PubMed:7643015 JSONTXT

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    jnlpba-st-training

    {"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":37,"end":46},"obj":"protein"},{"id":"T2","span":{"begin":69,"end":73},"obj":"protein"},{"id":"T3","span":{"begin":78,"end":83},"obj":"protein"},{"id":"T4","span":{"begin":89,"end":107},"obj":"cell_line"},{"id":"T5","span":{"begin":109,"end":125},"obj":"protein"},{"id":"T6","span":{"begin":127,"end":136},"obj":"protein"},{"id":"T7","span":{"begin":154,"end":178},"obj":"protein"},{"id":"T8","span":{"begin":205,"end":212},"obj":"cell_type"},{"id":"T9","span":{"begin":217,"end":243},"obj":"cell_type"},{"id":"T10","span":{"begin":245,"end":248},"obj":"cell_type"},{"id":"T11","span":{"begin":317,"end":329},"obj":"protein"},{"id":"T12","span":{"begin":331,"end":334},"obj":"protein"},{"id":"T13","span":{"begin":337,"end":341},"obj":"protein"},{"id":"T14","span":{"begin":346,"end":351},"obj":"protein"},{"id":"T15","span":{"begin":394,"end":403},"obj":"protein"},{"id":"T16","span":{"begin":428,"end":435},"obj":"cell_type"},{"id":"T17","span":{"begin":440,"end":443},"obj":"cell_type"},{"id":"T18","span":{"begin":495,"end":507},"obj":"cell_line"},{"id":"T19","span":{"begin":521,"end":530},"obj":"protein"},{"id":"T20","span":{"begin":611,"end":640},"obj":"cell_line"},{"id":"T21","span":{"begin":720,"end":735},"obj":"cell_line"},{"id":"T22","span":{"begin":749,"end":763},"obj":"cell_type"},{"id":"T23","span":{"begin":782,"end":786},"obj":"protein"},{"id":"T24","span":{"begin":791,"end":796},"obj":"protein"},{"id":"T25","span":{"begin":826,"end":835},"obj":"protein"},{"id":"T26","span":{"begin":840,"end":888},"obj":"protein"},{"id":"T27","span":{"begin":890,"end":896},"obj":"protein"},{"id":"T28","span":{"begin":971,"end":975},"obj":"protein"},{"id":"T29","span":{"begin":980,"end":985},"obj":"protein"},{"id":"T30","span":{"begin":1017,"end":1026},"obj":"protein"},{"id":"T31","span":{"begin":1031,"end":1037},"obj":"protein"},{"id":"T32","span":{"begin":1120,"end":1146},"obj":"RNA"},{"id":"T33","span":{"begin":1256,"end":1287},"obj":"protein"},{"id":"T34","span":{"begin":1374,"end":1378},"obj":"protein"},{"id":"T35","span":{"begin":1383,"end":1388},"obj":"protein"},{"id":"T36","span":{"begin":1392,"end":1403},"obj":"cell_line"},{"id":"T37","span":{"begin":1444,"end":1460},"obj":"protein"},{"id":"T38","span":{"begin":1509,"end":1513},"obj":"protein"},{"id":"T39","span":{"begin":1527,"end":1564},"obj":"RNA"},{"id":"T40","span":{"begin":1579,"end":1584},"obj":"protein"},{"id":"T41","span":{"begin":1598,"end":1624},"obj":"RNA"},{"id":"T42","span":{"begin":1675,"end":1691},"obj":"protein"},{"id":"T43","span":{"begin":1711,"end":1742},"obj":"protein"},{"id":"T44","span":{"begin":1802,"end":1806},"obj":"protein"},{"id":"T45","span":{"begin":1811,"end":1816},"obj":"protein"},{"id":"T46","span":{"begin":1900,"end":1913},"obj":"DNA"},{"id":"T47","span":{"begin":2006,"end":2010},"obj":"protein"},{"id":"T48","span":{"begin":2019,"end":2024},"obj":"protein"},{"id":"T49","span":{"begin":2033,"end":2048},"obj":"protein"},{"id":"T50","span":{"begin":2049,"end":2059},"obj":"protein"},{"id":"T51","span":{"begin":2064,"end":2067},"obj":"protein"},{"id":"T52","span":{"begin":2119,"end":2148},"obj":"protein"},{"id":"T53","span":{"begin":2231,"end":2235},"obj":"protein"},{"id":"T54","span":{"begin":2240,"end":2245},"obj":"protein"},{"id":"T55","span":{"begin":2311,"end":2320},"obj":"protein"},{"id":"T56","span":{"begin":2325,"end":2331},"obj":"protein"},{"id":"T57","span":{"begin":2362,"end":2377},"obj":"cell_line"}],"text":"Cellular and molecular mechanisms of IFN-gamma production induced by IL-2 and IL-12 in a human NK cell line.\nInterferon-gamma (IFN-gamma) is an important immunoregulatory protein produced predominantly by T cells and large granular lymphocytes (LGL) in response to different extracellular signals. In particular, two interleukins (ILs), IL-2 and IL-12, have been shown to be potent inducers of IFN-gamma gene expression in both T cells and LGL. Although it has been reported that there are some T cell lines that produce IFN-gamma in response to IL-2 and IL-12 stimulation, there has as yet been no report of a natural killer (NK) cell line that responds in a similar manner. In this report we present evidence that the cell line NK3.3 derived from human NK cells, responds to both IL-2 and IL-12, as measured by increases in IFN-gamma and granulocyte-macrophage colony-stimulating factor (GM-CSF) cytoplasmic mRNA and protein expression. In addition, when used together IL-2 and IL-12 synergized in the induction of IFN-gamma and GM-CSF and this synergy was attributed to an increased accumulation and stability of the IFN-gamma and GM-CSF mRNAs. To investigate the signaling pathways involved in the gene induction, five inhibitors, cyclosporin A (CsA), transforming growth factor-beta, cycloheximide, genistein, and staurosporine A, were used in analyzing the effects of IL-2 and IL-12 on NK3.3 cells. The results suggest that activation of protein kinase C, but not new protein synthesis, is required for IL-2 induction of IFN-gamma and GM-CSF cytoplasmic mRNA. In contrast, IL-12 induction of IFN-gamma cytoplasmic mRNA appears to only partially depend on activation of protein kinase C. Furthermore, both transforming growth factor-beta and genistein, a tyrosine kinase inhibitor, could suppress IL-2 and IL-12 signaling but CsA was generally inactive. It also was observed that suppression of cytokine gene expression by these agents was independent of the inhibition of proliferation. In addition, IL-2 but not IL-12 induced nuclear factors NF-kappa B and AP1, and regulation of the nuclear levels of these two DNA binding protein complexes is correlated with IFN-gamma and GM-CSF gene expression. These data indicate that IL-2 and IL-12 may have distinct signaling pathways leading to the induction of IFN-gamma and GM-CSF gene expression, and that the NK3.3 cell line may serve as a novel model for dissecting the biochemical and molecular events involved in these pathways."}

    genia-medco-coref

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and molecular mechanisms of IFN-gamma production induced by IL-2 and IL-12 in a human NK cell line.\nInterferon-gamma (IFN-gamma) is an important immunoregulatory protein produced predominantly by T cells and large granular lymphocytes (LGL) in response to different extracellular signals. In particular, two interleukins (ILs), IL-2 and IL-12, have been shown to be potent inducers of IFN-gamma gene expression in both T cells and LGL. Although it has been reported that there are some T cell lines that produce IFN-gamma in response to IL-2 and IL-12 stimulation, there has as yet been no report of a natural killer (NK) cell line that responds in a similar manner. In this report we present evidence that the cell line NK3.3 derived from human NK cells, responds to both IL-2 and IL-12, as measured by increases in IFN-gamma and granulocyte-macrophage colony-stimulating factor (GM-CSF) cytoplasmic mRNA and protein expression. In addition, when used together IL-2 and IL-12 synergized in the induction of IFN-gamma and GM-CSF and this synergy was attributed to an increased accumulation and stability of the IFN-gamma and GM-CSF mRNAs. To investigate the signaling pathways involved in the gene induction, five inhibitors, cyclosporin A (CsA), transforming growth factor-beta, cycloheximide, genistein, and staurosporine A, were used in analyzing the effects of IL-2 and IL-12 on NK3.3 cells. The results suggest that activation of protein kinase C, but not new protein synthesis, is required for IL-2 induction of IFN-gamma and GM-CSF cytoplasmic mRNA. In contrast, IL-12 induction of IFN-gamma cytoplasmic mRNA appears to only partially depend on activation of protein kinase C. Furthermore, both transforming growth factor-beta and genistein, a tyrosine kinase inhibitor, could suppress IL-2 and IL-12 signaling but CsA was generally inactive. It also was observed that suppression of cytokine gene expression by these agents was independent of the inhibition of proliferation. In addition, IL-2 but not IL-12 induced nuclear factors NF-kappa B and AP1, and regulation of the nuclear levels of these two DNA binding protein complexes is correlated with IFN-gamma and GM-CSF gene expression. These data indicate that IL-2 and IL-12 may have distinct signaling pathways leading to the induction of IFN-gamma and GM-CSF gene expression, and that the NK3.3 cell line may serve as a novel model for dissecting the biochemical and molecular events involved in these pathways."}

    pubmed-sentences-benchmark

    {"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":108},"obj":"Sentence"},{"id":"S2","span":{"begin":109,"end":297},"obj":"Sentence"},{"id":"S3","span":{"begin":298,"end":444},"obj":"Sentence"},{"id":"S4","span":{"begin":445,"end":675},"obj":"Sentence"},{"id":"S5","span":{"begin":676,"end":938},"obj":"Sentence"},{"id":"S6","span":{"begin":939,"end":1147},"obj":"Sentence"},{"id":"S7","span":{"begin":1148,"end":1404},"obj":"Sentence"},{"id":"S8","span":{"begin":1405,"end":1565},"obj":"Sentence"},{"id":"S9","span":{"begin":1566,"end":1692},"obj":"Sentence"},{"id":"S10","span":{"begin":1693,"end":1858},"obj":"Sentence"},{"id":"S11","span":{"begin":1859,"end":1992},"obj":"Sentence"},{"id":"S12","span":{"begin":1993,"end":2205},"obj":"Sentence"},{"id":"S13","span":{"begin":2206,"end":2484},"obj":"Sentence"}],"text":"Cellular and molecular mechanisms of IFN-gamma production induced by IL-2 and IL-12 in a human NK cell line.\nInterferon-gamma (IFN-gamma) is an important immunoregulatory protein produced predominantly by T cells and large granular lymphocytes (LGL) in response to different extracellular signals. In particular, two interleukins (ILs), IL-2 and IL-12, have been shown to be potent inducers of IFN-gamma gene expression in both T cells and LGL. Although it has been reported that there are some T cell lines that produce IFN-gamma in response to IL-2 and IL-12 stimulation, there has as yet been no report of a natural killer (NK) cell line that responds in a similar manner. In this report we present evidence that the cell line NK3.3 derived from human NK cells, responds to both IL-2 and IL-12, as measured by increases in IFN-gamma and granulocyte-macrophage colony-stimulating factor (GM-CSF) cytoplasmic mRNA and protein expression. In addition, when used together IL-2 and IL-12 synergized in the induction of IFN-gamma and GM-CSF and this synergy was attributed to an increased accumulation and stability of the IFN-gamma and GM-CSF mRNAs. To investigate the signaling pathways involved in the gene induction, five inhibitors, cyclosporin A (CsA), transforming growth factor-beta, cycloheximide, genistein, and staurosporine A, were used in analyzing the effects of IL-2 and IL-12 on NK3.3 cells. The results suggest that activation of protein kinase C, but not new protein synthesis, is required for IL-2 induction of IFN-gamma and GM-CSF cytoplasmic mRNA. In contrast, IL-12 induction of IFN-gamma cytoplasmic mRNA appears to only partially depend on activation of protein kinase C. Furthermore, both transforming growth factor-beta and genistein, a tyrosine kinase inhibitor, could suppress IL-2 and IL-12 signaling but CsA was generally inactive. It also was observed that suppression of cytokine gene expression by these agents was independent of the inhibition of proliferation. In addition, IL-2 but not IL-12 induced nuclear factors NF-kappa B and AP1, and regulation of the nuclear levels of these two DNA binding protein complexes is correlated with IFN-gamma and GM-CSF gene expression. These data indicate that IL-2 and IL-12 may have distinct signaling pathways leading to the induction of IFN-gamma and GM-CSF gene expression, and that the NK3.3 cell line may serve as a novel model for dissecting the biochemical and molecular events involved in these pathways."}

    GENIAcorpus

    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and molecular mechanisms of IFN-gamma production induced by IL-2 and IL-12 in a human NK cell line.\nInterferon-gamma (IFN-gamma) is an important immunoregulatory protein produced predominantly by T cells and large granular lymphocytes (LGL) in response to different extracellular signals. In particular, two interleukins (ILs), IL-2 and IL-12, have been shown to be potent inducers of IFN-gamma gene expression in both T cells and LGL. Although it has been reported that there are some T cell lines that produce IFN-gamma in response to IL-2 and IL-12 stimulation, there has as yet been no report of a natural killer (NK) cell line that responds in a similar manner. In this report we present evidence that the cell line NK3.3 derived from human NK cells, responds to both IL-2 and IL-12, as measured by increases in IFN-gamma and granulocyte-macrophage colony-stimulating factor (GM-CSF) cytoplasmic mRNA and protein expression. In addition, when used together IL-2 and IL-12 synergized in the induction of IFN-gamma and GM-CSF and this synergy was attributed to an increased accumulation and stability of the IFN-gamma and GM-CSF mRNAs. To investigate the signaling pathways involved in the gene induction, five inhibitors, cyclosporin A (CsA), transforming growth factor-beta, cycloheximide, genistein, and staurosporine A, were used in analyzing the effects of IL-2 and IL-12 on NK3.3 cells. The results suggest that activation of protein kinase C, but not new protein synthesis, is required for IL-2 induction of IFN-gamma and GM-CSF cytoplasmic mRNA. In contrast, IL-12 induction of IFN-gamma cytoplasmic mRNA appears to only partially depend on activation of protein kinase C. Furthermore, both transforming growth factor-beta and genistein, a tyrosine kinase inhibitor, could suppress IL-2 and IL-12 signaling but CsA was generally inactive. It also was observed that suppression of cytokine gene expression by these agents was independent of the inhibition of proliferation. In addition, IL-2 but not IL-12 induced nuclear factors NF-kappa B and AP1, and regulation of the nuclear levels of these two DNA binding protein complexes is correlated with IFN-gamma and GM-CSF gene expression. These data indicate that IL-2 and IL-12 may have distinct signaling pathways leading to the induction of IFN-gamma and GM-CSF gene expression, and that the NK3.3 cell line may serve as a novel model for dissecting the biochemical and molecular events involved in these pathways."}