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bionlp-st-ge-2016-uniprot

bionlp-st-ge-2016-reference

bionlp-st-ge-2016-reference-tees

events-check-again

GO-CC

{"project":"GO-CC","denotations":[{"id":"T6786","span":{"begin":113,"end":117},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6787","span":{"begin":175,"end":179},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6788","span":{"begin":2004,"end":2008},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6789","span":{"begin":2019,"end":2024},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6790","span":{"begin":2258,"end":2263},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23992","span":{"begin":1114,"end":1119},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23993","span":{"begin":1716,"end":1721},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23994","span":{"begin":1754,"end":1759},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T23995","span":{"begin":1229,"end":1237},"obj":"http://purl.obolibrary.org/obo/GO_0019815"},{"id":"T23996","span":{"begin":1229,"end":1237},"obj":"http://purl.obolibrary.org/obo/GO_0042571"}],"text":"NF-κB and PKC(s) Mediate Human MDM Survival in Response to M-CSF Stimulation\nSince PKC and NF-κB are critical in cell survival [37], [38], we hypothesized that M-CSF promoted cell survival through PKC in human MDMs. To detect apoptosis, the expression of cleaved caspase-3, a marker of apoptosis, was analyzed in the presence or absence of M-CSF and PKC inhibitors. In MDMs pretreated with PKC inhibitors (Ro-31-8220, Gö-6976, or BAPTA/AM) and stimulated with M-CSF, cleaved caspase-3 was elevated to levels of cells treated with vehicle alone (Figure 3A). In contrast, cells incubated with M-CSF and vehicle had less cleaved caspase-3 than cells incubated with vehicle alone or M-CSF with PKC inhibitors. These data supported the hypothesis that M-CSF-induced NF-κB activity was regulated by conventional PKCs, not novel PKCs.\n10.1371/journal.pone.0028081.g003 Figure 3 Inhibition of PKC or NF-κB induces apoptosis in MDMs.\n(A) MDMs were pre-incubated in RPMI medium containing inhibitors (Ro-31-8220: 5 µM, Gö-6976: 5 µM, BAPTA/AM: 2.5 µM) for 30 minutes prior to the addition of M-CSF. As a control, untreated cells were incubated with dimethyl sulfoxide (DMSO). Cell lysates were resolved by SDS-PAGE and immunoblotted with antibody recognizing the active cleaved form of caspase-3. The blots were reblotted with β-actin that served as a loading control. The ratio of active caspase-3 bands (17 kD and 19 kD) to β-actin control was determined by densitometry analysis (bottom panel). Data represents the mean ± S.E.M from two independent donors. (B) Apoptosis of the treated MDMs was also measured by Annexin V-FITC and propidium iodine (PI) staining and analyzed by flow cytometry. The percentage of surviving cells (Annexin V/PI negative) for the cells treated with vehicle/M-CSF was arbitrarily set as 100. Data shown represent the mean ± S.E.M from three independent experiments. *The p-values of inhibitors/M-CSF compared to vehicle/M-CSF were ≤0.05. To confirm that PKC inhibition decreased cell survival, cells were treated with M-CSF in the absence or presence of PKC inhibitors and then also examined for apoptosis by Annexin V/PI staining. PKC inhibitors in the presence of M-CSF reduced the number of Annexin V/PI negative MDMs compared to cells treated with M-CSF alone (Figure 3B). These observations further suggested that MDM survival is promoted by M-CSF and critically involves conventional PKCs and NF-κB activity."}

GO-MF

{"project":"GO-MF","denotations":[{"id":"T6777","span":{"begin":10,"end":13},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6778","span":{"begin":83,"end":86},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6779","span":{"begin":197,"end":200},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6780","span":{"begin":350,"end":353},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6781","span":{"begin":390,"end":393},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6782","span":{"begin":690,"end":693},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6783","span":{"begin":1979,"end":1982},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6784","span":{"begin":2079,"end":2082},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6785","span":{"begin":2157,"end":2160},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T23990","span":{"begin":886,"end":889},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T23991","span":{"begin":1229,"end":1237},"obj":"http://purl.obolibrary.org/obo/GO_0003823"}],"text":"NF-κB and PKC(s) Mediate Human MDM Survival in Response to M-CSF Stimulation\nSince PKC and NF-κB are critical in cell survival [37], [38], we hypothesized that M-CSF promoted cell survival through PKC in human MDMs. To detect apoptosis, the expression of cleaved caspase-3, a marker of apoptosis, was analyzed in the presence or absence of M-CSF and PKC inhibitors. In MDMs pretreated with PKC inhibitors (Ro-31-8220, Gö-6976, or BAPTA/AM) and stimulated with M-CSF, cleaved caspase-3 was elevated to levels of cells treated with vehicle alone (Figure 3A). In contrast, cells incubated with M-CSF and vehicle had less cleaved caspase-3 than cells incubated with vehicle alone or M-CSF with PKC inhibitors. These data supported the hypothesis that M-CSF-induced NF-κB activity was regulated by conventional PKCs, not novel PKCs.\n10.1371/journal.pone.0028081.g003 Figure 3 Inhibition of PKC or NF-κB induces apoptosis in MDMs.\n(A) MDMs were pre-incubated in RPMI medium containing inhibitors (Ro-31-8220: 5 µM, Gö-6976: 5 µM, BAPTA/AM: 2.5 µM) for 30 minutes prior to the addition of M-CSF. As a control, untreated cells were incubated with dimethyl sulfoxide (DMSO). Cell lysates were resolved by SDS-PAGE and immunoblotted with antibody recognizing the active cleaved form of caspase-3. The blots were reblotted with β-actin that served as a loading control. The ratio of active caspase-3 bands (17 kD and 19 kD) to β-actin control was determined by densitometry analysis (bottom panel). Data represents the mean ± S.E.M from two independent donors. (B) Apoptosis of the treated MDMs was also measured by Annexin V-FITC and propidium iodine (PI) staining and analyzed by flow cytometry. The percentage of surviving cells (Annexin V/PI negative) for the cells treated with vehicle/M-CSF was arbitrarily set as 100. Data shown represent the mean ± S.E.M from three independent experiments. *The p-values of inhibitors/M-CSF compared to vehicle/M-CSF were ≤0.05. To confirm that PKC inhibition decreased cell survival, cells were treated with M-CSF in the absence or presence of PKC inhibitors and then also examined for apoptosis by Annexin V/PI staining. PKC inhibitors in the presence of M-CSF reduced the number of Annexin V/PI negative MDMs compared to cells treated with M-CSF alone (Figure 3B). These observations further suggested that MDM survival is promoted by M-CSF and critically involves conventional PKCs and NF-κB activity."}

GO-BP

{"project":"GO-BP","denotations":[{"id":"T6987","span":{"begin":47,"end":64},"obj":"http://purl.obolibrary.org/obo/GO_1903969"},{"id":"T6988","span":{"begin":47,"end":64},"obj":"http://purl.obolibrary.org/obo/GO_0036005"},{"id":"T6989","span":{"begin":47,"end":64},"obj":"http://purl.obolibrary.org/obo/GO_1903970"},{"id":"T6990","span":{"begin":47,"end":64},"obj":"http://purl.obolibrary.org/obo/GO_1903971"},{"id":"T6991","span":{"begin":226,"end":235},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T6992","span":{"begin":286,"end":295},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T6993","span":{"begin":2121,"end":2130},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T6994","span":{"begin":226,"end":235},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T6995","span":{"begin":286,"end":295},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T6996","span":{"begin":2121,"end":2130},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T24072","span":{"begin":907,"end":916},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T24073","span":{"begin":1555,"end":1564},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T24074","span":{"begin":907,"end":916},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T24075","span":{"begin":1555,"end":1564},"obj":"http://purl.obolibrary.org/obo/GO_0097194"}],"text":"NF-κB and PKC(s) Mediate Human MDM Survival in Response to M-CSF Stimulation\nSince PKC and NF-κB are critical in cell survival [37], [38], we hypothesized that M-CSF promoted cell survival through PKC in human MDMs. To detect apoptosis, the expression of cleaved caspase-3, a marker of apoptosis, was analyzed in the presence or absence of M-CSF and PKC inhibitors. In MDMs pretreated with PKC inhibitors (Ro-31-8220, Gö-6976, or BAPTA/AM) and stimulated with M-CSF, cleaved caspase-3 was elevated to levels of cells treated with vehicle alone (Figure 3A). In contrast, cells incubated with M-CSF and vehicle had less cleaved caspase-3 than cells incubated with vehicle alone or M-CSF with PKC inhibitors. These data supported the hypothesis that M-CSF-induced NF-κB activity was regulated by conventional PKCs, not novel PKCs.\n10.1371/journal.pone.0028081.g003 Figure 3 Inhibition of PKC or NF-κB induces apoptosis in MDMs.\n(A) MDMs were pre-incubated in RPMI medium containing inhibitors (Ro-31-8220: 5 µM, Gö-6976: 5 µM, BAPTA/AM: 2.5 µM) for 30 minutes prior to the addition of M-CSF. As a control, untreated cells were incubated with dimethyl sulfoxide (DMSO). Cell lysates were resolved by SDS-PAGE and immunoblotted with antibody recognizing the active cleaved form of caspase-3. The blots were reblotted with β-actin that served as a loading control. The ratio of active caspase-3 bands (17 kD and 19 kD) to β-actin control was determined by densitometry analysis (bottom panel). Data represents the mean ± S.E.M from two independent donors. (B) Apoptosis of the treated MDMs was also measured by Annexin V-FITC and propidium iodine (PI) staining and analyzed by flow cytometry. The percentage of surviving cells (Annexin V/PI negative) for the cells treated with vehicle/M-CSF was arbitrarily set as 100. Data shown represent the mean ± S.E.M from three independent experiments. *The p-values of inhibitors/M-CSF compared to vehicle/M-CSF were ≤0.05. To confirm that PKC inhibition decreased cell survival, cells were treated with M-CSF in the absence or presence of PKC inhibitors and then also examined for apoptosis by Annexin V/PI staining. PKC inhibitors in the presence of M-CSF reduced the number of Annexin V/PI negative MDMs compared to cells treated with M-CSF alone (Figure 3B). These observations further suggested that MDM survival is promoted by M-CSF and critically involves conventional PKCs and NF-κB activity."}

pmc-enju-pas

sentences

2_test

{"project":"2_test","denotations":[{"id":"22216091-12861375-90609711","span":{"begin":128,"end":130},"obj":"12861375"},{"id":"22216091-16248967-90609712","span":{"begin":134,"end":136},"obj":"16248967"}],"text":"NF-κB and PKC(s) Mediate Human MDM Survival in Response to M-CSF Stimulation\nSince PKC and NF-κB are critical in cell survival [37], [38], we hypothesized that M-CSF promoted cell survival through PKC in human MDMs. To detect apoptosis, the expression of cleaved caspase-3, a marker of apoptosis, was analyzed in the presence or absence of M-CSF and PKC inhibitors. In MDMs pretreated with PKC inhibitors (Ro-31-8220, Gö-6976, or BAPTA/AM) and stimulated with M-CSF, cleaved caspase-3 was elevated to levels of cells treated with vehicle alone (Figure 3A). In contrast, cells incubated with M-CSF and vehicle had less cleaved caspase-3 than cells incubated with vehicle alone or M-CSF with PKC inhibitors. These data supported the hypothesis that M-CSF-induced NF-κB activity was regulated by conventional PKCs, not novel PKCs.\n10.1371/journal.pone.0028081.g003 Figure 3 Inhibition of PKC or NF-κB induces apoptosis in MDMs.\n(A) MDMs were pre-incubated in RPMI medium containing inhibitors (Ro-31-8220: 5 µM, Gö-6976: 5 µM, BAPTA/AM: 2.5 µM) for 30 minutes prior to the addition of M-CSF. As a control, untreated cells were incubated with dimethyl sulfoxide (DMSO). Cell lysates were resolved by SDS-PAGE and immunoblotted with antibody recognizing the active cleaved form of caspase-3. The blots were reblotted with β-actin that served as a loading control. The ratio of active caspase-3 bands (17 kD and 19 kD) to β-actin control was determined by densitometry analysis (bottom panel). Data represents the mean ± S.E.M from two independent donors. (B) Apoptosis of the treated MDMs was also measured by Annexin V-FITC and propidium iodine (PI) staining and analyzed by flow cytometry. The percentage of surviving cells (Annexin V/PI negative) for the cells treated with vehicle/M-CSF was arbitrarily set as 100. Data shown represent the mean ± S.E.M from three independent experiments. *The p-values of inhibitors/M-CSF compared to vehicle/M-CSF were ≤0.05. To confirm that PKC inhibition decreased cell survival, cells were treated with M-CSF in the absence or presence of PKC inhibitors and then also examined for apoptosis by Annexin V/PI staining. PKC inhibitors in the presence of M-CSF reduced the number of Annexin V/PI negative MDMs compared to cells treated with M-CSF alone (Figure 3B). These observations further suggested that MDM survival is promoted by M-CSF and critically involves conventional PKCs and NF-κB activity."}

bionlp-st-ge-2016-spacy-parsed

test2

PMC:3245220 / 13205-15644 JSONTXT

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PMC:3245220 / 13205-15644 JSON TXT