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    bionlp-st-ge-2016-uniprot

    {"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T5134","span":{"begin":0,"end":5},"obj":"P09603"},{"id":"T5135","span":{"begin":2,"end":5},"obj":"P04141"},{"id":"T5136","span":{"begin":148,"end":153},"obj":"P09603"},{"id":"T5137","span":{"begin":150,"end":153},"obj":"P04141"},{"id":"T5138","span":{"begin":253,"end":258},"obj":"P09603"},{"id":"T5139","span":{"begin":255,"end":258},"obj":"P04141"},{"id":"T5140","span":{"begin":409,"end":414},"obj":"P09603"},{"id":"T5141","span":{"begin":411,"end":414},"obj":"P04141"},{"id":"T5142","span":{"begin":590,"end":595},"obj":"P09603"},{"id":"T5143","span":{"begin":592,"end":595},"obj":"P04141"},{"id":"T5144","span":{"begin":938,"end":943},"obj":"P09603"},{"id":"T5145","span":{"begin":940,"end":943},"obj":"P04141"},{"id":"T5146","span":{"begin":2016,"end":2021},"obj":"P09603"},{"id":"T5147","span":{"begin":2018,"end":2021},"obj":"P04141"},{"id":"T5148","span":{"begin":2215,"end":2220},"obj":"P09603"},{"id":"T5149","span":{"begin":2217,"end":2220},"obj":"P04141"},{"id":"T5150","span":{"begin":2364,"end":2369},"obj":"P09603"},{"id":"T5151","span":{"begin":2366,"end":2369},"obj":"P04141"},{"id":"T23146","span":{"begin":1001,"end":1006},"obj":"P09603"},{"id":"T23147","span":{"begin":1003,"end":1006},"obj":"P04141"},{"id":"T23148","span":{"begin":1128,"end":1133},"obj":"P09603"},{"id":"T23149","span":{"begin":1130,"end":1133},"obj":"P04141"},{"id":"T23150","span":{"begin":1389,"end":1394},"obj":"P09603"},{"id":"T23151","span":{"begin":1391,"end":1394},"obj":"P04141"},{"id":"T23152","span":{"begin":1842,"end":1847},"obj":"P09603"},{"id":"T23153","span":{"begin":1844,"end":1847},"obj":"P04141"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    bionlp-st-ge-2016-reference

    {"project":"bionlp-st-ge-2016-reference","denotations":[{"id":"T5152","span":{"begin":2250,"end":2259},"obj":"Positive_regulation"},{"id":"T5153","span":{"begin":2275,"end":2283},"obj":"Positive_regulation"},{"id":"T5154","span":{"begin":2260,"end":2265},"obj":"Protein"},{"id":"T5155","span":{"begin":0,"end":5},"obj":"Protein"},{"id":"T5156","span":{"begin":148,"end":153},"obj":"Protein"},{"id":"T5157","span":{"begin":253,"end":258},"obj":"Protein"},{"id":"T5158","span":{"begin":409,"end":414},"obj":"Protein"},{"id":"T5159","span":{"begin":590,"end":595},"obj":"Protein"},{"id":"T5160","span":{"begin":938,"end":943},"obj":"Protein"},{"id":"T5161","span":{"begin":2016,"end":2021},"obj":"Protein"},{"id":"T5162","span":{"begin":2215,"end":2220},"obj":"Protein"},{"id":"T5163","span":{"begin":2364,"end":2369},"obj":"Protein"},{"id":"T23154","span":{"begin":1001,"end":1006},"obj":"Protein"},{"id":"T23155","span":{"begin":1128,"end":1133},"obj":"Protein"},{"id":"T23156","span":{"begin":1389,"end":1394},"obj":"Protein"},{"id":"T23157","span":{"begin":1842,"end":1847},"obj":"Protein"}],"relations":[{"id":"R3885","pred":"themeOf","subj":"T5153","obj":"T5152"},{"id":"R3886","pred":"themeOf","subj":"T5154","obj":"T5153"},{"id":"R3887","pred":"causeOf","subj":"T5162","obj":"T5152"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    bionlp-st-ge-2016-reference-tees

    {"project":"bionlp-st-ge-2016-reference-tees","denotations":[{"id":"T5264","span":{"begin":0,"end":5},"obj":"Protein"},{"id":"T5265","span":{"begin":14,"end":19},"obj":"Protein"},{"id":"T5266","span":{"begin":148,"end":153},"obj":"Protein"},{"id":"T5267","span":{"begin":162,"end":171},"obj":"Protein"},{"id":"T5268","span":{"begin":253,"end":258},"obj":"Protein"},{"id":"T5269","span":{"begin":172,"end":179},"obj":"Binding"},{"id":"T5270","span":{"begin":154,"end":161},"obj":"Positive_regulation"},{"id":"T5271","span":{"begin":307,"end":320},"obj":"Protein"},{"id":"T5272","span":{"begin":336,"end":341},"obj":"Binding"},{"id":"T5273","span":{"begin":409,"end":414},"obj":"Protein"},{"id":"T5274","span":{"begin":429,"end":434},"obj":"Protein"},{"id":"T5275","span":{"begin":439,"end":446},"obj":"Binding"},{"id":"T5276","span":{"begin":423,"end":428},"obj":"Regulation"},{"id":"T5277","span":{"begin":516,"end":538},"obj":"Protein"},{"id":"T5278","span":{"begin":555,"end":560},"obj":"Protein"},{"id":"T5279","span":{"begin":590,"end":595},"obj":"Protein"},{"id":"T5280","span":{"begin":666,"end":678},"obj":"Protein"},{"id":"T5281","span":{"begin":487,"end":499},"obj":"Gene_expression"},{"id":"T5282","span":{"begin":654,"end":662},"obj":"Positive_regulation"},{"id":"T5283","span":{"begin":782,"end":786},"obj":"Protein"},{"id":"T5284","span":{"begin":787,"end":791},"obj":"Protein"},{"id":"T5285","span":{"begin":810,"end":829},"obj":"Protein"},{"id":"T5286","span":{"begin":802,"end":809},"obj":"Negative_regulation"},{"id":"T5287","span":{"begin":867,"end":886},"obj":"Protein"},{"id":"T5288","span":{"begin":903,"end":907},"obj":"Protein"},{"id":"T5289","span":{"begin":938,"end":943},"obj":"Protein"},{"id":"T5290","span":{"begin":846,"end":857},"obj":"Gene_expression"},{"id":"T5291","span":{"begin":846,"end":857},"obj":"Positive_regulation"},{"id":"T5292","span":{"begin":895,"end":902},"obj":"Gene_expression"},{"id":"T5293","span":{"begin":2016,"end":2021},"obj":"Protein"},{"id":"T5294","span":{"begin":2030,"end":2035},"obj":"Protein"},{"id":"T5295","span":{"begin":2022,"end":2029},"obj":"Positive_regulation"},{"id":"T5296","span":{"begin":2140,"end":2145},"obj":"Protein"},{"id":"T5297","span":{"begin":2146,"end":2150},"obj":"Protein"},{"id":"T5298","span":{"begin":2260,"end":2274},"obj":"Protein"},{"id":"T5299","span":{"begin":2250,"end":2259},"obj":"Positive_regulation"},{"id":"T5300","span":{"begin":2364,"end":2369},"obj":"Protein"},{"id":"T5301","span":{"begin":2378,"end":2383},"obj":"Protein"},{"id":"T23195","span":{"begin":1001,"end":1006},"obj":"Protein"},{"id":"T23196","span":{"begin":1015,"end":1020},"obj":"Protein"},{"id":"T23197","span":{"begin":1007,"end":1014},"obj":"Positive_regulation"},{"id":"T23198","span":{"begin":1128,"end":1133},"obj":"Protein"},{"id":"T23199","span":{"begin":1156,"end":1161},"obj":"Protein"},{"id":"T23200","span":{"begin":1166,"end":1173},"obj":"Binding"},{"id":"T23201","span":{"begin":1348,"end":1370},"obj":"Protein"},{"id":"T23202","span":{"begin":1389,"end":1394},"obj":"Protein"},{"id":"T23203","span":{"begin":1471,"end":1476},"obj":"Protein"},{"id":"T23204","span":{"begin":1526,"end":1530},"obj":"Protein"},{"id":"T23205","span":{"begin":1599,"end":1603},"obj":"Protein"},{"id":"T23206","span":{"begin":1531,"end":1539},"obj":"Localization"},{"id":"T23207","span":{"begin":1531,"end":1539},"obj":"Localization"},{"id":"T23208","span":{"begin":1587,"end":1595},"obj":"Positive_regulation"},{"id":"T23209","span":{"begin":1730,"end":1733},"obj":"Protein"},{"id":"T23210","span":{"begin":1734,"end":1736},"obj":"Protein"},{"id":"T23211","span":{"begin":1737,"end":1741},"obj":"Protein"},{"id":"T23212","span":{"begin":1824,"end":1847},"obj":"Protein"}],"relations":[{"id":"R3907","pred":"causeOf","subj":"T5266","obj":"T5270"},{"id":"R3908","pred":"themeOf","subj":"T5267","obj":"T5269"},{"id":"R3909","pred":"themeOf","subj":"T5269","obj":"T5270"},{"id":"R3910","pred":"themeOf","subj":"T5271","obj":"T5272"},{"id":"R3911","pred":"causeOf","subj":"T5273","obj":"T5276"},{"id":"R3912","pred":"themeOf","subj":"T5274","obj":"T5275"},{"id":"R3913","pred":"themeOf","subj":"T5275","obj":"T5276"},{"id":"R3914","pred":"themeOf","subj":"T5277","obj":"T5281"},{"id":"R3915","pred":"themeOf","subj":"T5280","obj":"T5282"},{"id":"R3916","pred":"themeOf","subj":"T5285","obj":"T5286"},{"id":"R3917","pred":"themeOf","subj":"T5287","obj":"T5290"},{"id":"R3918","pred":"themeOf","subj":"T5288","obj":"T5292"},{"id":"R3919","pred":"themeOf","subj":"T5290","obj":"T5291"},{"id":"R3920","pred":"causeOf","subj":"T5293","obj":"T5295"},{"id":"R3921","pred":"themeOf","subj":"T5294","obj":"T5295"},{"id":"R3922","pred":"themeOf","subj":"T5298","obj":"T5299"},{"id":"R17695","pred":"causeOf","subj":"T23195","obj":"T23197"},{"id":"R17696","pred":"themeOf","subj":"T23196","obj":"T23197"},{"id":"R17697","pred":"themeOf","subj":"T23199","obj":"T23200"},{"id":"R17698","pred":"themeOf","subj":"T23203","obj":"T23206"},{"id":"R17699","pred":"themeOf","subj":"T23204","obj":"T23207"},{"id":"R17700","pred":"themeOf","subj":"T23205","obj":"T23208"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    events-check-again

    {"project":"events-check-again","denotations":[{"id":"T5252","span":{"begin":0,"end":5},"obj":"Protein"},{"id":"T5253","span":{"begin":148,"end":153},"obj":"Protein"},{"id":"T5254","span":{"begin":253,"end":258},"obj":"Protein"},{"id":"T5255","span":{"begin":409,"end":414},"obj":"Protein"},{"id":"T5256","span":{"begin":590,"end":595},"obj":"Protein"},{"id":"T5257","span":{"begin":938,"end":943},"obj":"Protein"},{"id":"T5258","span":{"begin":2016,"end":2021},"obj":"Protein"},{"id":"T5259","span":{"begin":2215,"end":2220},"obj":"Protein"},{"id":"T5260","span":{"begin":2250,"end":2259},"obj":"Positive_regulation"},{"id":"T5261","span":{"begin":2260,"end":2265},"obj":"Protein"},{"id":"T5262","span":{"begin":2275,"end":2283},"obj":"Positive_regulation"},{"id":"T5263","span":{"begin":2364,"end":2369},"obj":"Protein"},{"id":"T23191","span":{"begin":1001,"end":1006},"obj":"Protein"},{"id":"T23192","span":{"begin":1128,"end":1133},"obj":"Protein"},{"id":"T23193","span":{"begin":1389,"end":1394},"obj":"Protein"},{"id":"T23194","span":{"begin":1842,"end":1847},"obj":"Protein"}],"relations":[{"id":"R3904","pred":"causeOf","subj":"T5259","obj":"T5260"},{"id":"R3905","pred":"themeOf","subj":"T5261","obj":"T5262"},{"id":"R3906","pred":"themeOf","subj":"T5262","obj":"T5260"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    GO-CC

    {"project":"GO-CC","denotations":[{"id":"T5184","span":{"begin":111,"end":115},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T5185","span":{"begin":625,"end":630},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T5186","span":{"begin":2101,"end":2106},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T5187","span":{"begin":2244,"end":2249},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T5188","span":{"begin":2321,"end":2326},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23169","span":{"begin":1656,"end":1661},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23170","span":{"begin":1677,"end":1682},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    GO-MF

    {"project":"GO-MF","denotations":[{"id":"T5176","span":{"begin":168,"end":179},"obj":"http://purl.obolibrary.org/obo/GO_0003677"},{"id":"T5177","span":{"begin":435,"end":446},"obj":"http://purl.obolibrary.org/obo/GO_0003677"},{"id":"T5178","span":{"begin":172,"end":179},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T5179","span":{"begin":439,"end":446},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T5180","span":{"begin":571,"end":578},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T5181","span":{"begin":816,"end":823},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T5182","span":{"begin":810,"end":823},"obj":"http://purl.obolibrary.org/obo/GO_0051059"},{"id":"T5183","span":{"begin":2022,"end":2044},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T23167","span":{"begin":1162,"end":1173},"obj":"http://purl.obolibrary.org/obo/GO_0003677"},{"id":"T23168","span":{"begin":1166,"end":1173},"obj":"http://purl.obolibrary.org/obo/GO_0005488"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    GO-BP

    {"project":"GO-BP","denotations":[{"id":"T5174","span":{"begin":2022,"end":2044},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5175","span":{"begin":2384,"end":2399},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T23166","span":{"begin":1021,"end":1036},"obj":"http://purl.obolibrary.org/obo/GO_0006351"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    UBERON-AE

    {"project":"UBERON-AE","denotations":[{"id":"T22809","span":{"begin":1764,"end":1769},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    pmc-enju-pas

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Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    sentences

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    2_test

    {"project":"2_test","denotations":[{"id":"22216091-11073986-90609709","span":{"begin":302,"end":304},"obj":"11073986"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    bionlp-st-ge-2016-spacy-parsed

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Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}

    test2

    {"project":"test2","denotations":[{"id":"T4653","span":{"begin":0,"end":5},"obj":"Protein"},{"id":"T4654","span":{"begin":148,"end":153},"obj":"Protein"},{"id":"T4655","span":{"begin":253,"end":258},"obj":"Protein"},{"id":"T4656","span":{"begin":409,"end":414},"obj":"Protein"},{"id":"T4657","span":{"begin":590,"end":595},"obj":"Protein"},{"id":"T4658","span":{"begin":938,"end":943},"obj":"Protein"},{"id":"T4659","span":{"begin":2016,"end":2021},"obj":"Protein"},{"id":"T4660","span":{"begin":2215,"end":2220},"obj":"Protein"},{"id":"T4661","span":{"begin":2250,"end":2259},"obj":"Positive_regulation"},{"id":"T4662","span":{"begin":2260,"end":2265},"obj":"Protein"},{"id":"T4663","span":{"begin":2364,"end":2369},"obj":"Protein"},{"id":"T22805","span":{"begin":1001,"end":1006},"obj":"Protein"},{"id":"T22806","span":{"begin":1128,"end":1133},"obj":"Protein"},{"id":"T22807","span":{"begin":1389,"end":1394},"obj":"Protein"},{"id":"T22808","span":{"begin":1842,"end":1847},"obj":"Protein"}],"relations":[{"id":"R3428","pred":"causeOf","subj":"T4660","obj":"T4661"}],"text":"M-CSF Induces NF-κB Transcriptional Activity in Human Monocyte–Derived Macrophages (MDMs) and Mouse Macrophage Cell Line, RAW 264.7\nTo determine if M-CSF induced NF-κB DNA binding in human macrophages, we performed EMSA analysis on nuclear lysates from M-CSF-treated MDMs. Similar to previous reports [11], nuclear NF-κB constitutively bound DNA in non-stimulated monocytes (Figure 1A). Interestingly, adding M-CSF did not alter NF-κB DNA binding by EMSA. In contrast, after transiently transfecting human MDMs with pNF-κB-SEAP constructs containing four NF-κB consensus binding sequences, M-CSF treatment of the transfected cells resulted in a 2.3-fold increase in SEAP release in the culture media compared to PBS (vehicle)-treated transfected MDMs (Figure 1B). As a control, the pTAL-SEAP construct lacking NF-κB binding sites was used. Cells transfected with the pTAL-SEAP construct did not produce SEAP in the absence or presence of M-CSF (Figure 1B).\n10.1371/journal.pone.0028081.g001 Figure 1 M-CSF induces NF-κB transcriptional activity in macrophages.\n(A) Nuclei were extracted from human MDMs treated without or with M-CSF for 15 or 30 minutes. NF-κB DNA binding activity was analyzed by EMSA Shown is a representative blot from three independent experiments. NS: non-stimulated. (B) Human MDMs transiently transfected with pTAL-SEAP or pNF-κB-SEAP constructs were treated with M-CSF in X-vivo medium and incubated for 6 hours before the collection of medium. NF-κB activity was analyzed by measuring the amount of SEAP secreted into the medium and data are expressed as fold increase of SEAP activity over that in pTAL-SEAP transfected resting cells. (C) RAW 264.7 cells were transiently transfected with pTAL-SEAP or pNF-κB-SEAP construct. Cells were serum starved for 4 hours prior to 2 hours stimulation with mouse recombinant M-CSF (100 ng/ml). Culture media was collected to measure SEAP production. Data are expressed mean ± S.E.M, for three independent experiments. We next investigated whether M-CSF induced NF-κB activity in the mouse macrophage cell line, RAW 264.7. RAW 264.7 cells were transfected with either the NF-κB-SEAP reporter or control pTAL-SEAP construct. As shown in Figure 1C, M-CSF treatment of RAW 264.7 cells increased NF-κB reporter activity by 2.5-fold over that of non-treated cells. Together, our data demonstrate that M-CSF induced NF-κB transcriptional activity in macrophages."}