PubMed:10201899
Annnotations
jnlpba-st-training
{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":0,"end":36},"obj":"protein"},{"id":"T2","span":{"begin":68,"end":71},"obj":"protein"},{"id":"T3","span":{"begin":71,"end":76},"obj":"protein"},{"id":"T4","span":{"begin":94,"end":116},"obj":"cell_type"},{"id":"T5","span":{"begin":183,"end":186},"obj":"protein"},{"id":"T6","span":{"begin":206,"end":233},"obj":"protein"},{"id":"T7","span":{"begin":306,"end":338},"obj":"protein"},{"id":"T8","span":{"begin":340,"end":344},"obj":"protein"},{"id":"T9","span":{"begin":360,"end":381},"obj":"cell_type"},{"id":"T10","span":{"begin":416,"end":436},"obj":"cell_type"},{"id":"T11","span":{"begin":452,"end":460},"obj":"protein"},{"id":"T12","span":{"begin":470,"end":493},"obj":"protein"},{"id":"T13","span":{"begin":495,"end":498},"obj":"protein"},{"id":"T14","span":{"begin":550,"end":558},"obj":"protein"},{"id":"T15","span":{"begin":562,"end":571},"obj":"protein"},{"id":"T16","span":{"begin":575,"end":592},"obj":"cell_type"},{"id":"T17","span":{"begin":597,"end":612},"obj":"cell_type"},{"id":"T18","span":{"begin":623,"end":631},"obj":"protein"},{"id":"T19","span":{"begin":684,"end":692},"obj":"protein"},{"id":"T20","span":{"begin":752,"end":755},"obj":"protein"},{"id":"T21","span":{"begin":756,"end":764},"obj":"protein"},{"id":"T22","span":{"begin":799,"end":807},"obj":"protein"},{"id":"T23","span":{"begin":898,"end":901},"obj":"protein"},{"id":"T24","span":{"begin":984,"end":988},"obj":"protein"},{"id":"T25","span":{"begin":990,"end":994},"obj":"protein"},{"id":"T26","span":{"begin":1000,"end":1009},"obj":"protein"},{"id":"T27","span":{"begin":1026,"end":1029},"obj":"protein"},{"id":"T28","span":{"begin":1034,"end":1037},"obj":"protein"},{"id":"T29","span":{"begin":1037,"end":1042},"obj":"protein"},{"id":"T30","span":{"begin":1086,"end":1110},"obj":"protein"},{"id":"T31","span":{"begin":1135,"end":1143},"obj":"protein"},{"id":"T32","span":{"begin":1194,"end":1202},"obj":"protein"},{"id":"T33","span":{"begin":1276,"end":1297},"obj":"cell_type"},{"id":"T34","span":{"begin":1338,"end":1343},"obj":"protein"},{"id":"T35","span":{"begin":1375,"end":1379},"obj":"protein"},{"id":"T36","span":{"begin":1431,"end":1438},"obj":"cell_type"}],"text":"p38 mitogen-activated protein kinase mediates signal integration of TCR/CD28 costimulation in primary murine T cells.\nOptimal T cell activation requires two signals, one generated by TCR and another by the CD28 costimulatory receptor. In this study, we investigated the regulation of costimulation-induced mitogen-activated protein kinase (MAPK) activation in primary mouse T cells. In contrast to that reported for human Jurkat T cells, we found that p38 MAPK, but not Jun NH2-terminal kinase (JNK), is weakly activated upon stimulation with either anti-CD3 or anti-CD28 in murine thymocytes and splenic T cells. However, p38 MAPK is activated strongly and synergistically by either CD3/CD28 coligation or PMA/Ca2+ ionophore stimulation, which mimics TCR-CD3/CD28-mediated signaling. Activation of p38 MAPK correlates closely with the stimulation of T cell proliferation. In contrast, PMA-induced JNK activation is inhibited by Ca2+ ionophore. T cell proliferation and production of IL-2, IL-4, and IFN-gamma induced by both CD3 and CD3/CD28 ligation and the nuclear expression of the c-Jun and ATF-2 proteins are each blocked by the p38 MAPK inhibitor SB203580. Our findings demonstrate that p38 MAPK 1) plays an important role in signal integration during costimulation of primary mouse T cells, 2) may be involved in the induction of c-Jun activation and augmentation of AP-1 transcriptional activity, and 3) regulates whether T cells enter a state of functional unresponsiveness."}
pubmed-sentences-benchmark
{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":117},"obj":"Sentence"},{"id":"S2","span":{"begin":118,"end":234},"obj":"Sentence"},{"id":"S3","span":{"begin":235,"end":382},"obj":"Sentence"},{"id":"S4","span":{"begin":383,"end":613},"obj":"Sentence"},{"id":"S5","span":{"begin":614,"end":784},"obj":"Sentence"},{"id":"S6","span":{"begin":785,"end":872},"obj":"Sentence"},{"id":"S7","span":{"begin":873,"end":944},"obj":"Sentence"},{"id":"S8","span":{"begin":945,"end":1163},"obj":"Sentence"},{"id":"S9","span":{"begin":1164,"end":1484},"obj":"Sentence"}],"text":"p38 mitogen-activated protein kinase mediates signal integration of TCR/CD28 costimulation in primary murine T cells.\nOptimal T cell activation requires two signals, one generated by TCR and another by the CD28 costimulatory receptor. In this study, we investigated the regulation of costimulation-induced mitogen-activated protein kinase (MAPK) activation in primary mouse T cells. In contrast to that reported for human Jurkat T cells, we found that p38 MAPK, but not Jun NH2-terminal kinase (JNK), is weakly activated upon stimulation with either anti-CD3 or anti-CD28 in murine thymocytes and splenic T cells. However, p38 MAPK is activated strongly and synergistically by either CD3/CD28 coligation or PMA/Ca2+ ionophore stimulation, which mimics TCR-CD3/CD28-mediated signaling. Activation of p38 MAPK correlates closely with the stimulation of T cell proliferation. In contrast, PMA-induced JNK activation is inhibited by Ca2+ ionophore. T cell proliferation and production of IL-2, IL-4, and IFN-gamma induced by both CD3 and CD3/CD28 ligation and the nuclear expression of the c-Jun and ATF-2 proteins are each blocked by the p38 MAPK inhibitor SB203580. Our findings demonstrate that p38 MAPK 1) plays an important role in signal integration during costimulation of primary mouse T cells, 2) may be involved in the induction of c-Jun activation and augmentation of AP-1 transcriptional activity, and 3) regulates whether T cells enter a state of functional unresponsiveness."}
genia-medco-coref
{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":0,"end":36},"obj":"NP"},{"id":"C2","span":{"begin":94,"end":116},"obj":"NP"},{"id":"C3","span":{"begin":153,"end":164},"obj":"NP"},{"id":"C4","span":{"begin":166,"end":233},"obj":"NP"},{"id":"C5","span":{"begin":360,"end":381},"obj":"NP"},{"id":"C6","span":{"begin":416,"end":436},"obj":"NP"},{"id":"C7","span":{"begin":452,"end":460},"obj":"NP"},{"id":"C8","span":{"begin":623,"end":631},"obj":"NP"},{"id":"C9","span":{"begin":707,"end":737},"obj":"NP"},{"id":"C10","span":{"begin":739,"end":744},"obj":"NP"},{"id":"C11","span":{"begin":799,"end":807},"obj":"NP"},{"id":"C12","span":{"begin":1194,"end":1202},"obj":"NP"},{"id":"C13","span":{"begin":1276,"end":1297},"obj":"NP"},{"id":"C14","span":{"begin":1431,"end":1438},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-appos","subj":"C4","obj":"C3"},{"id":"R2","pred":"coref-ident","subj":"C5","obj":"C2"},{"id":"R3","pred":"coref-ident","subj":"C7","obj":"C1"},{"id":"R4","pred":"coref-ident","subj":"C8","obj":"C7"},{"id":"R5","pred":"coref-relat","subj":"C10","obj":"C9"},{"id":"R6","pred":"coref-ident","subj":"C11","obj":"C8"},{"id":"R7","pred":"coref-ident","subj":"C12","obj":"C11"},{"id":"R8","pred":"coref-ident","subj":"C13","obj":"C5"},{"id":"R9","pred":"coref-ident","subj":"C14","obj":"C6"}],"text":"p38 mitogen-activated protein kinase mediates signal integration of TCR/CD28 costimulation in primary murine T cells.\nOptimal T cell activation requires two signals, one generated by TCR and another by the CD28 costimulatory receptor. In this study, we investigated the regulation of costimulation-induced mitogen-activated protein kinase (MAPK) activation in primary mouse T cells. In contrast to that reported for human Jurkat T cells, we found that p38 MAPK, but not Jun NH2-terminal kinase (JNK), is weakly activated upon stimulation with either anti-CD3 or anti-CD28 in murine thymocytes and splenic T cells. However, p38 MAPK is activated strongly and synergistically by either CD3/CD28 coligation or PMA/Ca2+ ionophore stimulation, which mimics TCR-CD3/CD28-mediated signaling. Activation of p38 MAPK correlates closely with the stimulation of T cell proliferation. In contrast, PMA-induced JNK activation is inhibited by Ca2+ ionophore. T cell proliferation and production of IL-2, IL-4, and IFN-gamma induced by both CD3 and CD3/CD28 ligation and the nuclear expression of the c-Jun and ATF-2 proteins are each blocked by the p38 MAPK inhibitor SB203580. Our findings demonstrate that p38 MAPK 1) plays an important role in signal integration during costimulation of primary mouse T cells, 2) may be involved in the induction of c-Jun activation and augmentation of AP-1 transcriptional activity, and 3) regulates whether T cells enter a state of functional unresponsiveness."}
GENIAcorpus
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