PubMed:7929104 JSON TXT

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sentences

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":135},"obj":"Sentence"},{"id":"T2","span":{"begin":136,"end":182},"obj":"Sentence"},{"id":"T3","span":{"begin":183,"end":359},"obj":"Sentence"},{"id":"T4","span":{"begin":360,"end":495},"obj":"Sentence"},{"id":"T5","span":{"begin":496,"end":731},"obj":"Sentence"},{"id":"T6","span":{"begin":732,"end":953},"obj":"Sentence"},{"id":"T7","span":{"begin":954,"end":1090},"obj":"Sentence"},{"id":"T8","span":{"begin":1091,"end":1260},"obj":"Sentence"},{"id":"T9","span":{"begin":1261,"end":1513},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":135},"obj":"Sentence"},{"id":"T2","span":{"begin":136,"end":182},"obj":"Sentence"},{"id":"T3","span":{"begin":183,"end":359},"obj":"Sentence"},{"id":"T4","span":{"begin":360,"end":495},"obj":"Sentence"},{"id":"T5","span":{"begin":496,"end":731},"obj":"Sentence"},{"id":"T6","span":{"begin":732,"end":953},"obj":"Sentence"},{"id":"T7","span":{"begin":954,"end":1090},"obj":"Sentence"},{"id":"T8","span":{"begin":1091,"end":1260},"obj":"Sentence"},{"id":"T9","span":{"begin":1261,"end":1513},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Regulation of interleukin-2 receptor alpha chain expression and nuclear factor.kappa B activation by protein kinase C in T lymphocytes. Autocrine role of tumor necrosis factor alpha.\nThe regulation of interleukin-2 receptor alpha chain (IL-2R alpha) expression and nuclear factor (NF) activation by protein kinase C (PKC) in resting T cells, has been studied. Treatment of human resting T cells with phorbol esters strongly induced the expression of IL-2R alpha and the activation of NF.kappa B. This activation was due to the translocation of p65 and c-Rel NF.kappa B proteins from cytoplasmic stores to the nucleus, where they bound the kappa B sequence of the IL-2R alpha promoter either as p50.p65 or as p50.c-Rel heterodimers. Interestingly, all of those events were largely indirect and mediated by endogenously secreted tumor necrosis factor alpha (TNF alpha), as they were strongly inhibited by a neutralizing anti-TNF alpha monoclonal antibody. Furthermore, cyclosporin A, which blocked TNF alpha production induced by PKC, strongly inhibited IL-2R alpha and NF.kappa B activation. The addition of either TNF alpha or IL-2 partially recovered cyclosporin A-induced IL-2R alpha inhibition, but only TNF alpha completely recovered NF.kappa B activation. Those results indicate that, in resting T cells, PKC activation has only a triggering role, whereas the endogenously secreted TNF alpha plays an essential role in the quantitative control of the expression of IL-2R alpha chain or NF.kappa B activation."}

jnlpba-st-training

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":14,"end":48},"obj":"protein"},{"id":"T2","span":{"begin":64,"end":86},"obj":"protein"},{"id":"T3","span":{"begin":101,"end":117},"obj":"protein"},{"id":"T4","span":{"begin":121,"end":134},"obj":"cell_type"},{"id":"T5","span":{"begin":154,"end":181},"obj":"protein"},{"id":"T6","span":{"begin":201,"end":235},"obj":"protein"},{"id":"T7","span":{"begin":237,"end":248},"obj":"protein"},{"id":"T8","span":{"begin":265,"end":279},"obj":"protein"},{"id":"T9","span":{"begin":299,"end":315},"obj":"protein"},{"id":"T10","span":{"begin":317,"end":320},"obj":"protein"},{"id":"T11","span":{"begin":325,"end":340},"obj":"cell_type"},{"id":"T12","span":{"begin":379,"end":394},"obj":"cell_type"},{"id":"T13","span":{"begin":450,"end":461},"obj":"protein"},{"id":"T14","span":{"begin":484,"end":494},"obj":"protein"},{"id":"T15","span":{"begin":544,"end":547},"obj":"protein"},{"id":"T16","span":{"begin":552,"end":557},"obj":"protein"},{"id":"T17","span":{"begin":558,"end":568},"obj":"protein"},{"id":"T18","span":{"begin":639,"end":655},"obj":"DNA"},{"id":"T19","span":{"begin":663,"end":683},"obj":"DNA"},{"id":"T20","span":{"begin":694,"end":701},"obj":"protein"},{"id":"T21","span":{"begin":708,"end":717},"obj":"protein"},{"id":"T22","span":{"begin":827,"end":854},"obj":"protein"},{"id":"T23","span":{"begin":856,"end":865},"obj":"protein"},{"id":"T24","span":{"begin":905,"end":952},"obj":"protein"},{"id":"T25","span":{"begin":996,"end":1005},"obj":"protein"},{"id":"T26","span":{"begin":1028,"end":1031},"obj":"protein"},{"id":"T27","span":{"begin":1052,"end":1063},"obj":"protein"},{"id":"T28","span":{"begin":1068,"end":1078},"obj":"protein"},{"id":"T29","span":{"begin":1114,"end":1123},"obj":"protein"},{"id":"T30","span":{"begin":1127,"end":1131},"obj":"protein"},{"id":"T31","span":{"begin":1174,"end":1185},"obj":"protein"},{"id":"T32","span":{"begin":1207,"end":1216},"obj":"protein"},{"id":"T33","span":{"begin":1238,"end":1248},"obj":"protein"},{"id":"T34","span":{"begin":1293,"end":1308},"obj":"cell_type"},{"id":"T35","span":{"begin":1310,"end":1313},"obj":"protein"},{"id":"T36","span":{"begin":1387,"end":1396},"obj":"protein"},{"id":"T37","span":{"begin":1470,"end":1481},"obj":"protein"},{"id":"T38","span":{"begin":1491,"end":1501},"obj":"protein"}],"text":"Regulation of interleukin-2 receptor alpha chain expression and nuclear factor.kappa B activation by protein kinase C in T lymphocytes. Autocrine role of tumor necrosis factor alpha.\nThe regulation of interleukin-2 receptor alpha chain (IL-2R alpha) expression and nuclear factor (NF) activation by protein kinase C (PKC) in resting T cells, has been studied. Treatment of human resting T cells with phorbol esters strongly induced the expression of IL-2R alpha and the activation of NF.kappa B. This activation was due to the translocation of p65 and c-Rel NF.kappa B proteins from cytoplasmic stores to the nucleus, where they bound the kappa B sequence of the IL-2R alpha promoter either as p50.p65 or as p50.c-Rel heterodimers. Interestingly, all of those events were largely indirect and mediated by endogenously secreted tumor necrosis factor alpha (TNF alpha), as they were strongly inhibited by a neutralizing anti-TNF alpha monoclonal antibody. Furthermore, cyclosporin A, which blocked TNF alpha production induced by PKC, strongly inhibited IL-2R alpha and NF.kappa B activation. The addition of either TNF alpha or IL-2 partially recovered cyclosporin A-induced IL-2R alpha inhibition, but only TNF alpha completely recovered NF.kappa B activation. Those results indicate that, in resting T cells, PKC activation has only a triggering role, whereas the endogenously secreted TNF alpha plays an essential role in the quantitative control of the expression of IL-2R alpha chain or NF.kappa B activation."}

genia-medco-coref

pubmed-sentences-benchmark

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":135},"obj":"Sentence"},{"id":"S2","span":{"begin":136,"end":182},"obj":"Sentence"},{"id":"S3","span":{"begin":183,"end":359},"obj":"Sentence"},{"id":"S4","span":{"begin":360,"end":495},"obj":"Sentence"},{"id":"S5","span":{"begin":496,"end":731},"obj":"Sentence"},{"id":"S6","span":{"begin":732,"end":953},"obj":"Sentence"},{"id":"S7","span":{"begin":954,"end":1090},"obj":"Sentence"},{"id":"S8","span":{"begin":1091,"end":1260},"obj":"Sentence"},{"id":"S9","span":{"begin":1261,"end":1513},"obj":"Sentence"}],"text":"Regulation of interleukin-2 receptor alpha chain expression and nuclear factor.kappa B activation by protein kinase C in T lymphocytes. Autocrine role of tumor necrosis factor alpha.\nThe regulation of interleukin-2 receptor alpha chain (IL-2R alpha) expression and nuclear factor (NF) activation by protein kinase C (PKC) in resting T cells, has been studied. Treatment of human resting T cells with phorbol esters strongly induced the expression of IL-2R alpha and the activation of NF.kappa B. This activation was due to the translocation of p65 and c-Rel NF.kappa B proteins from cytoplasmic stores to the nucleus, where they bound the kappa B sequence of the IL-2R alpha promoter either as p50.p65 or as p50.c-Rel heterodimers. Interestingly, all of those events were largely indirect and mediated by endogenously secreted tumor necrosis factor alpha (TNF alpha), as they were strongly inhibited by a neutralizing anti-TNF alpha monoclonal antibody. Furthermore, cyclosporin A, which blocked TNF alpha production induced by PKC, strongly inhibited IL-2R alpha and NF.kappa B activation. The addition of either TNF alpha or IL-2 partially recovered cyclosporin A-induced IL-2R alpha inhibition, but only TNF alpha completely recovered NF.kappa B activation. Those results indicate that, in resting T cells, PKC activation has only a triggering role, whereas the endogenously secreted TNF alpha plays an essential role in the quantitative control of the expression of IL-2R alpha chain or NF.kappa B activation."}

GENIAcorpus

mondo_disease

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":154,"end":159},"obj":"Disease"},{"id":"T2","span":{"begin":827,"end":832},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0005070"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0005070"}],"text":"Regulation of interleukin-2 receptor alpha chain expression and nuclear factor.kappa B activation by protein kinase C in T lymphocytes. Autocrine role of tumor necrosis factor alpha.\nThe regulation of interleukin-2 receptor alpha chain (IL-2R alpha) expression and nuclear factor (NF) activation by protein kinase C (PKC) in resting T cells, has been studied. Treatment of human resting T cells with phorbol esters strongly induced the expression of IL-2R alpha and the activation of NF.kappa B. This activation was due to the translocation of p65 and c-Rel NF.kappa B proteins from cytoplasmic stores to the nucleus, where they bound the kappa B sequence of the IL-2R alpha promoter either as p50.p65 or as p50.c-Rel heterodimers. Interestingly, all of those events were largely indirect and mediated by endogenously secreted tumor necrosis factor alpha (TNF alpha), as they were strongly inhibited by a neutralizing anti-TNF alpha monoclonal antibody. Furthermore, cyclosporin A, which blocked TNF alpha production induced by PKC, strongly inhibited IL-2R alpha and NF.kappa B activation. The addition of either TNF alpha or IL-2 partially recovered cyclosporin A-induced IL-2R alpha inhibition, but only TNF alpha completely recovered NF.kappa B activation. Those results indicate that, in resting T cells, PKC activation has only a triggering role, whereas the endogenously secreted TNF alpha plays an essential role in the quantitative control of the expression of IL-2R alpha chain or NF.kappa B activation."}

NCBITAXON

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":373,"end":378},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"}],"text":"Regulation of interleukin-2 receptor alpha chain expression and nuclear factor.kappa B activation by protein kinase C in T lymphocytes. Autocrine role of tumor necrosis factor alpha.\nThe regulation of interleukin-2 receptor alpha chain (IL-2R alpha) expression and nuclear factor (NF) activation by protein kinase C (PKC) in resting T cells, has been studied. Treatment of human resting T cells with phorbol esters strongly induced the expression of IL-2R alpha and the activation of NF.kappa B. This activation was due to the translocation of p65 and c-Rel NF.kappa B proteins from cytoplasmic stores to the nucleus, where they bound the kappa B sequence of the IL-2R alpha promoter either as p50.p65 or as p50.c-Rel heterodimers. Interestingly, all of those events were largely indirect and mediated by endogenously secreted tumor necrosis factor alpha (TNF alpha), as they were strongly inhibited by a neutralizing anti-TNF alpha monoclonal antibody. Furthermore, cyclosporin A, which blocked TNF alpha production induced by PKC, strongly inhibited IL-2R alpha and NF.kappa B activation. The addition of either TNF alpha or IL-2 partially recovered cyclosporin A-induced IL-2R alpha inhibition, but only TNF alpha completely recovered NF.kappa B activation. Those results indicate that, in resting T cells, PKC activation has only a triggering role, whereas the endogenously secreted TNF alpha plays an essential role in the quantitative control of the expression of IL-2R alpha chain or NF.kappa B activation."}

Anatomy-UBERON

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":121,"end":134},"obj":"Body_part"},{"id":"T2","span":{"begin":583,"end":594},"obj":"Body_part"},{"id":"T3","span":{"begin":609,"end":616},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/GO_0005737"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/GO_0005634"},{"id":"A4","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0000125"}],"text":"Regulation of interleukin-2 receptor alpha chain expression and nuclear factor.kappa B activation by protein kinase C in T lymphocytes. Autocrine role of tumor necrosis factor alpha.\nThe regulation of interleukin-2 receptor alpha chain (IL-2R alpha) expression and nuclear factor (NF) activation by protein kinase C (PKC) in resting T cells, has been studied. Treatment of human resting T cells with phorbol esters strongly induced the expression of IL-2R alpha and the activation of NF.kappa B. This activation was due to the translocation of p65 and c-Rel NF.kappa B proteins from cytoplasmic stores to the nucleus, where they bound the kappa B sequence of the IL-2R alpha promoter either as p50.p65 or as p50.c-Rel heterodimers. Interestingly, all of those events were largely indirect and mediated by endogenously secreted tumor necrosis factor alpha (TNF alpha), as they were strongly inhibited by a neutralizing anti-TNF alpha monoclonal antibody. Furthermore, cyclosporin A, which blocked TNF alpha production induced by PKC, strongly inhibited IL-2R alpha and NF.kappa B activation. The addition of either TNF alpha or IL-2 partially recovered cyclosporin A-induced IL-2R alpha inhibition, but only TNF alpha completely recovered NF.kappa B activation. Those results indicate that, in resting T cells, PKC activation has only a triggering role, whereas the endogenously secreted TNF alpha plays an essential role in the quantitative control of the expression of IL-2R alpha chain or NF.kappa B activation."}

HP-phenotype

{"project":"HP-phenotype","denotations":[{"id":"T1","span":{"begin":154,"end":159},"obj":"Phenotype"},{"id":"T2","span":{"begin":827,"end":832},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0002664"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0002664"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"Regulation of interleukin-2 receptor alpha chain expression and nuclear factor.kappa B activation by protein kinase C in T lymphocytes. Autocrine role of tumor necrosis factor alpha.\nThe regulation of interleukin-2 receptor alpha chain (IL-2R alpha) expression and nuclear factor (NF) activation by protein kinase C (PKC) in resting T cells, has been studied. Treatment of human resting T cells with phorbol esters strongly induced the expression of IL-2R alpha and the activation of NF.kappa B. This activation was due to the translocation of p65 and c-Rel NF.kappa B proteins from cytoplasmic stores to the nucleus, where they bound the kappa B sequence of the IL-2R alpha promoter either as p50.p65 or as p50.c-Rel heterodimers. Interestingly, all of those events were largely indirect and mediated by endogenously secreted tumor necrosis factor alpha (TNF alpha), as they were strongly inhibited by a neutralizing anti-TNF alpha monoclonal antibody. Furthermore, cyclosporin A, which blocked TNF alpha production induced by PKC, strongly inhibited IL-2R alpha and NF.kappa B activation. The addition of either TNF alpha or IL-2 partially recovered cyclosporin A-induced IL-2R alpha inhibition, but only TNF alpha completely recovered NF.kappa B activation. Those results indicate that, in resting T cells, PKC activation has only a triggering role, whereas the endogenously secreted TNF alpha plays an essential role in the quantitative control of the expression of IL-2R alpha chain or NF.kappa B activation."}

CL-cell

{"project":"CL-cell","denotations":[{"id":"T1","span":{"begin":121,"end":134},"obj":"Cell"},{"id":"T2","span":{"begin":333,"end":340},"obj":"Cell"},{"id":"T3","span":{"begin":387,"end":394},"obj":"Cell"},{"id":"T4","span":{"begin":1301,"end":1308},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A3","pred":"cl_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A4","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0000084"}],"text":"Regulation of interleukin-2 receptor alpha chain expression and nuclear factor.kappa B activation by protein kinase C in T lymphocytes. Autocrine role of tumor necrosis factor alpha.\nThe regulation of interleukin-2 receptor alpha chain (IL-2R alpha) expression and nuclear factor (NF) activation by protein kinase C (PKC) in resting T cells, has been studied. Treatment of human resting T cells with phorbol esters strongly induced the expression of IL-2R alpha and the activation of NF.kappa B. This activation was due to the translocation of p65 and c-Rel NF.kappa B proteins from cytoplasmic stores to the nucleus, where they bound the kappa B sequence of the IL-2R alpha promoter either as p50.p65 or as p50.c-Rel heterodimers. Interestingly, all of those events were largely indirect and mediated by endogenously secreted tumor necrosis factor alpha (TNF alpha), as they were strongly inhibited by a neutralizing anti-TNF alpha monoclonal antibody. Furthermore, cyclosporin A, which blocked TNF alpha production induced by PKC, strongly inhibited IL-2R alpha and NF.kappa B activation. The addition of either TNF alpha or IL-2 partially recovered cyclosporin A-induced IL-2R alpha inhibition, but only TNF alpha completely recovered NF.kappa B activation. Those results indicate that, in resting T cells, PKC activation has only a triggering role, whereas the endogenously secreted TNF alpha plays an essential role in the quantitative control of the expression of IL-2R alpha chain or NF.kappa B activation."}