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SOCS3 has recently been shown to specifically inhibit STAT3 activation induced by IL-6 but not by IL-10, thereby regulating the divergent action of IL-6 and IL-10 [8,9]. On the contrary, SOCS1 is able to partially inhibit IL-10-mediated STAT3 activation and cellular responses, as well as IFN-γ-mediated STAT1 activation [32]. To determine whether SOCSs were involved in the defective IL-10-induced STAT3 activation of RA CD4+ T cells, the levels of SOCS1 and SOCS3 mRNA expression in PB CD4+ T cells from active RA patients and from healthy controls were compared by semiquantitative real-time PCR. The RA CD4+ T cells contained higher levels of SOCS1 but lower levels of SOCS3 transcripts than did control CD4+ T cells (Fig. 6a). Constitutive expression of SOCS1 mRNA in RA CD4+ T cells was comparable with the expression in normal CD4+ T cells stimulated by 10 ng/ml IL-6 (Fig. 6b), supporting its functional significance. 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expression of SOCS1 mRNA in RA CD4+ T cells\nIL-6 induces two potent inhibitors of JAKs (SOCS1 and SOCS3 proteins) that not only act as mediators of negative feedback inhibition, but also play a major role in crosstalk inhibition by opposing other cytokine-signaling pathways [7]. SOCS3 has recently been shown to specifically inhibit STAT3 activation induced by IL-6 but not by IL-10, thereby regulating the divergent action of IL-6 and IL-10 [8,9]. On the contrary, SOCS1 is able to partially inhibit IL-10-mediated STAT3 activation and cellular responses, as well as IFN-γ-mediated STAT1 activation [32]. To determine whether SOCSs were involved in the defective IL-10-induced STAT3 activation of RA CD4+ T cells, the levels of SOCS1 and SOCS3 mRNA expression in PB CD4+ T cells from active RA patients and from healthy controls were compared by semiquantitative real-time PCR. The RA CD4+ T cells contained higher levels of SOCS1 but lower levels of SOCS3 transcripts than did control CD4+ T cells (Fig. 6a). Constitutive expression of SOCS1 mRNA in RA CD4+ T cells was comparable with the expression in normal CD4+ T cells stimulated by 10 ng/ml IL-6 (Fig. 6b), supporting its functional significance. Defective IL-10-induced STAT3 activation therefore appears to be due at least in part to an abundance of SOCS1 in RA CD4+ T cells."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T20502","span":{"begin":1328,"end":1331},"obj":"Protein"},{"id":"T20501","span":{"begin":1316,"end":1321},"obj":"Protein"},{"id":"T20500","span":{"begin":1235,"end":1240},"obj":"Protein"},{"id":"T20499","span":{"begin":1221,"end":1226},"obj":"Protein"},{"id":"T20498","span":{"begin":1155,"end":1159},"obj":"Protein"},{"id":"T20497","span":{"begin":1119,"end":1122},"obj":"Protein"},{"id":"T20496","span":{"begin":1061,"end":1064},"obj":"Protein"},{"id":"T20495","span":{"begin":1044,"end":1049},"obj":"Protein"},{"id":"T20494","span":{"begin":993,"end":996},"obj":"Protein"},{"id":"T20493","span":{"begin":958,"end":963},"obj":"Protein"},{"id":"T20492","span":{"begin":932,"end":937},"obj":"Protein"},{"id":"T20491","span":{"begin":892,"end":895},"obj":"Protein"},{"id":"T20490","span":{"begin":773,"end":776},"obj":"Protein"},{"id":"T20489","span":{"begin":745,"end":750},"obj":"Protein"},{"id":"T20488","span":{"begin":735,"end":740},"obj":"Protein"},{"id":"T20487","span":{"begin":707,"end":710},"obj":"Protein"},{"id":"T20486","span":{"begin":684,"end":689},"obj":"Protein"},{"id":"T20485","span":{"begin":670,"end":675},"obj":"Protein"},{"id":"T20484","span":{"begin":589,"end":594},"obj":"Protein"},{"id":"T20483","span":{"begin":574,"end":579},"obj":"Protein"},{"id":"T20482","span":{"begin":522,"end":527},"obj":"Protein"},{"id":"T20481","span":{"begin":507,"end":512},"obj":"Protein"},{"id":"T20480","span":{"begin":472,"end":477},"obj":"Protein"},{"id":"T20475","span":{"begin":339,"end":344},"obj":"Protein"},{"id":"T20474","span":{"begin":285,"end":290},"obj":"Protein"},{"id":"T20473","span":{"begin":103,"end":108},"obj":"Protein"},{"id":"T20472","span":{"begin":93,"end":98},"obj":"Protein"},{"id":"T20471","span":{"begin":49,"end":53},"obj":"Protein"},{"id":"T20470","span":{"begin":36,"end":39},"obj":"Protein"},{"id":"T20469","span":{"begin":19,"end":24},"obj":"Protein"},{"id":"T20479","span":{"begin":442,"end":447},"obj":"Protein"},{"id":"T20478","span":{"begin":433,"end":437},"obj":"Protein"},{"id":"T20477","span":{"begin":383,"end":388},"obj":"Protein"},{"id":"T20476","span":{"begin":367,"end":371},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"High expression of SOCS1 mRNA in RA CD4+ T cells\nIL-6 induces two potent inhibitors of JAKs (SOCS1 and SOCS3 proteins) that not only act as mediators of negative feedback inhibition, but also play a major role in crosstalk inhibition by opposing other cytokine-signaling pathways [7]. SOCS3 has recently been shown to specifically inhibit STAT3 activation induced by IL-6 but not by IL-10, thereby regulating the divergent action of IL-6 and IL-10 [8,9]. On the contrary, SOCS1 is able to partially inhibit IL-10-mediated STAT3 activation and cellular responses, as well as IFN-γ-mediated STAT1 activation [32]. To determine whether SOCSs were involved in the defective IL-10-induced STAT3 activation of RA CD4+ T cells, the levels of SOCS1 and SOCS3 mRNA expression in PB CD4+ T cells from active RA patients and from healthy controls were compared by semiquantitative real-time PCR. The RA CD4+ T cells contained higher levels of SOCS1 but lower levels of SOCS3 transcripts than did control CD4+ T cells (Fig. 6a). Constitutive expression of SOCS1 mRNA in RA CD4+ T cells was comparable with the expression in normal CD4+ T cells stimulated by 10 ng/ml IL-6 (Fig. 6b), supporting its functional significance. Defective IL-10-induced STAT3 activation therefore appears to be due at least in part to an abundance of SOCS1 in RA CD4+ T cells."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T20638","span":{"begin":574,"end":579},"obj":"http://www.uniprot.org/uniprot/P01579"},{"id":"T20637","span":{"begin":1221,"end":1226},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20636","span":{"begin":670,"end":675},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20635","span":{"begin":507,"end":512},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20634","span":{"begin":442,"end":447},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20633","span":{"begin":383,"end":388},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20632","span":{"begin":1235,"end":1240},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T20631","span":{"begin":684,"end":689},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T20630","span":{"begin":522,"end":527},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T20629","span":{"begin":339,"end":344},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T20628","span":{"begin":1155,"end":1159},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T20627","span":{"begin":433,"end":437},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T20626","span":{"begin":367,"end":371},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T20625","span":{"begin":49,"end":53},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T20624","span":{"begin":1328,"end":1331},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20623","span":{"begin":1119,"end":1122},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20622","span":{"begin":1061,"end":1064},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20621","span":{"begin":993,"end":996},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20620","span":{"begin":892,"end":895},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20619","span":{"begin":773,"end":776},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20618","span":{"begin":707,"end":710},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20617","span":{"begin":36,"end":39},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20616","span":{"begin":1316,"end":1321},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20615","span":{"begin":1044,"end":1049},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20614","span":{"begin":932,"end":937},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20613","span":{"begin":735,"end":740},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20612","span":{"begin":472,"end":477},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20611","span":{"begin":93,"end":98},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20610","span":{"begin":19,"end":24},"obj":"http://www.uniprot.org/uniprot/O15524"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"High expression of SOCS1 mRNA in RA CD4+ T cells\nIL-6 induces two potent inhibitors of JAKs (SOCS1 and SOCS3 proteins) that not only act as mediators of negative feedback inhibition, but also play a major role in crosstalk inhibition by opposing other cytokine-signaling pathways [7]. SOCS3 has recently been shown to specifically inhibit STAT3 activation induced by IL-6 but not by IL-10, thereby regulating the divergent action of IL-6 and IL-10 [8,9]. On the contrary, SOCS1 is able to partially inhibit IL-10-mediated STAT3 activation and cellular responses, as well as IFN-γ-mediated STAT1 activation [32]. To determine whether SOCSs were involved in the defective IL-10-induced STAT3 activation of RA CD4+ T cells, the levels of SOCS1 and SOCS3 mRNA expression in PB CD4+ T cells from active RA patients and from healthy controls were compared by semiquantitative real-time PCR. The RA CD4+ T cells contained higher levels of SOCS1 but lower levels of SOCS3 transcripts than did control CD4+ T cells (Fig. 6a). Constitutive expression of SOCS1 mRNA in RA CD4+ T cells was comparable with the expression in normal CD4+ T cells stimulated by 10 ng/ml IL-6 (Fig. 6b), supporting its functional significance. Defective IL-10-induced STAT3 activation therefore appears to be due at least in part to an abundance of SOCS1 in RA CD4+ T cells."}

{"project":"GO-BP","denotations":[{"id":"T20406","span":{"begin":543,"end":551},"obj":"http://purl.obolibrary.org/obo/GO_0007349"},{"id":"T20405","span":{"begin":528,"end":561},"obj":"http://purl.obolibrary.org/obo/GO_1900039"},{"id":"T20404","span":{"begin":528,"end":561},"obj":"http://purl.obolibrary.org/obo/GO_1900036"},{"id":"T20403","span":{"begin":528,"end":561},"obj":"http://purl.obolibrary.org/obo/GO_0010186"},{"id":"T20402","span":{"begin":261,"end":279},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T20401","span":{"begin":261,"end":270},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T20400","span":{"begin":252,"end":279},"obj":"http://purl.obolibrary.org/obo/GO_0019221"}],"text":"High expression of SOCS1 mRNA in RA CD4+ T cells\nIL-6 induces two potent inhibitors of JAKs (SOCS1 and SOCS3 proteins) that not only act as mediators of negative feedback inhibition, but also play a major role in crosstalk inhibition by opposing other cytokine-signaling pathways [7]. SOCS3 has recently been shown to specifically inhibit STAT3 activation induced by IL-6 but not by IL-10, thereby regulating the divergent action of IL-6 and IL-10 [8,9]. On the contrary, SOCS1 is able to partially inhibit IL-10-mediated STAT3 activation and cellular responses, as well as IFN-γ-mediated STAT1 activation [32]. To determine whether SOCSs were involved in the defective IL-10-induced STAT3 activation of RA CD4+ T cells, the levels of SOCS1 and SOCS3 mRNA expression in PB CD4+ T cells from active RA patients and from healthy controls were compared by semiquantitative real-time PCR. The RA CD4+ T cells contained higher levels of SOCS1 but lower levels of SOCS3 transcripts than did control CD4+ T cells (Fig. 6a). Constitutive expression of SOCS1 mRNA in RA CD4+ T cells was comparable with the expression in normal CD4+ T cells stimulated by 10 ng/ml IL-6 (Fig. 6b), supporting its functional significance. Defective IL-10-induced STAT3 activation therefore appears to be due at least in part to an abundance of SOCS1 in RA CD4+ T cells."}

{"project":"GO-CC","denotations":[{"id":"T20519","span":{"begin":1335,"end":1340},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20518","span":{"begin":1126,"end":1131},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20517","span":{"begin":1068,"end":1073},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20516","span":{"begin":1000,"end":1005},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20515","span":{"begin":899,"end":904},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20514","span":{"begin":780,"end":785},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20513","span":{"begin":714,"end":719},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20512","span":{"begin":43,"end":48},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"High expression of SOCS1 mRNA in RA CD4+ T cells\nIL-6 induces two potent inhibitors of JAKs (SOCS1 and SOCS3 proteins) that not only act as mediators of negative feedback inhibition, but also play a major role in crosstalk inhibition by opposing other cytokine-signaling pathways [7]. SOCS3 has recently been shown to specifically inhibit STAT3 activation induced by IL-6 but not by IL-10, thereby regulating the divergent action of IL-6 and IL-10 [8,9]. On the contrary, SOCS1 is able to partially inhibit IL-10-mediated STAT3 activation and cellular responses, as well as IFN-γ-mediated STAT1 activation [32]. To determine whether SOCSs were involved in the defective IL-10-induced STAT3 activation of RA CD4+ T cells, the levels of SOCS1 and SOCS3 mRNA expression in PB CD4+ T cells from active RA patients and from healthy controls were compared by semiquantitative real-time PCR. The RA CD4+ T cells contained higher levels of SOCS1 but lower levels of SOCS3 transcripts than did control CD4+ T cells (Fig. 6a). Constitutive expression of SOCS1 mRNA in RA CD4+ T cells was comparable with the expression in normal CD4+ T cells stimulated by 10 ng/ml IL-6 (Fig. 6b), supporting its functional significance. Defective IL-10-induced STAT3 activation therefore appears to be due at least in part to an abundance of SOCS1 in RA CD4+ T cells."}

{"project":"GO-MF","denotations":[{"id":"T20511","span":{"begin":1221,"end":1226},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20510","span":{"begin":670,"end":675},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20509","span":{"begin":507,"end":512},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20508","span":{"begin":442,"end":447},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20507","span":{"begin":383,"end":388},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20506","span":{"begin":1155,"end":1159},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T20505","span":{"begin":433,"end":437},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T20504","span":{"begin":367,"end":371},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T20503","span":{"begin":49,"end":53},"obj":"http://purl.obolibrary.org/obo/GO_0005138"}],"text":"High expression of SOCS1 mRNA in RA CD4+ T cells\nIL-6 induces two potent inhibitors of JAKs (SOCS1 and SOCS3 proteins) that not only act as mediators of negative feedback inhibition, but also play a major role in crosstalk inhibition by opposing other cytokine-signaling pathways [7]. SOCS3 has recently been shown to specifically inhibit STAT3 activation induced by IL-6 but not by IL-10, thereby regulating the divergent action of IL-6 and IL-10 [8,9]. On the contrary, SOCS1 is able to partially inhibit IL-10-mediated STAT3 activation and cellular responses, as well as IFN-γ-mediated STAT1 activation [32]. To determine whether SOCSs were involved in the defective IL-10-induced STAT3 activation of RA CD4+ T cells, the levels of SOCS1 and SOCS3 mRNA expression in PB CD4+ T cells from active RA patients and from healthy controls were compared by semiquantitative real-time PCR. The RA CD4+ T cells contained higher levels of SOCS1 but lower levels of SOCS3 transcripts than did control CD4+ T cells (Fig. 6a). Constitutive expression of SOCS1 mRNA in RA CD4+ T cells was comparable with the expression in normal CD4+ T cells stimulated by 10 ng/ml IL-6 (Fig. 6b), supporting its functional significance. Defective IL-10-induced STAT3 activation therefore appears to be due at least in part to an abundance of SOCS1 in RA CD4+ T cells."}

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expression of SOCS1 mRNA in RA CD4+ T cells\nIL-6 induces two potent inhibitors of JAKs (SOCS1 and SOCS3 proteins) that not only act as mediators of negative feedback inhibition, but also play a major role in crosstalk inhibition by opposing other cytokine-signaling pathways [7]. SOCS3 has recently been shown to specifically inhibit STAT3 activation induced by IL-6 but not by IL-10, thereby regulating the divergent action of IL-6 and IL-10 [8,9]. On the contrary, SOCS1 is able to partially inhibit IL-10-mediated STAT3 activation and cellular responses, as well as IFN-γ-mediated STAT1 activation [32]. To determine whether SOCSs were involved in the defective IL-10-induced STAT3 activation of RA CD4+ T cells, the levels of SOCS1 and SOCS3 mRNA expression in PB CD4+ T cells from active RA patients and from healthy controls were compared by semiquantitative real-time PCR. The RA CD4+ T cells contained higher levels of SOCS1 but lower levels of SOCS3 transcripts than did control CD4+ T cells (Fig. 6a). Constitutive expression of SOCS1 mRNA in RA CD4+ T cells was comparable with the expression in normal CD4+ T cells stimulated by 10 ng/ml IL-6 (Fig. 6b), supporting its functional significance. Defective IL-10-induced STAT3 activation therefore appears to be due at least in part to an abundance of SOCS1 in RA CD4+ T cells."}