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jnlpba-st-training

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":65,"end":75},"obj":"protein"},{"id":"T2","span":{"begin":146,"end":156},"obj":"protein"},{"id":"T3","span":{"begin":250,"end":259},"obj":"protein"},{"id":"T4","span":{"begin":261,"end":288},"obj":"protein"},{"id":"T5","span":{"begin":537,"end":547},"obj":"protein"},{"id":"T6","span":{"begin":651,"end":661},"obj":"protein"},{"id":"T7","span":{"begin":692,"end":710},"obj":"cell_line"},{"id":"T8","span":{"begin":712,"end":720},"obj":"cell_line"},{"id":"T9","span":{"begin":729,"end":735},"obj":"cell_line"},{"id":"T10","span":{"begin":746,"end":773},"obj":"protein"},{"id":"T11","span":{"begin":1105,"end":1115},"obj":"protein"},{"id":"T12","span":{"begin":1130,"end":1142},"obj":"cell_line"},{"id":"T13","span":{"begin":1177,"end":1187},"obj":"protein"},{"id":"T14","span":{"begin":1340,"end":1350},"obj":"protein"},{"id":"T15","span":{"begin":1489,"end":1497},"obj":"protein"},{"id":"T16","span":{"begin":1523,"end":1533},"obj":"protein"},{"id":"T17","span":{"begin":1689,"end":1699},"obj":"protein"},{"id":"T18","span":{"begin":1789,"end":1799},"obj":"protein"}],"text":"Separation of oxidant-initiated and redox-regulated steps in the NF-kappa B signal transduction pathway.\nStudies presented here show that overall NF-kappa B signal transduction begins with a parallel series of stimuli-specific pathways through which cytokines (tumor necrosis factor alpha), oxidants (hydrogen peroxide and mitomycin C), and phorbol ester (phorbol 12-myristate 13-acetate) individually initiate signaling. These initial pathways culminate in a common pathway through which all of the stimulating agents ultimately signal NF-kappa B activation. We distinguish the stimuli-specific pathways by showing that the oxidative stimuli trigger NF-kappa B activation in only one of two human T-cell lines (Wurzburg but not Jurkat), whereas tumor necrosis factor alpha and phorbol 12-myristate 13-acetate readily stimulate in both lines. We propose the common pathway as the simplest way of accounting for the common requirements and properties of the signaling pathway. We include a redox-regulatory mechanism(s) in this common pathway to account for the previously demonstrated redox regulation of NF-kappa B activation in Jurkat cells (in which oxidants don't activate NF-kappa B); we put tyrosine phosphorylation in the common pathway by showing that kinase activity (inhibitable by herbimycin A and tyrphostin 47) is required for NF-kappa B activation by all stimuli tested in both cell lines. Since internal sites of oxidant production have been shown to play a key role in the cytokine-stimulated activation of NF-kappa B, and since tyrosine kinase and phosphatase activities are known to be altered by oxidants, these findings suggest that intracellular redox status controls NF-kappa B activation by regulating tyrosine phosphorylation event(s) within the common step of the NF-kappa B signal transduction pathway."}

genia-medco-coref

pubmed-sentences-benchmark

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":104},"obj":"Sentence"},{"id":"S2","span":{"begin":105,"end":421},"obj":"Sentence"},{"id":"S3","span":{"begin":422,"end":559},"obj":"Sentence"},{"id":"S4","span":{"begin":560,"end":842},"obj":"Sentence"},{"id":"S5","span":{"begin":843,"end":975},"obj":"Sentence"},{"id":"S6","span":{"begin":976,"end":1403},"obj":"Sentence"},{"id":"S7","span":{"begin":1404,"end":1828},"obj":"Sentence"}],"text":"Separation of oxidant-initiated and redox-regulated steps in the NF-kappa B signal transduction pathway.\nStudies presented here show that overall NF-kappa B signal transduction begins with a parallel series of stimuli-specific pathways through which cytokines (tumor necrosis factor alpha), oxidants (hydrogen peroxide and mitomycin C), and phorbol ester (phorbol 12-myristate 13-acetate) individually initiate signaling. These initial pathways culminate in a common pathway through which all of the stimulating agents ultimately signal NF-kappa B activation. We distinguish the stimuli-specific pathways by showing that the oxidative stimuli trigger NF-kappa B activation in only one of two human T-cell lines (Wurzburg but not Jurkat), whereas tumor necrosis factor alpha and phorbol 12-myristate 13-acetate readily stimulate in both lines. We propose the common pathway as the simplest way of accounting for the common requirements and properties of the signaling pathway. We include a redox-regulatory mechanism(s) in this common pathway to account for the previously demonstrated redox regulation of NF-kappa B activation in Jurkat cells (in which oxidants don't activate NF-kappa B); we put tyrosine phosphorylation in the common pathway by showing that kinase activity (inhibitable by herbimycin A and tyrphostin 47) is required for NF-kappa B activation by all stimuli tested in both cell lines. Since internal sites of oxidant production have been shown to play a key role in the cytokine-stimulated activation of NF-kappa B, and since tyrosine kinase and phosphatase activities are known to be altered by oxidants, these findings suggest that intracellular redox status controls NF-kappa B activation by regulating tyrosine phosphorylation event(s) within the common step of the NF-kappa B signal transduction pathway."}

GENIAcorpus

PubMed:7526398 JSONTXT

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jnlpba-st-training

genia-medco-coref

pubmed-sentences-benchmark

GENIAcorpus

PubMed:7526398 JSON TXT