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weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T12411","span":{"begin":864,"end":870},"obj":"Protein"},{"id":"T12410","span":{"begin":538,"end":542},"obj":"Protein"},{"id":"T12409","span":{"begin":442,"end":447},"obj":"Protein"},{"id":"T12408","span":{"begin":427,"end":433},"obj":"Protein"},{"id":"T12407","span":{"begin":202,"end":208},"obj":"Protein"},{"id":"T12406","span":{"begin":186,"end":192},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"The weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T14305","span":{"begin":442,"end":447},"obj":"http://www.uniprot.org/uniprot/P01584"},{"id":"T14276","span":{"begin":864,"end":870},"obj":"http://www.uniprot.org/uniprot/P18510"},{"id":"T14325","span":{"begin":202,"end":208},"obj":"http://www.uniprot.org/uniprot/P06886"},{"id":"T14324","span":{"begin":186,"end":192},"obj":"http://www.uniprot.org/uniprot/P06886"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"The weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}

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{"project":"simple1","denotations":[{"id":"T12790","span":{"begin":864,"end":870},"obj":"Protein"},{"id":"T12789","span":{"begin":538,"end":542},"obj":"Protein"},{"id":"T12788","span":{"begin":442,"end":447},"obj":"Protein"},{"id":"T12787","span":{"begin":427,"end":433},"obj":"Protein"},{"id":"T12786","span":{"begin":202,"end":208},"obj":"Protein"},{"id":"T12785","span":{"begin":186,"end":192},"obj":"Protein"}],"text":"The weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}

{"project":"BioNLP16_DUT","denotations":[{"id":"T16685","span":{"begin":850,"end":859},"obj":"Positive_regulation"},{"id":"T16684","span":{"begin":524,"end":534},"obj":"Positive_regulation"},{"id":"T16683","span":{"begin":448,"end":458},"obj":"Gene_expression"},{"id":"T16682","span":{"begin":417,"end":425},"obj":"Regulation"},{"id":"T16628","span":{"begin":864,"end":870},"obj":"Protein"},{"id":"T16627","span":{"begin":538,"end":542},"obj":"Protein"},{"id":"T16626","span":{"begin":442,"end":447},"obj":"Protein"},{"id":"T16625","span":{"begin":427,"end":433},"obj":"Protein"},{"id":"T16624","span":{"begin":202,"end":208},"obj":"Protein"},{"id":"T16623","span":{"begin":186,"end":192},"obj":"Protein"}],"relations":[{"id":"R11405","pred":"themeOf","subj":"T16683","obj":"T16682"},{"id":"R11424","pred":"themeOf","subj":"T16626","obj":"T16683"},{"id":"R11425","pred":"themeOf","subj":"T16627","obj":"T16684"},{"id":"R11428","pred":"themeOf","subj":"T16628","obj":"T16685"}],"text":"The weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}

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weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T12514","span":{"begin":836,"end":849},"obj":"Protein"},{"id":"T12513","span":{"begin":828,"end":831},"obj":"Protein"},{"id":"T12512","span":{"begin":823,"end":826},"obj":"Protein"},{"id":"T12511","span":{"begin":560,"end":570},"obj":"Positive_regulation"},{"id":"T12510","span":{"begin":687,"end":691},"obj":"Protein"},{"id":"T12509","span":{"begin":683,"end":685},"obj":"Protein"},{"id":"T12508","span":{"begin":574,"end":578},"obj":"Protein"},{"id":"T12507","span":{"begin":524,"end":534},"obj":"Positive_regulation"},{"id":"T12506","span":{"begin":538,"end":542},"obj":"Protein"},{"id":"T12505","span":{"begin":479,"end":483},"obj":"Protein"},{"id":"T12504","span":{"begin":417,"end":425},"obj":"Regulation"},{"id":"T12503","span":{"begin":417,"end":425},"obj":"Regulation"},{"id":"T12502","span":{"begin":448,"end":458},"obj":"Gene_expression"},{"id":"T12501","span":{"begin":448,"end":458},"obj":"Gene_expression"},{"id":"T12500","span":{"begin":442,"end":447},"obj":"Protein"},{"id":"T12499","span":{"begin":426,"end":433},"obj":"Protein"},{"id":"T12498","span":{"begin":392,"end":396},"obj":"Protein"},{"id":"T12497","span":{"begin":235,"end":239},"obj":"Protein"},{"id":"T12496","span":{"begin":202,"end":208},"obj":"Protein"},{"id":"T12516","span":{"begin":850,"end":859},"obj":"Positive_regulation"},{"id":"T12515","span":{"begin":864,"end":870},"obj":"Protein"},{"id":"T12517","span":{"begin":850,"end":859},"obj":"Positive_regulation"}],"relations":[{"id":"R7937","pred":"themeOf","subj":"T12499","obj":"T12501"},{"id":"R7938","pred":"themeOf","subj":"T12500","obj":"T12502"},{"id":"R7939","pred":"themeOf","subj":"T12501","obj":"T12503"},{"id":"R7940","pred":"themeOf","subj":"T12502","obj":"T12504"},{"id":"R7941","pred":"themeOf","subj":"T12506","obj":"T12507"},{"id":"R7942","pred":"themeOf","subj":"T12508","obj":"T12511"},{"id":"R7943","pred":"causeOf","subj":"T12513","obj":"T12516"},{"id":"R7944","pred":"causeOf","subj":"T12514","obj":"T12517"},{"id":"R7945","pred":"themeOf","subj":"T12515","obj":"T12516"},{"id":"R7946","pred":"themeOf","subj":"T12515","obj":"T12517"}],"text":"The weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}

{"project":"testone","denotations":[{"id":"T11460","span":{"begin":864,"end":870},"obj":"Protein"},{"id":"T11459","span":{"begin":538,"end":542},"obj":"Protein"},{"id":"T11458","span":{"begin":442,"end":447},"obj":"Protein"},{"id":"T11457","span":{"begin":427,"end":433},"obj":"Protein"},{"id":"T11456","span":{"begin":202,"end":208},"obj":"Protein"},{"id":"T11455","span":{"begin":186,"end":192},"obj":"Protein"},{"id":"T11556","span":{"begin":850,"end":859},"obj":"Positive_regulation"},{"id":"T11555","span":{"begin":524,"end":534},"obj":"Positive_regulation"},{"id":"T11554","span":{"begin":508,"end":516},"obj":"Regulation"},{"id":"T11553","span":{"begin":448,"end":458},"obj":"Gene_expression"}],"relations":[{"id":"R7486","pred":"themeOf","subj":"T11458","obj":"T11553"},{"id":"R7487","pred":"themeOf","subj":"T11459","obj":"T11555"},{"id":"R7488","pred":"themeOf","subj":"T11460","obj":"T11556"},{"id":"R7532","pred":"themeOf","subj":"T11555","obj":"T11554"}],"text":"The weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}

{"project":"test3","denotations":[{"id":"T11850","span":{"begin":864,"end":870},"obj":"Protein"},{"id":"T11849","span":{"begin":850,"end":859},"obj":"Positive_regulation"},{"id":"T11848","span":{"begin":538,"end":542},"obj":"Protein"},{"id":"T11847","span":{"begin":448,"end":458},"obj":"Gene_expression"},{"id":"T11846","span":{"begin":442,"end":447},"obj":"Protein"},{"id":"T11845","span":{"begin":429,"end":433},"obj":"Protein"},{"id":"T11844","span":{"begin":417,"end":425},"obj":"Regulation"},{"id":"T11843","span":{"begin":202,"end":208},"obj":"Protein"},{"id":"T11842","span":{"begin":186,"end":192},"obj":"Protein"},{"id":"T11663","span":{"begin":864,"end":870},"obj":"Protein"},{"id":"T11662","span":{"begin":538,"end":542},"obj":"Protein"},{"id":"T11661","span":{"begin":442,"end":447},"obj":"Protein"},{"id":"T11660","span":{"begin":427,"end":433},"obj":"Protein"},{"id":"T11659","span":{"begin":202,"end":208},"obj":"Protein"},{"id":"T11658","span":{"begin":186,"end":192},"obj":"Protein"}],"relations":[{"id":"R7631","pred":"themeOf","subj":"T11845","obj":"T11847"},{"id":"R7632","pred":"themeOf","subj":"T11846","obj":"T11847"},{"id":"R7633","pred":"themeOf","subj":"T11847","obj":"T11844"},{"id":"R7634","pred":"themeOf","subj":"T11850","obj":"T11849"}],"text":"The weaker modulating effects of GP on the LPS-induced immune response observed in this study, may be attributed to delicately balanced differences in signaling pathways between LPS and TSST-1 [43-45]. TSST-1 has been shown to use the PI3K pathway for signaling [44] and this effect may be sustained by GP treatment [22,37]. It has been demonstrated that in septic/LPS-adapted leukocytes the PI3K pathway selectively controls sIL-1RA but not IL-1β production [48]. Signaling via PI3K has been reported to be involved in the activation of NFAT in T cells [49]. Activation of NFκB can also take place via PI3K [50], which may offer an explanation for a difference in signaling between GP (PI3K) and LPS (mitogen-activated kinase signaling). This idea may be supported by another study showing that despite the use of similar PRR, LPS and peptidoglycan activated the IL-1RA gene through different mechanisms/DNA-binding proteins and acted synergistically in combination, suggestive of signals which are not equivalent in all parts [51]."}