respectively. Palmitic Acid 17-33 DNA damage inducible transcript 3 Homo sapiens 102-106 25938832-7 2015 Moreover, Pretreatment with LY294002 inhibited the palmitate sodium induced-phosphorylation of PI3K and Akt, and promoted upregulation of CHOP and Bax induced by palmitate sodium. Palmitic Acid 162-178 DNA damage inducible transcript 3 Homo sapiens 138-142 24368569-5 2013 Palmitic acid was the main compound responsible for this apoptotic effect by a ceramide-independent mechanism that involved endoplasmic reticulum (ER)-stress with upregulation of CCAAT/-enhancer-binding protein homologous protein (CHOP). Palmitic Acid 0-13 DNA damage inducible transcript 3 Homo sapiens 231-235 20506110-11 2010 Furthermore, PA decreased GRP78 expression and induced increases in the endoplasmic reticulum (ER) stress signaling pathways p-PERK, p-eIF2alpha, p-ATF4, and CHOP, which were blocked by AM251 treatment. Palmitic Acid 13-15 DNA damage inducible transcript 3 Homo sapiens 158-162 22246806-9 2012 Knockdown of PERK gene expression suppressed the PERK/ATF4/CHOP signaling pathway during sodium palmitate-induced ER stress and significantly inhibited sodium palmitate-induced apoptosis in L02 and HepG2 cells. Palmitic Acid 89-105 DNA damage inducible transcript 3 Homo sapiens 59-63 21078775-5 2011 PA induced ER stress, as determined by phosphorylation of PERK, eIF2alpha, and JNK, as well as induction of CHOP in macrophage-like THP-1 cells. Palmitic Acid 0-2 DNA damage inducible transcript 3 Homo sapiens 108-112 20668104-5 2010 Palmitic acid induces podocyte ER stress, leading to an unfolded protein response as reflected by the induction of the ER chaperone immunoglobulin heavy chain binding protein (BiP) and proapoptotic C/EBP homologous protein (CHOP) transcription factor. Palmitic Acid 0-13 DNA damage inducible transcript 3 Homo sapiens 198-222 20668104-5 2010 Palmitic acid induces podocyte ER stress, leading to an unfolded protein response as reflected by the induction of the ER chaperone immunoglobulin heavy chain binding protein (BiP) and proapoptotic C/EBP homologous protein (CHOP) transcription factor. Palmitic Acid 0-13 DNA damage inducible transcript 3 Homo sapiens 224-228 20668104-6 2010 Of note, the monounsaturated palmitoleic and oleic acid can attenuate the palmitic acid-induced upregulation of CHOP, thereby preventing cell death. Palmitic Acid 74-87 DNA damage inducible transcript 3 Homo sapiens 112-116 20668104-7 2010 Similarly, gene silencing of CHOP protects against palmitic acid-induced podocyte apoptosis. Palmitic Acid 51-64 DNA damage inducible transcript 3 Homo sapiens 29-33