PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28482072-8 2017 In contrast, CHOP overexpression mimicked inhibition of PGC-1alpha by high glucose. Glucose 75-82 DNA damage inducible transcript 3 Homo sapiens 13-17 28482072-10 2017 Moreover, maternal diabetes in vivo and high glucose in vitro promoted the interaction between CHOP and the PGC-1alpha transcriptional regulator CCAAT/enhancer binding protein-beta (C/EBPbeta), and reduced C/EBPbeta binding to the PGC-1alpha promoter leading to markedly decrease in PGC-1alpha expression. Glucose 45-52 DNA damage inducible transcript 3 Homo sapiens 95-99 28024901-4 2017 The results showed that along with induction of Cdk5 and apoptosis, GRP78 and its two sensors as well as CHOP and cleaved caspase-12 were induced in high glucose treated podocytes. Glucose 154-161 DNA damage inducible transcript 3 Homo sapiens 105-109 27530507-12 2017 Teneligliptin ameliorates high glucose-induced endoplasmic reticulum stress reducing the expression of several markers (BIP, PERK, ATF4, CHOP, IRE1a and ATF6). Glucose 31-38 DNA damage inducible transcript 3 Homo sapiens 137-141 25958041-9 2015 Along with the induction of FABP4 and apoptosis, GRP78 and its three sensors as well as C/EBP homologous protein (CHOP) and Caspase-12 were induced in HMCs treated with NEFA or high glucose and these responses were attenuated or even abrogated by treating with FABP4 inhibitor or FABP4 siRNA. Glucose 182-189 DNA damage inducible transcript 3 Homo sapiens 88-112 27481183-5 2016 In cultured PBMCs, high glucose and FFAs induced GRP78, CHOP and XBP-1 mRNA, and high glucose also induced APP, PS1 and PS2 mRNA. Glucose 24-31 DNA damage inducible transcript 3 Homo sapiens 56-60 25958041-9 2015 Along with the induction of FABP4 and apoptosis, GRP78 and its three sensors as well as C/EBP homologous protein (CHOP) and Caspase-12 were induced in HMCs treated with NEFA or high glucose and these responses were attenuated or even abrogated by treating with FABP4 inhibitor or FABP4 siRNA. Glucose 182-189 DNA damage inducible transcript 3 Homo sapiens 114-118 24362844-9 2014 CONCLUSION: The results suggest a guideline for plasma glucose monitoring during CHOP chemotherapy in patients with no history of DM. Glucose 55-62 DNA damage inducible transcript 3 Homo sapiens 81-85 25857226-0 2015 CHOP mediates XBP1S-induced renal mesangial cell necrosis following high glucose treatment. Glucose 73-80 DNA damage inducible transcript 3 Homo sapiens 0-4 25448036-5 2015 Adipogenesis proceeded in both normal and high glucose with concomitant activation of the UPR, but only high glucose was associated with increased levels of ER stress and mitochondrial stress as observed by parallel increases in CHOP and protein succination. Glucose 109-116 DNA damage inducible transcript 3 Homo sapiens 229-233 24851895-6 2014 Compared with control group, the mRNA and protein expressions of GRP78, CHOP and caspase 12 were all up-regulated significantly in high glucose group (P < 0.05). Glucose 136-143 DNA damage inducible transcript 3 Homo sapiens 72-76 24851895-7 2014 The high glucose with adiponectin group could reduce the podocyte apoptosis by 10% and down-regulated the mRNA and protein expressions of GRP78, CHOP and caspase 12 versus high glucose group (all P < 0.05). Glucose 9-16 DNA damage inducible transcript 3 Homo sapiens 145-149 20424162-5 2010 In addition, prolonged exposure to high glucose further increases IL-1beta-triggered CHOP expression. Glucose 40-47 DNA damage inducible transcript 3 Homo sapiens 85-89 24177007-5 2013 These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition. Glucose 277-284 DNA damage inducible transcript 3 Homo sapiens 131-135 23241730-7 2013 The expression of CHOP and caspase-3 in mesangial cells was also found to be significantly enhanced under high glucose conditions compared with the normal group (P<0.01). Glucose 111-118 DNA damage inducible transcript 3 Homo sapiens 18-22 24177007-5 2013 These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition. Glucose 142-149 DNA damage inducible transcript 3 Homo sapiens 131-135 33390989-7 2020 Interestingly, melatonin treatment significantly alleviates the high-glucose induced changes in cell growth, apoptosis, and calcium influx by inhibiting the PERK-eIF2alpha-ATF4-CHOP signaling pathway. Glucose 69-76 DNA damage inducible transcript 3 Homo sapiens 177-181 17620318-7 2007 CHOP may play a role in altered beta-cell glucose metabolism, in beta-cell apoptosis, and in lack of beta-cell replication. Glucose 42-49 DNA damage inducible transcript 3 Homo sapiens 0-4 16770736-1 2006 Endoplasmic reticulum (ER) dysfunction is known to activate the unfolded protein response, which is characterized by the activation of two divergent processes, i.e., suppression of the initiation process in global protein synthesis and expression of glucose-regulated protein 78 (Bip/Grp78) and the C/EBP homologous transcription factor CHOP/Gadd153. Glucose 250-257 DNA damage inducible transcript 3 Homo sapiens 337-341 16770736-1 2006 Endoplasmic reticulum (ER) dysfunction is known to activate the unfolded protein response, which is characterized by the activation of two divergent processes, i.e., suppression of the initiation process in global protein synthesis and expression of glucose-regulated protein 78 (Bip/Grp78) and the C/EBP homologous transcription factor CHOP/Gadd153. Glucose 250-257 DNA damage inducible transcript 3 Homo sapiens 342-349 16000304-4 2005 Here we report that glucose withdrawal, tunicamycin, and thapsigargin induce up-regulation of GADD153 and caspase-12, two markers of endoplasmic reticulum stress, in both primary chondrocytes and a chondrocyte cell line. Glucose 20-27 DNA damage inducible transcript 3 Homo sapiens 94-101 8336711-3 1993 Here we examined the role of glucose in regulating gadd153 expression. Glucose 29-36 DNA damage inducible transcript 3 Homo sapiens 51-58 8336711-9 1993 Frequent addition of fresh medium to the cells during the differentiation process, as well as supplementation of medium with glucose, reduced gadd153 expression without preventing C/EBP alpha expression or interfering with cellular differentiation. Glucose 125-132 DNA damage inducible transcript 3 Homo sapiens 142-149 8336711-10 1993 Thus, gadd153 expression is not essential for the process of adipocyte differentiation but is significantly influenced by the availability of glucose to the cell. Glucose 142-149 DNA damage inducible transcript 3 Homo sapiens 6-13 33826840-4 2021 Our study found that after oxygen-glucose deprivation/reoxygenation (OGD/R) treatment, the levels of GPR4 and CHOP in SH-SY5Y cells were significantly increased, which was accompanied by a decrease in cell viability, and an increase in LDH release and apoptosis. Glucose 34-41 DNA damage inducible transcript 3 Homo sapiens 110-114 32504504-9 2021 BeWo cells cultured with high glucose and insulin showed decreased SDF2 expression, while high glucose increased CHOP and sXBP1 expression, which was then significantly reverted with insulin treatment. Glucose 95-102 DNA damage inducible transcript 3 Homo sapiens 113-117 17615236-3 2007 Here we show that CHOP expression is induced in cultured pancreatic beta-cells maintained in a basal glucose concentration of 5.5 mM and repressed by stimulatory glucose (>or=11 mM). Glucose 101-108 DNA damage inducible transcript 3 Homo sapiens 18-22 17615236-3 2007 Here we show that CHOP expression is induced in cultured pancreatic beta-cells maintained in a basal glucose concentration of 5.5 mM and repressed by stimulatory glucose (>or=11 mM). Glucose 162-169 DNA damage inducible transcript 3 Homo sapiens 18-22 34479965-11 2021 Human CHOP-ASOs efficiently reduced glucose-induced CHOP and prevented cell death of human kidney cells in vitro Conclusions: The ASO-based approach efficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to an ACEi in particular at later timepoints. Glucose 36-43 DNA damage inducible transcript 3 Homo sapiens 6-10 34479965-11 2021 Human CHOP-ASOs efficiently reduced glucose-induced CHOP and prevented cell death of human kidney cells in vitro Conclusions: The ASO-based approach efficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to an ACEi in particular at later timepoints. Glucose 36-43 DNA damage inducible transcript 3 Homo sapiens 52-56 32515472-7 2020 Moreover, high glucose increased mRNA and protein expression of CHOP, ATF-6 and GRP78. Glucose 15-22 DNA damage inducible transcript 3 Homo sapiens 64-68 31883977-5 2020 CHOP protein stability was investigated in conditions of nutrient stress due to high glucose or elevated fumarate (fumarase knockdown model); where cysteine succination is specifically elevated. Glucose 85-92 DNA damage inducible transcript 3 Homo sapiens 0-4 31883977-6 2020 CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation. Glucose 69-76 DNA damage inducible transcript 3 Homo sapiens 0-4 31883977-6 2020 CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation. Glucose 69-76 DNA damage inducible transcript 3 Homo sapiens 114-118 31883977-6 2020 CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation. Glucose 69-76 DNA damage inducible transcript 3 Homo sapiens 114-118 31883977-13 2020 This study demonstrates that physiological increases in the metabolite fumarate during high glucose exposure contributes to the presence of oxidative stress and sustained CHOP levels in the adipocyte during diabetes. Glucose 92-99 DNA damage inducible transcript 3 Homo sapiens 171-175 30671964-4 2019 TUG1 was highly expressed in a cell following treatment with high glucose, and PGC-1alpha and cleaved caspase-3 levels were much lower, while CHOP level was much higher in high glucose group (HG), furthermore, CHOP inhibited PGC-1alpha expression. Glucose 177-184 DNA damage inducible transcript 3 Homo sapiens 142-146 31524237-0 2019 High glucose and bupivacaine-induced cytotoxicity is mediated by enhanced apoptosis and impaired autophagy via the PERK-ATF4-CHOP and IRE1-TRAF2 signaling pathways. Glucose 5-12 DNA damage inducible transcript 3 Homo sapiens 125-129 31524237-7 2019 Compared with the control group, high glucose and bupivacaine significantly increased ATF4, CHOP and caspase-12 expression, increased apoptosis, and decreased p-IRE1, TRAF2, LC3-II/LC3-I and Beclin1 expression. Glucose 38-45 DNA damage inducible transcript 3 Homo sapiens 92-96 31524237-9 2019 High glucose and bupivacaine induced cytotoxicity in SH-SY5Y cells, at least in part, through enhancing cell apoptosis and inhibiting autophagy via the PERK-ATF4-CHOP and IRE1-TRAF2 signaling pathways. Glucose 5-12 DNA damage inducible transcript 3 Homo sapiens 162-166 31212679-5 2019 The C. turczaninowii extract attenuated the increased mRNA expression of IL-6, TNF-alpha, and CHOP in hASMCs under high glucose conditions. Glucose 120-127 DNA damage inducible transcript 3 Homo sapiens 94-98 31084986-3 2019 We investigated whether high-glucose concentrations augment lipopolysaccharide-induced reduction in macrophage phagocytosis via the endoplasmic stress-C/EBP homologous protein (CHOP) pathway using animal and laboratory investigations. Glucose 29-36 DNA damage inducible transcript 3 Homo sapiens 144-175 31084986-3 2019 We investigated whether high-glucose concentrations augment lipopolysaccharide-induced reduction in macrophage phagocytosis via the endoplasmic stress-C/EBP homologous protein (CHOP) pathway using animal and laboratory investigations. Glucose 29-36 DNA damage inducible transcript 3 Homo sapiens 177-181 30625303-7 2019 Exocrine acinar cells exposed to high Ins or Ins+Glu concentrations (but not Glu alone) exhibited ER-stress UPR, demonstrated by significant increase of transcript and protein levels of downstream markers in the ATF6 and IRE1 transduction arms, including: sXBP1, cleaved ATF6, XBP1, CHOP, IRE1-p and caspase-12. Glucose 49-52 DNA damage inducible transcript 3 Homo sapiens 283-287