PMC:3342329 / 25171-26254 JSONTXT

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    test3

    {"project":"test3","denotations":[{"id":"T8994","span":{"begin":1070,"end":1074},"obj":"Protein"},{"id":"T8993","span":{"begin":1012,"end":1018},"obj":"Protein"},{"id":"T8992","span":{"begin":1000,"end":1008},"obj":"Positive_regulation"},{"id":"T8991","span":{"begin":861,"end":867},"obj":"Protein"},{"id":"T8990","span":{"begin":848,"end":857},"obj":"Positive_regulation"},{"id":"T8989","span":{"begin":829,"end":837},"obj":"Negative_regulation"},{"id":"T8988","span":{"begin":823,"end":828},"obj":"Protein"},{"id":"T8987","span":{"begin":812,"end":819},"obj":"Negative_regulation"},{"id":"T8986","span":{"begin":654,"end":660},"obj":"Protein"},{"id":"T8985","span":{"begin":267,"end":273},"obj":"Protein"},{"id":"T8984","span":{"begin":258,"end":266},"obj":"Positive_regulation"},{"id":"T8983","span":{"begin":238,"end":247},"obj":"Negative_regulation"},{"id":"T8982","span":{"begin":211,"end":221},"obj":"Gene_expression"},{"id":"T8981","span":{"begin":206,"end":210},"obj":"Protein"},{"id":"T8980","span":{"begin":195,"end":205},"obj":"Negative_regulation"},{"id":"T8903","span":{"begin":1070,"end":1074},"obj":"Protein"},{"id":"T8902","span":{"begin":1012,"end":1018},"obj":"Protein"},{"id":"T8901","span":{"begin":861,"end":867},"obj":"Protein"},{"id":"T8900","span":{"begin":823,"end":828},"obj":"Protein"},{"id":"T8899","span":{"begin":654,"end":660},"obj":"Protein"},{"id":"T8898","span":{"begin":267,"end":273},"obj":"Protein"},{"id":"T8897","span":{"begin":206,"end":210},"obj":"Protein"}],"relations":[{"id":"R5911","pred":"themeOf","subj":"T8981","obj":"T8982"},{"id":"R5912","pred":"themeOf","subj":"T8982","obj":"T8980"},{"id":"R5913","pred":"themeOf","subj":"T8985","obj":"T8984"},{"id":"R5914","pred":"themeOf","subj":"T8988","obj":"T8989"},{"id":"R5915","pred":"themeOf","subj":"T8989","obj":"T8987"},{"id":"R5916","pred":"themeOf","subj":"T8991","obj":"T8990"},{"id":"R5917","pred":"themeOf","subj":"T8993","obj":"T8992"}],"text":"Activation of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    testone

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    BioNLP16_Messiy

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    BioNLP16_DUT

    {"project":"BioNLP16_DUT","denotations":[{"id":"T10837","span":{"begin":1070,"end":1074},"obj":"Protein"},{"id":"T10836","span":{"begin":1012,"end":1018},"obj":"Protein"},{"id":"T10835","span":{"begin":861,"end":867},"obj":"Protein"},{"id":"T10834","span":{"begin":823,"end":828},"obj":"Protein"},{"id":"T10833","span":{"begin":654,"end":660},"obj":"Protein"},{"id":"T10832","span":{"begin":267,"end":273},"obj":"Protein"},{"id":"T10831","span":{"begin":206,"end":210},"obj":"Protein"},{"id":"T10869","span":{"begin":1000,"end":1008},"obj":"Positive_regulation"},{"id":"T10868","span":{"begin":812,"end":819},"obj":"Negative_regulation"},{"id":"T10867","span":{"begin":829,"end":837},"obj":"Negative_regulation"},{"id":"T10866","span":{"begin":258,"end":266},"obj":"Positive_regulation"},{"id":"T10865","span":{"begin":211,"end":221},"obj":"Gene_expression"},{"id":"T10864","span":{"begin":195,"end":205},"obj":"Negative_regulation"}],"relations":[{"id":"R7321","pred":"themeOf","subj":"T10831","obj":"T10865"},{"id":"R7322","pred":"themeOf","subj":"T10832","obj":"T10866"},{"id":"R7323","pred":"themeOf","subj":"T10834","obj":"T10868"},{"id":"R7324","pred":"themeOf","subj":"T10834","obj":"T10867"},{"id":"R7325","pred":"themeOf","subj":"T10836","obj":"T10869"},{"id":"R7333","pred":"themeOf","subj":"T10865","obj":"T10864"}],"text":"Activation of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    2_test

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    pmc-enju-pas

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of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    bionlp-st-ge-2016-test-proteins

    {"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T9212","span":{"begin":1070,"end":1074},"obj":"Protein"},{"id":"T9211","span":{"begin":1012,"end":1018},"obj":"Protein"},{"id":"T9210","span":{"begin":861,"end":867},"obj":"Protein"},{"id":"T9209","span":{"begin":823,"end":828},"obj":"Protein"},{"id":"T9208","span":{"begin":654,"end":660},"obj":"Protein"},{"id":"T9207","span":{"begin":267,"end":273},"obj":"Protein"},{"id":"T9206","span":{"begin":206,"end":210},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Activation of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    bionlp-st-ge-2016-uniprot

    {"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T10932","span":{"begin":206,"end":210},"obj":"http://www.uniprot.org/uniprot/P05231"},{"id":"T10917","span":{"begin":1012,"end":1018},"obj":"http://www.uniprot.org/uniprot/P18510"},{"id":"T10916","span":{"begin":861,"end":867},"obj":"http://www.uniprot.org/uniprot/P18510"},{"id":"T10915","span":{"begin":654,"end":660},"obj":"http://www.uniprot.org/uniprot/P18510"},{"id":"T10914","span":{"begin":267,"end":273},"obj":"http://www.uniprot.org/uniprot/P18510"},{"id":"T10897","span":{"begin":1070,"end":1074},"obj":"http://www.uniprot.org/uniprot/P51681"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Activation of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    GO-BP

    {"project":"GO-BP","denotations":[{"id":"T9288","span":{"begin":206,"end":221},"obj":"http://purl.obolibrary.org/obo/GO_0032675"},{"id":"T9287","span":{"begin":206,"end":221},"obj":"http://purl.obolibrary.org/obo/GO_0032635"},{"id":"T9286","span":{"begin":76,"end":88},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T9285","span":{"begin":47,"end":59},"obj":"http://purl.obolibrary.org/obo/GO_0051179"},{"id":"T9238","span":{"begin":1049,"end":1066},"obj":"http://purl.obolibrary.org/obo/GO_0045926"},{"id":"T9237","span":{"begin":375,"end":392},"obj":"http://purl.obolibrary.org/obo/GO_0045926"},{"id":"T9233","span":{"begin":1049,"end":1055},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T9232","span":{"begin":686,"end":692},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T9231","span":{"begin":422,"end":428},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T9230","span":{"begin":375,"end":381},"obj":"http://purl.obolibrary.org/obo/GO_0040007"}],"text":"Activation of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    GO-MF

    {"project":"GO-MF","denotations":[{"id":"T9334","span":{"begin":407,"end":412},"obj":"http://purl.obolibrary.org/obo/GO_0045519"},{"id":"T9328","span":{"begin":206,"end":210},"obj":"http://purl.obolibrary.org/obo/GO_0005138"}],"text":"Activation of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    GO-CC

    {"project":"GO-CC","denotations":[{"id":"T9308","span":{"begin":907,"end":912},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T9307","span":{"begin":740,"end":745},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T9306","span":{"begin":620,"end":625},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T9305","span":{"begin":66,"end":71},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Activation of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    sentences

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    simple1

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of NF-κB could modulate subcellular localization of NK cells and pathogenesis [49]. Inhibition of NF-κB activity prevented NK cell depletion, and thus increased anti-tumor activity by decreasing IL-6 production [50]. Thus, the decreased NF-κB and elevated IL-1Ra could also be associated in the infiltration of cytotoxic lymphocytes into tumor, resulting in tumor growth inhibition. In contrast, IL-23, a tumor growth promoting cytokine, increased NF-κB and immune cell infiltration in oral tumor [51]. These data indicate that NF-κB could be involved in the cytokine mediated anti-tumor activities of immune cells. It is also noteworthy that IL-1Ra inhibited melanoma tumor growth by increasing the number of myeloid suppressor cells in tumor [25]. The 3-methylcholatrene-induced tumor incidence was reduced in IL-1α knockout mice, but increased in IL-1Ra mice with concomitant maturation of NK cells and anti-tumor immunity [52]. These data indicate that the decrease of NF-κB, and thus increase of IL-1Ra could be significant in tumor growth inhibition of CCR5−/− mice."}

    bionlp-st-ge-2016-test-tees

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