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PubMed:22337883 JSONTXT 24 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
T1 0-119 Sentence denotes The transcription factor Erg controls endothelial cell quiescence by repressing activity of nuclear factor (NF)-κB p65.
T1 0-119 Sentence denotes The transcription factor Erg controls endothelial cell quiescence by repressing activity of nuclear factor (NF)-κB p65.
T2 120-244 Sentence denotes The interaction of transcription factors with specific DNA sequences is critical for activation of gene expression programs.
T2 120-244 Sentence denotes The interaction of transcription factors with specific DNA sequences is critical for activation of gene expression programs.
T3 245-436 Sentence denotes In endothelial cells (EC), the transcription factor NF-κB is important in the switch from quiescence to activation, and is tightly controlled to avoid excessive inflammation and organ damage.
T3 245-436 Sentence denotes In endothelial cells (EC), the transcription factor NF-κB is important in the switch from quiescence to activation, and is tightly controlled to avoid excessive inflammation and organ damage.
T4 437-516 Sentence denotes Here we describe a novel mechanism that controls the activation of NF-κB in EC.
T4 437-516 Sentence denotes Here we describe a novel mechanism that controls the activation of NF-κB in EC.
T5 517-665 Sentence denotes The transcription factor Erg, the most highly expressed ETS member in resting EC, controls quiescence by repressing proinflammatory gene expression.
T5 517-665 Sentence denotes The transcription factor Erg, the most highly expressed ETS member in resting EC, controls quiescence by repressing proinflammatory gene expression.
T6 666-850 Sentence denotes Focusing on intercellular adhesion molecule 1(ICAM)-1 as a model, we identify two ETS binding sites (EBS -118 and -181) within the ICAM-1 promoter required for Erg-mediated repression.
T6 666-850 Sentence denotes Focusing on intercellular adhesion molecule 1(ICAM)-1 as a model, we identify two ETS binding sites (EBS -118 and -181) within the ICAM-1 promoter required for Erg-mediated repression.
T7 851-954 Sentence denotes We show that Erg binds to both EBS -118 and EBS -181, the latter located within the NF-κB binding site.
T7 851-954 Sentence denotes We show that Erg binds to both EBS -118 and EBS -181, the latter located within the NF-κB binding site.
T8 955-1122 Sentence denotes Interestingly, inhibition of Erg expression in quiescent EC results in increased NF-κB-dependent ICAM-1 expression, indicating that Erg represses basal NF-κB activity.
T8 955-1122 Sentence denotes Interestingly, inhibition of Erg expression in quiescent EC results in increased NF-κB-dependent ICAM-1 expression, indicating that Erg represses basal NF-κB activity.
T9 1123-1229 Sentence denotes Erg prevents NF-κB p65 from binding to the ICAM-1 promoter, suggesting a direct mechanism of interference.
T9 1123-1229 Sentence denotes Erg prevents NF-κB p65 from binding to the ICAM-1 promoter, suggesting a direct mechanism of interference.
T10 1230-1475 Sentence denotes Gene set enrichment analysis of transcriptome profiles of Erg and NF-κB-dependent genes, together with chromatin immunoprecipitation (ChIP) studies, reveals that this mechanism is common to other proinflammatory genes, including cIAP-2 and IL-8.
T10 1230-1475 Sentence denotes Gene set enrichment analysis of transcriptome profiles of Erg and NF-κB-dependent genes, together with chromatin immunoprecipitation (ChIP) studies, reveals that this mechanism is common to other proinflammatory genes, including cIAP-2 and IL-8.
T11 1476-1657 Sentence denotes These results identify a role for Erg as a gatekeeper controlling vascular inflammation, thus providing an important barrier to protect against inappropriate endothelial activation.
T11 1476-1657 Sentence denotes These results identify a role for Erg as a gatekeeper controlling vascular inflammation, thus providing an important barrier to protect against inappropriate endothelial activation.