PubMed:9973402 JSONTXT

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":27,"end":36},"obj":"DNA"},{"id":"T2","span":{"begin":51,"end":66},"obj":"cell_type"},{"id":"T3","span":{"begin":120,"end":124},"obj":"protein"},{"id":"T4","span":{"begin":214,"end":236},"obj":"cell_type"},{"id":"T5","span":{"begin":240,"end":269},"obj":"cell_type"},{"id":"T6","span":{"begin":287,"end":300},"obj":"cell_line"},{"id":"T7","span":{"begin":383,"end":399},"obj":"RNA"},{"id":"T8","span":{"begin":456,"end":465},"obj":"DNA"},{"id":"T9","span":{"begin":484,"end":497},"obj":"cell_line"},{"id":"T10","span":{"begin":522,"end":544},"obj":"cell_type"},{"id":"T11","span":{"begin":548,"end":569},"obj":"cell_type"},{"id":"T12","span":{"begin":596,"end":622},"obj":"protein"},{"id":"T13","span":{"begin":681,"end":684},"obj":"protein"},{"id":"T14","span":{"begin":689,"end":698},"obj":"protein"},{"id":"T15","span":{"begin":724,"end":740},"obj":"protein"},{"id":"T16","span":{"begin":906,"end":940},"obj":"protein"},{"id":"T17","span":{"begin":982,"end":991},"obj":"DNA"},{"id":"T18","span":{"begin":1006,"end":1021},"obj":"cell_type"}],"text":"Evidence for repression of IL-2 gene activation in anergic T cells.\nThe induction of clonal anergy in a T cell inhibits IL-2 secretion because of the development of a proximal signal transduction defect. Fusion of anergic murine T cells to human Jurkat T leukemia cells and formation of heterokaryons failed to result in a complementation of this signaling defect and restoration of murine IL-2 mRNA inducibility. Instead, signal transduction to the human IL-2 gene became disrupted. Heterokaryons formed by the fusion of anergic murine T cells to normal murine T cells also failed to accumulate intracellular IL-2 protein in response to stimulation either with the combination of CD3 and CD28 mAbs or with ionomycin plus a protein kinase C-activating phorbol ester. The results argue against a loss-of-function signaling defect as the sole basis for clonal anergy induction and document the presence of a dominant-acting repressor molecule that inhibits signal transduction to the IL-2 gene within viable anergic T cells."}

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":67},"obj":"Sentence"},{"id":"S2","span":{"begin":68,"end":203},"obj":"Sentence"},{"id":"S3","span":{"begin":204,"end":413},"obj":"Sentence"},{"id":"S4","span":{"begin":414,"end":483},"obj":"Sentence"},{"id":"S5","span":{"begin":484,"end":766},"obj":"Sentence"},{"id":"S6","span":{"begin":767,"end":1022},"obj":"Sentence"}],"text":"Evidence for repression of IL-2 gene activation in anergic T cells.\nThe induction of clonal anergy in a T cell inhibits IL-2 secretion because of the development of a proximal signal transduction defect. Fusion of anergic murine T cells to human Jurkat T leukemia cells and formation of heterokaryons failed to result in a complementation of this signaling defect and restoration of murine IL-2 mRNA inducibility. Instead, signal transduction to the human IL-2 gene became disrupted. Heterokaryons formed by the fusion of anergic murine T cells to normal murine T cells also failed to accumulate intracellular IL-2 protein in response to stimulation either with the combination of CD3 and CD28 mAbs or with ionomycin plus a protein kinase C-activating phorbol ester. The results argue against a loss-of-function signaling defect as the sole basis for clonal anergy induction and document the presence of a dominant-acting repressor molecule that inhibits signal transduction to the IL-2 gene within viable anergic T cells."}

{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":214,"end":236},"obj":"NP"},{"id":"C2","span":{"begin":446,"end":465},"obj":"NP"},{"id":"C3","span":{"begin":522,"end":544},"obj":"NP"},{"id":"C4","span":{"begin":904,"end":940},"obj":"NP"},{"id":"C5","span":{"begin":941,"end":945},"obj":"NP"},{"id":"C6","span":{"begin":978,"end":991},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C3","obj":"C1"},{"id":"R2","pred":"coref-relat","subj":"C5","obj":"C4"},{"id":"R3","pred":"coref-ident","subj":"C6","obj":"C2"}],"text":"Evidence for repression of IL-2 gene activation in anergic T cells.\nThe induction of clonal anergy in a T cell inhibits IL-2 secretion because of the development of a proximal signal transduction defect. Fusion of anergic murine T cells to human Jurkat T leukemia cells and formation of heterokaryons failed to result in a complementation of this signaling defect and restoration of murine IL-2 mRNA inducibility. Instead, signal transduction to the human IL-2 gene became disrupted. Heterokaryons formed by the fusion of anergic murine T cells to normal murine T cells also failed to accumulate intracellular IL-2 protein in response to stimulation either with the combination of CD3 and CD28 mAbs or with ionomycin plus a protein kinase C-activating phorbol ester. The results argue against a loss-of-function signaling defect as the sole basis for clonal anergy induction and document the presence of a dominant-acting repressor molecule that inhibits signal transduction to the IL-2 gene within viable anergic T cells."}

{"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":27,"end":36},"obj":"DNA_domain_or_region"},{"id":"T2","span":{"begin":51,"end":66},"obj":"cell_type"},{"id":"T3","span":{"begin":85,"end":98},"obj":"other_name"},{"id":"T4","span":{"begin":120,"end":124},"obj":"protein_molecule"},{"id":"T5","span":{"begin":167,"end":202},"obj":"other_name"},{"id":"T6","span":{"begin":214,"end":236},"obj":"cell_type"},{"id":"T7","span":{"begin":240,"end":269},"obj":"cell_type"},{"id":"T8","span":{"begin":287,"end":300},"obj":"cell_line"},{"id":"T9","span":{"begin":383,"end":399},"obj":"RNA_molecule"},{"id":"T10","span":{"begin":456,"end":465},"obj":"DNA_domain_or_region"},{"id":"T11","span":{"begin":484,"end":497},"obj":"cell_line"},{"id":"T12","span":{"begin":522,"end":544},"obj":"cell_type"},{"id":"T13","span":{"begin":548,"end":569},"obj":"cell_type"},{"id":"T14","span":{"begin":596,"end":622},"obj":"protein_molecule"},{"id":"T15","span":{"begin":681,"end":684},"obj":"protein_family_or_group"},{"id":"T16","span":{"begin":689,"end":698},"obj":"protein_family_or_group"},{"id":"T17","span":{"begin":707,"end":716},"obj":"other_organic_compound"},{"id":"T18","span":{"begin":724,"end":740},"obj":"protein_molecule"},{"id":"T19","span":{"begin":851,"end":864},"obj":"other_name"},{"id":"T20","span":{"begin":906,"end":940},"obj":"protein_family_or_group"},{"id":"T21","span":{"begin":982,"end":991},"obj":"DNA_domain_or_region"},{"id":"T22","span":{"begin":1006,"end":1021},"obj":"cell_type"}],"text":"Evidence for repression of IL-2 gene activation in anergic T cells.\nThe induction of clonal anergy in a T cell inhibits IL-2 secretion because of the development of a proximal signal transduction defect. Fusion of anergic murine T cells to human Jurkat T leukemia cells and formation of heterokaryons failed to result in a complementation of this signaling defect and restoration of murine IL-2 mRNA inducibility. Instead, signal transduction to the human IL-2 gene became disrupted. Heterokaryons formed by the fusion of anergic murine T cells to normal murine T cells also failed to accumulate intracellular IL-2 protein in response to stimulation either with the combination of CD3 and CD28 mAbs or with ionomycin plus a protein kinase C-activating phorbol ester. The results argue against a loss-of-function signaling defect as the sole basis for clonal anergy induction and document the presence of a dominant-acting repressor molecule that inhibits signal transduction to the IL-2 gene within viable anergic T cells."}