PubMed:10225377 JSONTXT

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    Inflammaging

    {"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":141},"obj":"Sentence"},{"id":"T2","span":{"begin":142,"end":247},"obj":"Sentence"},{"id":"T3","span":{"begin":248,"end":392},"obj":"Sentence"},{"id":"T4","span":{"begin":393,"end":584},"obj":"Sentence"},{"id":"T5","span":{"begin":585,"end":823},"obj":"Sentence"},{"id":"T6","span":{"begin":824,"end":943},"obj":"Sentence"},{"id":"T7","span":{"begin":944,"end":1085},"obj":"Sentence"},{"id":"T8","span":{"begin":1086,"end":1200},"obj":"Sentence"},{"id":"T9","span":{"begin":1201,"end":1264},"obj":"Sentence"},{"id":"T10","span":{"begin":1265,"end":1425},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":141},"obj":"Sentence"},{"id":"T2","span":{"begin":142,"end":247},"obj":"Sentence"},{"id":"T3","span":{"begin":248,"end":392},"obj":"Sentence"},{"id":"T4","span":{"begin":393,"end":584},"obj":"Sentence"},{"id":"T5","span":{"begin":585,"end":823},"obj":"Sentence"},{"id":"T6","span":{"begin":824,"end":943},"obj":"Sentence"},{"id":"T7","span":{"begin":944,"end":1085},"obj":"Sentence"},{"id":"T8","span":{"begin":1086,"end":1200},"obj":"Sentence"},{"id":"T9","span":{"begin":1201,"end":1264},"obj":"Sentence"},{"id":"T10","span":{"begin":1265,"end":1425},"obj":"Sentence"}],"text":"Activation of nuclear factor-kappaB by lipopolysaccharide in mononuclear leukocytes is prevented by inhibitors of cytosolic phospholipase A2.\nIn monocytes, lipopolysaccharide induces synthesis and activity of the 85-kDa cytosolic phospholipase A2. This enzyme releases arachidonic acid and lyso-phospholipids from membranes which are metabolized to eicosanoids and platelet-activating-factor. These lipid mediators increase activity of transcription factors and expression of cytokine genes indicating a function for cytosolic phospholipase A2 in signal transduction and inflammation. We have shown previously that trifluoromethylketone inhibitors of cytosolic phospholipase A2 suppressed interleukin-1beta protein and steady-state mRNA levels in human lipopolysaccharide-stimulated peripheral blood mononuclear leukocytes. In this study, the subcellular mechanisms were analyzed by which trifluoromethylketones interfere with gene expression. We found that they reduced the initial interleukin-1beta mRNA transcription rate through prevention of degradation of inhibitor-kappaB alpha. Consequently, cytosolic activation, nuclear translocation and DNA-binding of nuclear factor-kappaB were decreased. Trifluoromethylketones ameliorate chronic inflammation in vivo. Thus, this therapeutic potency may reside in retention of inactive nuclear factor-kappaB in the cytosol thereby abrogating interleukin-1beta gene transcription."}

    jnlpba-st-training

    {"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":14,"end":35},"obj":"protein"},{"id":"T2","span":{"begin":61,"end":83},"obj":"cell_type"},{"id":"T3","span":{"begin":114,"end":140},"obj":"protein"},{"id":"T4","span":{"begin":145,"end":154},"obj":"cell_type"},{"id":"T5","span":{"begin":220,"end":246},"obj":"protein"},{"id":"T6","span":{"begin":436,"end":457},"obj":"protein"},{"id":"T7","span":{"begin":476,"end":490},"obj":"DNA"},{"id":"T8","span":{"begin":517,"end":543},"obj":"protein"},{"id":"T9","span":{"begin":651,"end":677},"obj":"protein"},{"id":"T10","span":{"begin":753,"end":822},"obj":"cell_type"},{"id":"T11","span":{"begin":983,"end":1005},"obj":"RNA"},{"id":"T12","span":{"begin":1062,"end":1084},"obj":"protein"},{"id":"T13","span":{"begin":1163,"end":1184},"obj":"protein"},{"id":"T14","span":{"begin":1332,"end":1353},"obj":"protein"},{"id":"T15","span":{"begin":1361,"end":1368},"obj":"cell_type"},{"id":"T16","span":{"begin":1388,"end":1405},"obj":"protein"}],"text":"Activation of nuclear factor-kappaB by lipopolysaccharide in mononuclear leukocytes is prevented by inhibitors of cytosolic phospholipase A2.\nIn monocytes, lipopolysaccharide induces synthesis and activity of the 85-kDa cytosolic phospholipase A2. This enzyme releases arachidonic acid and lyso-phospholipids from membranes which are metabolized to eicosanoids and platelet-activating-factor. These lipid mediators increase activity of transcription factors and expression of cytokine genes indicating a function for cytosolic phospholipase A2 in signal transduction and inflammation. We have shown previously that trifluoromethylketone inhibitors of cytosolic phospholipase A2 suppressed interleukin-1beta protein and steady-state mRNA levels in human lipopolysaccharide-stimulated peripheral blood mononuclear leukocytes. In this study, the subcellular mechanisms were analyzed by which trifluoromethylketones interfere with gene expression. We found that they reduced the initial interleukin-1beta mRNA transcription rate through prevention of degradation of inhibitor-kappaB alpha. Consequently, cytosolic activation, nuclear translocation and DNA-binding of nuclear factor-kappaB were decreased. Trifluoromethylketones ameliorate chronic inflammation in vivo. Thus, this therapeutic potency may reside in retention of inactive nuclear factor-kappaB in the cytosol thereby abrogating interleukin-1beta gene transcription."}

    pubmed-sentences-benchmark

    {"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":141},"obj":"Sentence"},{"id":"S2","span":{"begin":142,"end":247},"obj":"Sentence"},{"id":"S3","span":{"begin":248,"end":392},"obj":"Sentence"},{"id":"S4","span":{"begin":393,"end":584},"obj":"Sentence"},{"id":"S5","span":{"begin":585,"end":823},"obj":"Sentence"},{"id":"S6","span":{"begin":824,"end":943},"obj":"Sentence"},{"id":"S7","span":{"begin":944,"end":1085},"obj":"Sentence"},{"id":"S8","span":{"begin":1086,"end":1200},"obj":"Sentence"},{"id":"S9","span":{"begin":1201,"end":1264},"obj":"Sentence"},{"id":"S10","span":{"begin":1265,"end":1425},"obj":"Sentence"}],"text":"Activation of nuclear factor-kappaB by lipopolysaccharide in mononuclear leukocytes is prevented by inhibitors of cytosolic phospholipase A2.\nIn monocytes, lipopolysaccharide induces synthesis and activity of the 85-kDa cytosolic phospholipase A2. This enzyme releases arachidonic acid and lyso-phospholipids from membranes which are metabolized to eicosanoids and platelet-activating-factor. These lipid mediators increase activity of transcription factors and expression of cytokine genes indicating a function for cytosolic phospholipase A2 in signal transduction and inflammation. We have shown previously that trifluoromethylketone inhibitors of cytosolic phospholipase A2 suppressed interleukin-1beta protein and steady-state mRNA levels in human lipopolysaccharide-stimulated peripheral blood mononuclear leukocytes. In this study, the subcellular mechanisms were analyzed by which trifluoromethylketones interfere with gene expression. We found that they reduced the initial interleukin-1beta mRNA transcription rate through prevention of degradation of inhibitor-kappaB alpha. Consequently, cytosolic activation, nuclear translocation and DNA-binding of nuclear factor-kappaB were decreased. Trifluoromethylketones ameliorate chronic inflammation in vivo. Thus, this therapeutic potency may reside in retention of inactive nuclear factor-kappaB in the cytosol thereby abrogating interleukin-1beta gene transcription."}

    genia-medco-coref

    {"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":14,"end":35},"obj":"NP"},{"id":"C2","span":{"begin":114,"end":140},"obj":"NP"},{"id":"C3","span":{"begin":213,"end":246},"obj":"NP"},{"id":"C4","span":{"begin":248,"end":259},"obj":"NP"},{"id":"C6","span":{"begin":314,"end":323},"obj":"NP"},{"id":"C7","span":{"begin":324,"end":329},"obj":"NP"},{"id":"C5","span":{"begin":269,"end":391},"obj":"NP"},{"id":"C8","span":{"begin":393,"end":414},"obj":"NP"},{"id":"C9","span":{"begin":517,"end":543},"obj":"NP"},{"id":"C10","span":{"begin":651,"end":677},"obj":"NP"},{"id":"C11","span":{"begin":839,"end":865},"obj":"NP"},{"id":"C12","span":{"begin":883,"end":888},"obj":"NP"},{"id":"C13","span":{"begin":889,"end":911},"obj":"NP"},{"id":"C14","span":{"begin":958,"end":962},"obj":"NP"},{"id":"C15","span":{"begin":1163,"end":1184},"obj":"NP"},{"id":"C16","span":{"begin":1201,"end":1223},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C3","obj":"C2"},{"id":"R2","pred":"coref-ident","subj":"C4","obj":"C3"},{"id":"R3","pred":"coref-relat","subj":"C7","obj":"C6"},{"id":"R4","pred":"coref-ident","subj":"C8","obj":"C5"},{"id":"R5","pred":"coref-ident","subj":"C9","obj":"C4"},{"id":"R6","pred":"coref-ident","subj":"C10","obj":"C9"},{"id":"R7","pred":"coref-relat","subj":"C12","obj":"C11"},{"id":"R8","pred":"coref-pron","subj":"C14","obj":"C13"},{"id":"R9","pred":"coref-ident","subj":"C15","obj":"C1"},{"id":"R10","pred":"coref-ident","subj":"C16","obj":"C13"}],"text":"Activation of nuclear factor-kappaB by lipopolysaccharide in mononuclear leukocytes is prevented by inhibitors of cytosolic phospholipase A2.\nIn monocytes, lipopolysaccharide induces synthesis and activity of the 85-kDa cytosolic phospholipase A2. This enzyme releases arachidonic acid and lyso-phospholipids from membranes which are metabolized to eicosanoids and platelet-activating-factor. These lipid mediators increase activity of transcription factors and expression of cytokine genes indicating a function for cytosolic phospholipase A2 in signal transduction and inflammation. We have shown previously that trifluoromethylketone inhibitors of cytosolic phospholipase A2 suppressed interleukin-1beta protein and steady-state mRNA levels in human lipopolysaccharide-stimulated peripheral blood mononuclear leukocytes. In this study, the subcellular mechanisms were analyzed by which trifluoromethylketones interfere with gene expression. We found that they reduced the initial interleukin-1beta mRNA transcription rate through prevention of degradation of inhibitor-kappaB alpha. Consequently, cytosolic activation, nuclear translocation and DNA-binding of nuclear factor-kappaB were decreased. Trifluoromethylketones ameliorate chronic inflammation in vivo. Thus, this therapeutic potency may reside in retention of inactive nuclear factor-kappaB in the cytosol thereby abrogating interleukin-1beta gene transcription."}

    GENIAcorpus

    {"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":14,"end":35},"obj":"protein_complex"},{"id":"T2","span":{"begin":39,"end":57},"obj":"lipid"},{"id":"T3","span":{"begin":61,"end":83},"obj":"cell_type"},{"id":"T4","span":{"begin":114,"end":140},"obj":"protein_molecule"},{"id":"T5","span":{"begin":145,"end":154},"obj":"cell_type"},{"id":"T6","span":{"begin":156,"end":174},"obj":"lipid"},{"id":"T7","span":{"begin":220,"end":246},"obj":"protein_molecule"},{"id":"T8","span":{"begin":269,"end":285},"obj":"other_organic_compound"},{"id":"T9","span":{"begin":290,"end":308},"obj":"lipid"},{"id":"T10","span":{"begin":349,"end":360},"obj":"other_organic_compound"},{"id":"T11","span":{"begin":365,"end":391},"obj":"other_organic_compound"},{"id":"T12","span":{"begin":436,"end":457},"obj":"protein_family_or_group"},{"id":"T13","span":{"begin":476,"end":490},"obj":"DNA_family_or_group"},{"id":"T14","span":{"begin":517,"end":543},"obj":"protein_molecule"},{"id":"T15","span":{"begin":547,"end":566},"obj":"other_name"},{"id":"T16","span":{"begin":571,"end":583},"obj":"other_name"},{"id":"T17","span":{"begin":615,"end":647},"obj":"other_organic_compound"},{"id":"T18","span":{"begin":651,"end":677},"obj":"protein_molecule"},{"id":"T19","span":{"begin":719,"end":743},"obj":"other_name"},{"id":"T20","span":{"begin":753,"end":771},"obj":"lipid"},{"id":"T21","span":{"begin":800,"end":822},"obj":"cell_type"},{"id":"T22","span":{"begin":843,"end":865},"obj":"other_name"},{"id":"T23","span":{"begin":889,"end":911},"obj":"other_organic_compound"},{"id":"T24","span":{"begin":927,"end":942},"obj":"other_organic_compound"},{"id":"T25","span":{"begin":983,"end":1005},"obj":"RNA_family_or_group"},{"id":"T26","span":{"begin":1062,"end":1084},"obj":"protein_molecule"},{"id":"T27","span":{"begin":1100,"end":1120},"obj":"other_name"},{"id":"T28","span":{"begin":1122,"end":1143},"obj":"other_name"},{"id":"T29","span":{"begin":1163,"end":1184},"obj":"protein_complex"},{"id":"T30","span":{"begin":1201,"end":1223},"obj":"other_organic_compound"},{"id":"T31","span":{"begin":1235,"end":1242},"obj":"other_name"},{"id":"T32","span":{"begin":1243,"end":1255},"obj":"other_name"},{"id":"T33","span":{"begin":1332,"end":1353},"obj":"protein_complex"},{"id":"T34","span":{"begin":1361,"end":1368},"obj":"cell_type"},{"id":"T35","span":{"begin":1388,"end":1405},"obj":"protein_molecule"}],"text":"Activation of nuclear factor-kappaB by lipopolysaccharide in mononuclear leukocytes is prevented by inhibitors of cytosolic phospholipase A2.\nIn monocytes, lipopolysaccharide induces synthesis and activity of the 85-kDa cytosolic phospholipase A2. This enzyme releases arachidonic acid and lyso-phospholipids from membranes which are metabolized to eicosanoids and platelet-activating-factor. These lipid mediators increase activity of transcription factors and expression of cytokine genes indicating a function for cytosolic phospholipase A2 in signal transduction and inflammation. We have shown previously that trifluoromethylketone inhibitors of cytosolic phospholipase A2 suppressed interleukin-1beta protein and steady-state mRNA levels in human lipopolysaccharide-stimulated peripheral blood mononuclear leukocytes. In this study, the subcellular mechanisms were analyzed by which trifluoromethylketones interfere with gene expression. We found that they reduced the initial interleukin-1beta mRNA transcription rate through prevention of degradation of inhibitor-kappaB alpha. Consequently, cytosolic activation, nuclear translocation and DNA-binding of nuclear factor-kappaB were decreased. Trifluoromethylketones ameliorate chronic inflammation in vivo. Thus, this therapeutic potency may reside in retention of inactive nuclear factor-kappaB in the cytosol thereby abrogating interleukin-1beta gene transcription."}