PMC:3245220 / 21378-23104
Annnotations
bionlp-st-ge-2016-uniprot
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bionlp-st-ge-2016-reference
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Among the IκB molecules, IκBα is highly induced by NF-κB activation [40]. Having shown that PKC regulated NF-κB activity in M-CSF-stimulated MDMs, we next determined whether inhibition of PKC activity decreased expression of NF-κB-regulated genes. We treated both MDMs and RAW 264.7 cells with the PKC inhibitor Ro-31-8220 for 30 minutes and then stimulated with M-CSF. IκBα gene was measured by qRT-PCR. As shown in Figures 6A and 6B, M-CSF enhanced IκBα gene expression and PKC inhibition by Ro-31-8220 decreased IκBα gene expression in both MDMs and RAW 264.7 cells (p\u003c0.01), demonstrating that PKC affected NF-κB-regulated gene expression in macrophages.\n10.1371/journal.pone.0028081.g006 Figure 6 Inhibition of M-CSF-induced PKC reduces NF-κB-regulated genes in both MDMs and RAW 264.7 cells.\nMDMs (A and C) and RAW 264.7 (B) cells were pretreated with Ro-31-8220 or solvent control DMSO for 30 minutes prior to M-CSF stimulation for the indicated times. Total RNA was isolated and converted to cDNA. Real-time RT PCR was performed using primers for IκBα, BCL-xl or GAPDH. Data are expressed as relative fold increase of IκBα or BCL-xl gene expression upon treatment over non-stimulated cells. Data represent the mean ± S.E.M for three independent experiments. To further define the role of PKC in mediating human MDM survival in response to M-CSF, we examined the expression of the anti-apoptotic gene BCL-xL, which is also regulated by NF-κB. As shown in Figure 6C, Ro-31-8220 reduced M-CSF-stimulated BCL-xL expression compared to cells treated with M-CSF and the vehicle control DMSO (p\u003c0.05)."}
bionlp-st-ge-2016-reference-tees
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t":"M-CSF-dependent PKC Regulates NF-κB-targeted Genes\nNF-κB induces a number of downstream genes, including the IκB family. Among the IκB molecules, IκBα is highly induced by NF-κB activation [40]. Having shown that PKC regulated NF-κB activity in M-CSF-stimulated MDMs, we next determined whether inhibition of PKC activity decreased expression of NF-κB-regulated genes. We treated both MDMs and RAW 264.7 cells with the PKC inhibitor Ro-31-8220 for 30 minutes and then stimulated with M-CSF. IκBα gene was measured by qRT-PCR. As shown in Figures 6A and 6B, M-CSF enhanced IκBα gene expression and PKC inhibition by Ro-31-8220 decreased IκBα gene expression in both MDMs and RAW 264.7 cells (p\u003c0.01), demonstrating that PKC affected NF-κB-regulated gene expression in macrophages.\n10.1371/journal.pone.0028081.g006 Figure 6 Inhibition of M-CSF-induced PKC reduces NF-κB-regulated genes in both MDMs and RAW 264.7 cells.\nMDMs (A and C) and RAW 264.7 (B) cells were pretreated with Ro-31-8220 or solvent control DMSO for 30 minutes prior to M-CSF stimulation for the indicated times. Total RNA was isolated and converted to cDNA. Real-time RT PCR was performed using primers for IκBα, BCL-xl or GAPDH. Data are expressed as relative fold increase of IκBα or BCL-xl gene expression upon treatment over non-stimulated cells. Data represent the mean ± S.E.M for three independent experiments. To further define the role of PKC in mediating human MDM survival in response to M-CSF, we examined the expression of the anti-apoptotic gene BCL-xL, which is also regulated by NF-κB. As shown in Figure 6C, Ro-31-8220 reduced M-CSF-stimulated BCL-xL expression compared to cells treated with M-CSF and the vehicle control DMSO (p\u003c0.05)."}
events-check-again
{"project":"events-check-again","denotations":[{"id":"T9984","span":{"begin":0,"end":5},"obj":"Protein"},{"id":"T9985","span":{"begin":146,"end":150},"obj":"Protein"},{"id":"T9986","span":{"begin":161,"end":168},"obj":"Positive_regulation"},{"id":"T9987","span":{"begin":245,"end":250},"obj":"Protein"},{"id":"T9988","span":{"begin":484,"end":489},"obj":"Protein"},{"id":"T9989","span":{"begin":491,"end":495},"obj":"Protein"},{"id":"T9990","span":{"begin":557,"end":562},"obj":"Protein"},{"id":"T9991","span":{"begin":563,"end":571},"obj":"Positive_regulation"},{"id":"T9992","span":{"begin":572,"end":576},"obj":"Protein"},{"id":"T9993","span":{"begin":582,"end":592},"obj":"Gene_expression"},{"id":"T9994","span":{"begin":626,"end":635},"obj":"Negative_regulation"},{"id":"T9995","span":{"begin":636,"end":640},"obj":"Protein"},{"id":"T9996","span":{"begin":646,"end":656},"obj":"Gene_expression"},{"id":"T9997","span":{"begin":1471,"end":1476},"obj":"Protein"},{"id":"T9998","span":{"begin":1494,"end":1504},"obj":"Gene_expression"},{"id":"T9999","span":{"begin":1532,"end":1538},"obj":"Protein"},{"id":"T10000","span":{"begin":1554,"end":1563},"obj":"Regulation"},{"id":"T10001","span":{"begin":1608,"end":1615},"obj":"Negative_regulation"},{"id":"T10002","span":{"begin":1616,"end":1621},"obj":"Protein"},{"id":"T10003","span":{"begin":1622,"end":1632},"obj":"Positive_regulation"},{"id":"T10004","span":{"begin":1633,"end":1639},"obj":"Protein"},{"id":"T10005","span":{"begin":1640,"end":1650},"obj":"Gene_expression"},{"id":"T10006","span":{"begin":1682,"end":1687},"obj":"Protein"},{"id":"T25398","span":{"begin":824,"end":834},"obj":"Negative_regulation"},{"id":"T25399","span":{"begin":838,"end":843},"obj":"Protein"},{"id":"T25400","span":{"begin":1039,"end":1044},"obj":"Protein"},{"id":"T25401","span":{"begin":1177,"end":1181},"obj":"Protein"},{"id":"T25402","span":{"begin":1183,"end":1189},"obj":"Protein"},{"id":"T25403","span":{"begin":1236,"end":1244},"obj":"Positive_regulation"},{"id":"T25404","span":{"begin":1236,"end":1244},"obj":"Positive_regulation"},{"id":"T25405","span":{"begin":1248,"end":1252},"obj":"Protein"},{"id":"T25406","span":{"begin":1256,"end":1262},"obj":"Protein"},{"id":"T25407","span":{"begin":1268,"end":1278},"obj":"Gene_expression"},{"id":"T25408","span":{"begin":1268,"end":1278},"obj":"Gene_expression"}],"relations":[{"id":"R7519","pred":"themeOf","subj":"T9985","obj":"T9986"},{"id":"R7520","pred":"causeOf","subj":"T9990","obj":"T9991"},{"id":"R7521","pred":"themeOf","subj":"T9992","obj":"T9993"},{"id":"R7522","pred":"themeOf","subj":"T9993","obj":"T9991"},{"id":"R7523","pred":"themeOf","subj":"T9995","obj":"T9996"},{"id":"R7524","pred":"themeOf","subj":"T9996","obj":"T9994"},{"id":"R7525","pred":"themeOf","subj":"T9999","obj":"T10000"},{"id":"R7526","pred":"themeOf","subj":"T9999","obj":"T9998"},{"id":"R7527","pred":"themeOf","subj":"T10003","obj":"T10001"},{"id":"R7528","pred":"themeOf","subj":"T10004","obj":"T10005"},{"id":"R7529","pred":"themeOf","subj":"T10005","obj":"T10003"},{"id":"R19401","pred":"themeOf","subj":"T25399","obj":"T25398"},{"id":"R19402","pred":"themeOf","subj":"T25405","obj":"T25407"},{"id":"R19403","pred":"themeOf","subj":"T25406","obj":"T25408"},{"id":"R19404","pred":"themeOf","subj":"T25407","obj":"T25403"},{"id":"R19405","pred":"themeOf","subj":"T25408","obj":"T25404"}],"attributes":[{"id":"M119","pred":"Speculation","subj":"T9998","obj":"true"}],"text":"M-CSF-dependent PKC Regulates NF-κB-targeted Genes\nNF-κB induces a number of downstream genes, including the IκB family. Among the IκB molecules, IκBα is highly induced by NF-κB activation [40]. Having shown that PKC regulated NF-κB activity in M-CSF-stimulated MDMs, we next determined whether inhibition of PKC activity decreased expression of NF-κB-regulated genes. We treated both MDMs and RAW 264.7 cells with the PKC inhibitor Ro-31-8220 for 30 minutes and then stimulated with M-CSF. IκBα gene was measured by qRT-PCR. As shown in Figures 6A and 6B, M-CSF enhanced IκBα gene expression and PKC inhibition by Ro-31-8220 decreased IκBα gene expression in both MDMs and RAW 264.7 cells (p\u003c0.01), demonstrating that PKC affected NF-κB-regulated gene expression in macrophages.\n10.1371/journal.pone.0028081.g006 Figure 6 Inhibition of M-CSF-induced PKC reduces NF-κB-regulated genes in both MDMs and RAW 264.7 cells.\nMDMs (A and C) and RAW 264.7 (B) cells were pretreated with Ro-31-8220 or solvent control DMSO for 30 minutes prior to M-CSF stimulation for the indicated times. Total RNA was isolated and converted to cDNA. Real-time RT PCR was performed using primers for IκBα, BCL-xl or GAPDH. Data are expressed as relative fold increase of IκBα or BCL-xl gene expression upon treatment over non-stimulated cells. Data represent the mean ± S.E.M for three independent experiments. To further define the role of PKC in mediating human MDM survival in response to M-CSF, we examined the expression of the anti-apoptotic gene BCL-xL, which is also regulated by NF-κB. As shown in Figure 6C, Ro-31-8220 reduced M-CSF-stimulated BCL-xL expression compared to cells treated with M-CSF and the vehicle control DMSO (p\u003c0.05)."}
GO-CC
{"project":"GO-CC","denotations":[{"id":"T9869","span":{"begin":404,"end":409},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T9870","span":{"begin":684,"end":689},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T9871","span":{"begin":1663,"end":1668},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T25344","span":{"begin":913,"end":918},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T25345","span":{"begin":953,"end":958},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T25346","span":{"begin":1314,"end":1319},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"M-CSF-dependent PKC Regulates NF-κB-targeted Genes\nNF-κB induces a number of downstream genes, including the IκB family. Among the IκB molecules, IκBα is highly induced by NF-κB activation [40]. Having shown that PKC regulated NF-κB activity in M-CSF-stimulated MDMs, we next determined whether inhibition of PKC activity decreased expression of NF-κB-regulated genes. We treated both MDMs and RAW 264.7 cells with the PKC inhibitor Ro-31-8220 for 30 minutes and then stimulated with M-CSF. IκBα gene was measured by qRT-PCR. As shown in Figures 6A and 6B, M-CSF enhanced IκBα gene expression and PKC inhibition by Ro-31-8220 decreased IκBα gene expression in both MDMs and RAW 264.7 cells (p\u003c0.01), demonstrating that PKC affected NF-κB-regulated gene expression in macrophages.\n10.1371/journal.pone.0028081.g006 Figure 6 Inhibition of M-CSF-induced PKC reduces NF-κB-regulated genes in both MDMs and RAW 264.7 cells.\nMDMs (A and C) and RAW 264.7 (B) cells were pretreated with Ro-31-8220 or solvent control DMSO for 30 minutes prior to M-CSF stimulation for the indicated times. Total RNA was isolated and converted to cDNA. Real-time RT PCR was performed using primers for IκBα, BCL-xl or GAPDH. Data are expressed as relative fold increase of IκBα or BCL-xl gene expression upon treatment over non-stimulated cells. Data represent the mean ± S.E.M for three independent experiments. To further define the role of PKC in mediating human MDM survival in response to M-CSF, we examined the expression of the anti-apoptotic gene BCL-xL, which is also regulated by NF-κB. As shown in Figure 6C, Ro-31-8220 reduced M-CSF-stimulated BCL-xL expression compared to cells treated with M-CSF and the vehicle control DMSO (p\u003c0.05)."}
GO-MF
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GO-BP
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bionlp-st-ge-2016-coref
{"project":"bionlp-st-ge-2016-coref","denotations":[{"id":"T9809","span":{"begin":1508,"end":1531},"obj":"Anaphor"},{"id":"T9810","span":{"begin":1532,"end":1538},"obj":"Antecedent"},{"id":"T9811","span":{"begin":1540,"end":1545},"obj":"Anaphor"}],"relations":[{"id":"R7454","pred":"boundBy","subj":"T9809","obj":"T9810"},{"id":"R7455","pred":"boundBy","subj":"T9811","obj":"T9810"}],"namespaces":[{"prefix":"_base","uri":"https://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"M-CSF-dependent PKC Regulates NF-κB-targeted Genes\nNF-κB induces a number of downstream genes, including the IκB family. Among the IκB molecules, IκBα is highly induced by NF-κB activation [40]. Having shown that PKC regulated NF-κB activity in M-CSF-stimulated MDMs, we next determined whether inhibition of PKC activity decreased expression of NF-κB-regulated genes. We treated both MDMs and RAW 264.7 cells with the PKC inhibitor Ro-31-8220 for 30 minutes and then stimulated with M-CSF. IκBα gene was measured by qRT-PCR. As shown in Figures 6A and 6B, M-CSF enhanced IκBα gene expression and PKC inhibition by Ro-31-8220 decreased IκBα gene expression in both MDMs and RAW 264.7 cells (p\u003c0.01), demonstrating that PKC affected NF-κB-regulated gene expression in macrophages.\n10.1371/journal.pone.0028081.g006 Figure 6 Inhibition of M-CSF-induced PKC reduces NF-κB-regulated genes in both MDMs and RAW 264.7 cells.\nMDMs (A and C) and RAW 264.7 (B) cells were pretreated with Ro-31-8220 or solvent control DMSO for 30 minutes prior to M-CSF stimulation for the indicated times. Total RNA was isolated and converted to cDNA. Real-time RT PCR was performed using primers for IκBα, BCL-xl or GAPDH. Data are expressed as relative fold increase of IκBα or BCL-xl gene expression upon treatment over non-stimulated cells. Data represent the mean ± S.E.M for three independent experiments. To further define the role of PKC in mediating human MDM survival in response to M-CSF, we examined the expression of the anti-apoptotic gene BCL-xL, which is also regulated by NF-κB. As shown in Figure 6C, Ro-31-8220 reduced M-CSF-stimulated BCL-xL expression compared to cells treated with M-CSF and the vehicle control DMSO (p\u003c0.05)."}
pmc-enju-pas
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sentences
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2_test
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,"subj":"T25220","obj":"T25217"},{"id":"R19277","pred":"punct","subj":"T25221","obj":"T25212"}],"text":"M-CSF-dependent PKC Regulates NF-κB-targeted Genes\nNF-κB induces a number of downstream genes, including the IκB family. Among the IκB molecules, IκBα is highly induced by NF-κB activation [40]. Having shown that PKC regulated NF-κB activity in M-CSF-stimulated MDMs, we next determined whether inhibition of PKC activity decreased expression of NF-κB-regulated genes. We treated both MDMs and RAW 264.7 cells with the PKC inhibitor Ro-31-8220 for 30 minutes and then stimulated with M-CSF. IκBα gene was measured by qRT-PCR. As shown in Figures 6A and 6B, M-CSF enhanced IκBα gene expression and PKC inhibition by Ro-31-8220 decreased IκBα gene expression in both MDMs and RAW 264.7 cells (p\u003c0.01), demonstrating that PKC affected NF-κB-regulated gene expression in macrophages.\n10.1371/journal.pone.0028081.g006 Figure 6 Inhibition of M-CSF-induced PKC reduces NF-κB-regulated genes in both MDMs and RAW 264.7 cells.\nMDMs (A and C) and RAW 264.7 (B) cells were pretreated with Ro-31-8220 or solvent control DMSO for 30 minutes prior to M-CSF stimulation for the indicated times. Total RNA was isolated and converted to cDNA. Real-time RT PCR was performed using primers for IκBα, BCL-xl or GAPDH. Data are expressed as relative fold increase of IκBα or BCL-xl gene expression upon treatment over non-stimulated cells. Data represent the mean ± S.E.M for three independent experiments. To further define the role of PKC in mediating human MDM survival in response to M-CSF, we examined the expression of the anti-apoptotic gene BCL-xL, which is also regulated by NF-κB. As shown in Figure 6C, Ro-31-8220 reduced M-CSF-stimulated BCL-xL expression compared to cells treated with M-CSF and the vehicle control DMSO (p\u003c0.05)."}
test2
{"project":"test2","denotations":[{"id":"T9395","span":{"begin":0,"end":5},"obj":"Protein"},{"id":"T9396","span":{"begin":146,"end":150},"obj":"Protein"},{"id":"T9397","span":{"begin":161,"end":168},"obj":"Positive_regulation"},{"id":"T9398","span":{"begin":245,"end":250},"obj":"Protein"},{"id":"T9399","span":{"begin":484,"end":489},"obj":"Protein"},{"id":"T9400","span":{"begin":491,"end":495},"obj":"Protein"},{"id":"T9401","span":{"begin":557,"end":562},"obj":"Protein"},{"id":"T9402","span":{"begin":563,"end":571},"obj":"Positive_regulation"},{"id":"T9403","span":{"begin":572,"end":576},"obj":"Protein"},{"id":"T9404","span":{"begin":582,"end":592},"obj":"Gene_expression"},{"id":"T9405","span":{"begin":626,"end":635},"obj":"Negative_regulation"},{"id":"T9406","span":{"begin":636,"end":640},"obj":"Protein"},{"id":"T9407","span":{"begin":646,"end":656},"obj":"Gene_expression"},{"id":"T9408","span":{"begin":1471,"end":1476},"obj":"Protein"},{"id":"T9409","span":{"begin":1494,"end":1504},"obj":"Gene_expression"},{"id":"T9410","span":{"begin":1532,"end":1538},"obj":"Protein"},{"id":"T9411","span":{"begin":1554,"end":1563},"obj":"Regulation"},{"id":"T9412","span":{"begin":1608,"end":1615},"obj":"Negative_regulation"},{"id":"T9413","span":{"begin":1616,"end":1621},"obj":"Protein"},{"id":"T9414","span":{"begin":1622,"end":1632},"obj":"Positive_regulation"},{"id":"T9415","span":{"begin":1633,"end":1639},"obj":"Protein"},{"id":"T9416","span":{"begin":1640,"end":1650},"obj":"Gene_expression"},{"id":"T9417","span":{"begin":1682,"end":1687},"obj":"Protein"},{"id":"T25107","span":{"begin":838,"end":843},"obj":"Protein"},{"id":"T25108","span":{"begin":1039,"end":1044},"obj":"Protein"},{"id":"T25109","span":{"begin":1177,"end":1181},"obj":"Protein"},{"id":"T25110","span":{"begin":1183,"end":1189},"obj":"Protein"},{"id":"T25111","span":{"begin":1236,"end":1244},"obj":"Positive_regulation"},{"id":"T25112","span":{"begin":1248,"end":1252},"obj":"Protein"},{"id":"T25113","span":{"begin":1256,"end":1262},"obj":"Protein"},{"id":"T25114","span":{"begin":1268,"end":1278},"obj":"Gene_expression"}],"relations":[{"id":"R7062","pred":"themeOf","subj":"T9396","obj":"T9397"},{"id":"R7063","pred":"causeOf","subj":"T9401","obj":"T9402"},{"id":"R7064","pred":"themeOf","subj":"T9403","obj":"T9404"},{"id":"R7065","pred":"themeOf","subj":"T9404","obj":"T9402"},{"id":"R7066","pred":"themeOf","subj":"T9406","obj":"T9407"},{"id":"R7067","pred":"themeOf","subj":"T9407","obj":"T9405"},{"id":"R7068","pred":"themeOf","subj":"T9409","obj":"T9411"},{"id":"R7069","pred":"themeOf","subj":"T9410","obj":"T9409"},{"id":"R7070","pred":"causeOf","subj":"T9413","obj":"T9414"},{"id":"R7071","pred":"themeOf","subj":"T9414","obj":"T9412"},{"id":"R7072","pred":"themeOf","subj":"T9415","obj":"T9416"},{"id":"R7073","pred":"themeOf","subj":"T9416","obj":"T9414"},{"id":"R19174","pred":"themeOf","subj":"T25112","obj":"T25114"},{"id":"R19175","pred":"themeOf","subj":"T25113","obj":"T25114"},{"id":"R19176","pred":"themeOf","subj":"T25114","obj":"T25111"}],"attributes":[{"id":"M112","pred":"Speculation","subj":"T9400","obj":"true"}],"text":"M-CSF-dependent PKC Regulates NF-κB-targeted Genes\nNF-κB induces a number of downstream genes, including the IκB family. Among the IκB molecules, IκBα is highly induced by NF-κB activation [40]. Having shown that PKC regulated NF-κB activity in M-CSF-stimulated MDMs, we next determined whether inhibition of PKC activity decreased expression of NF-κB-regulated genes. We treated both MDMs and RAW 264.7 cells with the PKC inhibitor Ro-31-8220 for 30 minutes and then stimulated with M-CSF. IκBα gene was measured by qRT-PCR. As shown in Figures 6A and 6B, M-CSF enhanced IκBα gene expression and PKC inhibition by Ro-31-8220 decreased IκBα gene expression in both MDMs and RAW 264.7 cells (p\u003c0.01), demonstrating that PKC affected NF-κB-regulated gene expression in macrophages.\n10.1371/journal.pone.0028081.g006 Figure 6 Inhibition of M-CSF-induced PKC reduces NF-κB-regulated genes in both MDMs and RAW 264.7 cells.\nMDMs (A and C) and RAW 264.7 (B) cells were pretreated with Ro-31-8220 or solvent control DMSO for 30 minutes prior to M-CSF stimulation for the indicated times. Total RNA was isolated and converted to cDNA. Real-time RT PCR was performed using primers for IκBα, BCL-xl or GAPDH. Data are expressed as relative fold increase of IκBα or BCL-xl gene expression upon treatment over non-stimulated cells. Data represent the mean ± S.E.M for three independent experiments. To further define the role of PKC in mediating human MDM survival in response to M-CSF, we examined the expression of the anti-apoptotic gene BCL-xL, which is also regulated by NF-κB. As shown in Figure 6C, Ro-31-8220 reduced M-CSF-stimulated BCL-xL expression compared to cells treated with M-CSF and the vehicle control DMSO (p\u003c0.05)."}