PMC:1064873 / 22128-23420 JSONTXT

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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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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":1279,"end":1282},"obj":"Protein"},{"id":"T20501","span":{"begin":1267,"end":1272},"obj":"Protein"},{"id":"T20500","span":{"begin":1186,"end":1191},"obj":"Protein"},{"id":"T20499","span":{"begin":1172,"end":1177},"obj":"Protein"},{"id":"T20498","span":{"begin":1106,"end":1110},"obj":"Protein"},{"id":"T20497","span":{"begin":1070,"end":1073},"obj":"Protein"},{"id":"T20496","span":{"begin":1012,"end":1015},"obj":"Protein"},{"id":"T20495","span":{"begin":995,"end":1000},"obj":"Protein"},{"id":"T20494","span":{"begin":944,"end":947},"obj":"Protein"},{"id":"T20493","span":{"begin":909,"end":914},"obj":"Protein"},{"id":"T20492","span":{"begin":883,"end":888},"obj":"Protein"},{"id":"T20491","span":{"begin":843,"end":846},"obj":"Protein"},{"id":"T20490","span":{"begin":724,"end":727},"obj":"Protein"},{"id":"T20489","span":{"begin":696,"end":701},"obj":"Protein"},{"id":"T20488","span":{"begin":686,"end":691},"obj":"Protein"},{"id":"T20487","span":{"begin":658,"end":661},"obj":"Protein"},{"id":"T20486","span":{"begin":635,"end":640},"obj":"Protein"},{"id":"T20485","span":{"begin":621,"end":626},"obj":"Protein"},{"id":"T20484","span":{"begin":540,"end":545},"obj":"Protein"},{"id":"T20483","span":{"begin":525,"end":530},"obj":"Protein"},{"id":"T20482","span":{"begin":473,"end":478},"obj":"Protein"},{"id":"T20481","span":{"begin":458,"end":463},"obj":"Protein"},{"id":"T20480","span":{"begin":423,"end":428},"obj":"Protein"},{"id":"T20475","span":{"begin":290,"end":295},"obj":"Protein"},{"id":"T20474","span":{"begin":236,"end":241},"obj":"Protein"},{"id":"T20473","span":{"begin":54,"end":59},"obj":"Protein"},{"id":"T20472","span":{"begin":44,"end":49},"obj":"Protein"},{"id":"T20471","span":{"begin":0,"end":4},"obj":"Protein"},{"id":"T20479","span":{"begin":393,"end":398},"obj":"Protein"},{"id":"T20478","span":{"begin":384,"end":388},"obj":"Protein"},{"id":"T20477","span":{"begin":334,"end":339},"obj":"Protein"},{"id":"T20476","span":{"begin":318,"end":322},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"IL-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":525,"end":530},"obj":"http://www.uniprot.org/uniprot/P01579"},{"id":"T20637","span":{"begin":1172,"end":1177},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20636","span":{"begin":621,"end":626},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20635","span":{"begin":458,"end":463},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20634","span":{"begin":393,"end":398},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20633","span":{"begin":334,"end":339},"obj":"http://www.uniprot.org/uniprot/P22301"},{"id":"T20632","span":{"begin":1186,"end":1191},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T20631","span":{"begin":635,"end":640},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T20630","span":{"begin":473,"end":478},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T20629","span":{"begin":290,"end":295},"obj":"http://www.uniprot.org/uniprot/P40763"},{"id":"T20628","span":{"begin":1106,"end":1110},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T20627","span":{"begin":384,"end":388},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T20626","span":{"begin":318,"end":322},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T20625","span":{"begin":0,"end":4},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T20624","span":{"begin":1279,"end":1282},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20623","span":{"begin":1070,"end":1073},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20622","span":{"begin":1012,"end":1015},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20621","span":{"begin":944,"end":947},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20620","span":{"begin":843,"end":846},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20619","span":{"begin":724,"end":727},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20618","span":{"begin":658,"end":661},"obj":"http://www.uniprot.org/uniprot/P01730"},{"id":"T20616","span":{"begin":1267,"end":1272},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20615","span":{"begin":995,"end":1000},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20614","span":{"begin":883,"end":888},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20613","span":{"begin":686,"end":691},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20612","span":{"begin":423,"end":428},"obj":"http://www.uniprot.org/uniprot/O15524"},{"id":"T20611","span":{"begin":44,"end":49},"obj":"http://www.uniprot.org/uniprot/O15524"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"IL-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":494,"end":502},"obj":"http://purl.obolibrary.org/obo/GO_0007349"},{"id":"T20405","span":{"begin":479,"end":512},"obj":"http://purl.obolibrary.org/obo/GO_1900039"},{"id":"T20404","span":{"begin":479,"end":512},"obj":"http://purl.obolibrary.org/obo/GO_1900036"},{"id":"T20403","span":{"begin":479,"end":512},"obj":"http://purl.obolibrary.org/obo/GO_0010186"},{"id":"T20402","span":{"begin":212,"end":230},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T20401","span":{"begin":212,"end":221},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T20400","span":{"begin":203,"end":230},"obj":"http://purl.obolibrary.org/obo/GO_0019221"}],"text":"IL-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":1286,"end":1291},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20518","span":{"begin":1077,"end":1082},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20517","span":{"begin":1019,"end":1024},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20516","span":{"begin":951,"end":956},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20515","span":{"begin":850,"end":855},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20514","span":{"begin":731,"end":736},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T20513","span":{"begin":665,"end":670},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"IL-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":1172,"end":1177},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20510","span":{"begin":621,"end":626},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20509","span":{"begin":458,"end":463},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20508","span":{"begin":393,"end":398},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20507","span":{"begin":334,"end":339},"obj":"http://purl.obolibrary.org/obo/GO_0005141"},{"id":"T20506","span":{"begin":1106,"end":1110},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T20505","span":{"begin":384,"end":388},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T20504","span":{"begin":318,"end":322},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T20503","span":{"begin":0,"end":4},"obj":"http://purl.obolibrary.org/obo/GO_0005138"}],"text":"IL-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":"sentences","denotations":[{"id":"T20399","span":{"begin":1162,"end":1292},"obj":"Sentence"},{"id":"T20398","span":{"begin":968,"end":1161},"obj":"Sentence"},{"id":"T20397","span":{"begin":836,"end":967},"obj":"Sentence"},{"id":"T20396","span":{"begin":563,"end":835},"obj":"Sentence"},{"id":"T20395","span":{"begin":406,"end":562},"obj":"Sentence"},{"id":"T20394","span":{"begin":236,"end":405},"obj":"Sentence"},{"id":"T20393","span":{"begin":0,"end":235},"obj":"Sentence"},{"id":"T132","span":{"begin":0,"end":235},"obj":"Sentence"},{"id":"T133","span":{"begin":236,"end":405},"obj":"Sentence"},{"id":"T134","span":{"begin":406,"end":562},"obj":"Sentence"},{"id":"T135","span":{"begin":563,"end":835},"obj":"Sentence"},{"id":"T136","span":{"begin":836,"end":967},"obj":"Sentence"},{"id":"T137","span":{"begin":968,"end":1161},"obj":"Sentence"},{"id":"T138","span":{"begin":1162,"end":1292},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"IL-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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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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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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