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PubMed:20829347 JSONTXT 23 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
T1 0-170 Sentence denotes Endoplasmic reticulum stress-activated C/EBP homologous protein enhances nuclear factor-kappaB signals via repression of peroxisome proliferator-activated receptor gamma.
T2 171-258 Sentence denotes Endoplasmic reticulum (ER) stress is a causative factor of inflammatory bowel diseases.
T3 259-440 Sentence denotes ER stress mediators, including CCAAT enhancer-binding protein (C/EBP) homologous protein (CHOP), are elevated in intestinal epithelia from patients with inflammatory bowel diseases.
T4 441-615 Sentence denotes The present study arose from the question of how chemical ER stress and CHOP protein were associated with nuclear factor-κB (NF-κB)-mediated epithelial inflammatory response.
T5 616-801 Sentence denotes In a human intestinal epithelial cell culture model, chemical ER stresses induced proinflammatory cytokine interleukin-8 (IL-8) expression and the nuclear translocation of CHOP protein.
T6 802-965 Sentence denotes CHOP was positively involved in ER-activated IL-8 production and was negatively associated with expression of peroxisome proliferator-activated receptor γ (PPARγ).
T7 966-1072 Sentence denotes ER stress-induced IL-8 production was enhanced by NF-κB activation that was negatively regulated by PPARγ.
T8 1073-1233 Sentence denotes Mechanistically, ER stress-induced CHOP suppressed PPARγ transcription by sequestering C/EBPβ and limiting availability of C/EBPβ binding to the PPARγ promoter.
T9 1234-1430 Sentence denotes Due to the CHOP-mediated regulation of PPARγ action, ER stress can enhance proinflammatory NF-κB activation and maintain an increased level of IL-8 production in human intestinal epithelial cells.
T10 1431-1549 Sentence denotes In contrast, PPARγ was a counteracting regulator of gut inflammatory response through attenuation of NF-κB activation.
T11 1550-1796 Sentence denotes The collective results support the view that balances between CHOP and PPARγ are crucial for epithelial homeostasis, and disruption of these balances in mucosal ER stress can etiologically affect the progress of human inflammatory bowel diseases.