PMC:3342329 / 20097-21381 JSONTXT

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{"project":"BioNLP16_DUT","denotations":[{"id":"T10796","span":{"begin":1181,"end":1185},"obj":"Protein"},{"id":"T10795","span":{"begin":1121,"end":1125},"obj":"Protein"},{"id":"T10794","span":{"begin":811,"end":814},"obj":"Protein"},{"id":"T10793","span":{"begin":803,"end":806},"obj":"Protein"},{"id":"T10792","span":{"begin":718,"end":722},"obj":"Protein"},{"id":"T10791","span":{"begin":449,"end":453},"obj":"Protein"},{"id":"T10853","span":{"begin":726,"end":735},"obj":"Negative_regulation"},{"id":"T10852","span":{"begin":815,"end":828},"obj":"Localization"},{"id":"T10851","span":{"begin":785,"end":795},"obj":"Negative_regulation"}],"relations":[{"id":"R7309","pred":"themeOf","subj":"T10792","obj":"T10853"},{"id":"R7310","pred":"themeOf","subj":"T10793","obj":"T10851"},{"id":"R7311","pred":"themeOf","subj":"T10793","obj":"T10852"},{"id":"R7312","pred":"themeOf","subj":"T10794","obj":"T10851"},{"id":"R7313","pred":"themeOf","subj":"T10794","obj":"T10852"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

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regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T9171","span":{"begin":1181,"end":1185},"obj":"Protein"},{"id":"T9170","span":{"begin":1121,"end":1125},"obj":"Protein"},{"id":"T9169","span":{"begin":811,"end":814},"obj":"Protein"},{"id":"T9168","span":{"begin":803,"end":806},"obj":"Protein"},{"id":"T9167","span":{"begin":718,"end":722},"obj":"Protein"},{"id":"T9166","span":{"begin":449,"end":453},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T10929","span":{"begin":811,"end":814},"obj":"http://www.uniprot.org/uniprot/P21579"},{"id":"T10928","span":{"begin":811,"end":814},"obj":"http://www.uniprot.org/uniprot/Q04206"},{"id":"T10927","span":{"begin":803,"end":806},"obj":"http://www.uniprot.org/uniprot/P19838"},{"id":"T10921","span":{"begin":517,"end":526},"obj":"http://www.uniprot.org/uniprot/P42574"},{"id":"T10879","span":{"begin":1181,"end":1185},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T10878","span":{"begin":1121,"end":1125},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T10877","span":{"begin":718,"end":722},"obj":"http://www.uniprot.org/uniprot/P51681"},{"id":"T10876","span":{"begin":449,"end":453},"obj":"http://www.uniprot.org/uniprot/P51681"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"UBERON-AE","denotations":[{"id":"T9008","span":{"begin":66,"end":79},"obj":"http://purl.obolibrary.org/obo/UBERON_0002405"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"GO-BP","denotations":[{"id":"T9258","span":{"begin":740,"end":762},"obj":"http://purl.obolibrary.org/obo/GO_0007252"},{"id":"T9257","span":{"begin":740,"end":755},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T9255","span":{"begin":630,"end":635},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T9254","span":{"begin":499,"end":504},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T9252","span":{"begin":625,"end":635},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T9251","span":{"begin":494,"end":504},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T9250","span":{"begin":376,"end":387},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T9246","span":{"begin":271,"end":287},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T9245","span":{"begin":238,"end":251},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T9244","span":{"begin":104,"end":116},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T9242","span":{"begin":88,"end":99},"obj":"http://purl.obolibrary.org/obo/GO_0016049"},{"id":"T9224","span":{"begin":1111,"end":1117},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T9223","span":{"begin":988,"end":994},"obj":"http://purl.obolibrary.org/obo/GO_0040007"},{"id":"T9222","span":{"begin":93,"end":99},"obj":"http://purl.obolibrary.org/obo/GO_0040007"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"GO-MF","denotations":[{"id":"T9316","span":{"begin":546,"end":553},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T9315","span":{"begin":542,"end":553},"obj":"http://purl.obolibrary.org/obo/GO_0003677"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"GO-CC","denotations":[{"id":"T9311","span":{"begin":838,"end":845},"obj":"http://purl.obolibrary.org/obo/GO_0005634"},{"id":"T9310","span":{"begin":233,"end":237},"obj":"http://purl.obolibrary.org/obo/GO_0019013"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"sentences","denotations":[{"id":"T9021","span":{"begin":1135,"end":1284},"obj":"Sentence"},{"id":"T9020","span":{"begin":996,"end":1134},"obj":"Sentence"},{"id":"T9019","span":{"begin":861,"end":995},"obj":"Sentence"},{"id":"T9018","span":{"begin":705,"end":860},"obj":"Sentence"},{"id":"T9017","span":{"begin":412,"end":704},"obj":"Sentence"},{"id":"T9016","span":{"begin":123,"end":411},"obj":"Sentence"},{"id":"T9015","span":{"begin":0,"end":122},"obj":"Sentence"},{"id":"T157","span":{"begin":0,"end":122},"obj":"Sentence"},{"id":"T158","span":{"begin":123,"end":411},"obj":"Sentence"},{"id":"T159","span":{"begin":412,"end":704},"obj":"Sentence"},{"id":"T160","span":{"begin":705,"end":860},"obj":"Sentence"},{"id":"T161","span":{"begin":861,"end":995},"obj":"Sentence"},{"id":"T162","span":{"begin":996,"end":1134},"obj":"Sentence"},{"id":"T163","span":{"begin":1135,"end":1284},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"simple1","denotations":[{"id":"T9364","span":{"begin":1181,"end":1185},"obj":"Protein"},{"id":"T9363","span":{"begin":1121,"end":1125},"obj":"Protein"},{"id":"T9362","span":{"begin":811,"end":814},"obj":"Protein"},{"id":"T9361","span":{"begin":803,"end":806},"obj":"Protein"},{"id":"T9360","span":{"begin":718,"end":722},"obj":"Protein"},{"id":"T9359","span":{"begin":449,"end":453},"obj":"Protein"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

{"project":"DLUT931","denotations":[{"id":"T11011","span":{"begin":1189,"end":1202},"obj":"Negative_regulation"},{"id":"T11010","span":{"begin":815,"end":828},"obj":"Localization"},{"id":"T11009","span":{"begin":785,"end":795},"obj":"Negative_regulation"},{"id":"T10953","span":{"begin":1181,"end":1185},"obj":"Protein"},{"id":"T10952","span":{"begin":1121,"end":1125},"obj":"Protein"},{"id":"T10951","span":{"begin":811,"end":814},"obj":"Protein"},{"id":"T10950","span":{"begin":803,"end":806},"obj":"Protein"},{"id":"T10949","span":{"begin":718,"end":722},"obj":"Protein"},{"id":"T10948","span":{"begin":449,"end":453},"obj":"Protein"}],"relations":[{"id":"R7327","pred":"themeOf","subj":"T11010","obj":"T11009"},{"id":"R7339","pred":"themeOf","subj":"T10950","obj":"T11009"},{"id":"R7340","pred":"themeOf","subj":"T10950","obj":"T11010"},{"id":"R7341","pred":"themeOf","subj":"T10951","obj":"T11009"},{"id":"R7342","pred":"themeOf","subj":"T10951","obj":"T11010"},{"id":"R7343","pred":"themeOf","subj":"T10953","obj":"T11011"},{"id":"R7345","pred":"themeOf","subj":"T11010","obj":"T11009"}],"text":"NF-κB regulates the expression of over 200 genes that control the immune system, cancer cell growth and inflammation [39]. Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. Thus, the inhibitions of NF-κB activity and the expression of target genes are critical in the inhibition of tumor growth in CCR5−/− mice. Although the mechanism is not clear as to how CCR5−/− downregulates NF-κB, it is noteworthy that NF-κB is activated or inactivated by many cytokines."}

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Because of its abilities to induce the expression of a large array of inflammatory mediators and its roles as core transcription factors in diverse immune responses, NF-κB has been recognized as a major factor responsible for cytokine-associated cancer development or anti-tumor immunity. In the melanoma tumor tissues of the CCR5−/− mice, the expression of NF-κB target cell death genes (Bax, caspase-3 and 9) and the DNA binding activity of NF-κB, were significantly inhibited, but the expression of cell death inhibitory NF-κB target genes, such as Bcl-2 and cIAP were enhanced. In addition, CCR5−/− prevented the phosphorylation of IκB, accompanied with the inhibition of the p50 and p65 translocation into the nucleus (Figure 2A-C). Many tumors, including melanoma, have increased levels of NF-κB [40], which is likely acting as a survival factor for melanoma growth. 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