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pmc-enju-pas

bionlp-st-ge-2016-spacy-parsed

GO-BP

{"project":"GO-BP","denotations":[{"id":"T6304","span":{"begin":24,"end":27},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6305","span":{"begin":122,"end":125},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6306","span":{"begin":44,"end":55},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T6307","span":{"begin":93,"end":103},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T6308","span":{"begin":263,"end":273},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T6309","span":{"begin":770,"end":786},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T16942","span":{"begin":836,"end":839},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T16943","span":{"begin":1004,"end":1007},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T16944","span":{"begin":856,"end":867},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T16945","span":{"begin":1021,"end":1036},"obj":"http://purl.obolibrary.org/obo/GO_1904627"},{"id":"T16946","span":{"begin":1132,"end":1148},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T16947","span":{"begin":1274,"end":1290},"obj":"http://purl.obolibrary.org/obo/GO_0051092"}],"text":"NF-κB inhibition due to PKC-dependent Bcl10 degradation\nWestern blot analysis revealed an up-regulation of phosphorylated-PKC after 24 h treatment of Jurkat T-cells with PMA or HK E. coli (figure 7a), while IκBβ levels remained unaffected (figure 7b). Bcl10 is a signalling protein that acts upstream of NF-κB in concert with CARMA1 and MALT1 and has been suggested to directly regulate NF-κB activity in T-cells [27]. Therefore, Bcl10 activation was evaluated in both control and PMA stimulated cells after 10 min, 1 h, 6 h, and 24 h using western blot analysis. The Bcl10 levels decreased following treatment with PMA, while in control cells, Bcl10 returned to higher levels by 24 h (figure 7c). This suggests that Bcl10 is involved in the PMA dependent inhibition of NF-κB activation.\nFigure 7 NF-κB inhibition by PMA correlated to PKC-dependent Bcl10 degradation. Levels of intracellular protein were assessed following 24 h stimulation with PMA (162 nM) or HK E. coli (5 × 107 CFU/ml). (A) Phospho-PKC increased in response to PMA and HK E. coli stimulation. (B) IκB decreased following stimulation with HK E. coli indicating NF-κB activation. (C) Bcl10 activation was inhibited following long-term stimulation with PMA, which explains the inhibitory effect of PMA on NF-κB activation. β-actin was used as a loading control. (n = 3).\n\nD"}

GO-MF

{"project":"GO-MF","denotations":[{"id":"T6310","span":{"begin":24,"end":27},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T6311","span":{"begin":122,"end":125},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T16948","span":{"begin":836,"end":839},"obj":"http://purl.obolibrary.org/obo/GO_0004697"},{"id":"T16949","span":{"begin":1004,"end":1007},"obj":"http://purl.obolibrary.org/obo/GO_0004697"}],"text":"NF-κB inhibition due to PKC-dependent Bcl10 degradation\nWestern blot analysis revealed an up-regulation of phosphorylated-PKC after 24 h treatment of Jurkat T-cells with PMA or HK E. coli (figure 7a), while IκBβ levels remained unaffected (figure 7b). Bcl10 is a signalling protein that acts upstream of NF-κB in concert with CARMA1 and MALT1 and has been suggested to directly regulate NF-κB activity in T-cells [27]. Therefore, Bcl10 activation was evaluated in both control and PMA stimulated cells after 10 min, 1 h, 6 h, and 24 h using western blot analysis. The Bcl10 levels decreased following treatment with PMA, while in control cells, Bcl10 returned to higher levels by 24 h (figure 7c). This suggests that Bcl10 is involved in the PMA dependent inhibition of NF-κB activation.\nFigure 7 NF-κB inhibition by PMA correlated to PKC-dependent Bcl10 degradation. Levels of intracellular protein were assessed following 24 h stimulation with PMA (162 nM) or HK E. coli (5 × 107 CFU/ml). (A) Phospho-PKC increased in response to PMA and HK E. coli stimulation. (B) IκB decreased following stimulation with HK E. coli indicating NF-κB activation. (C) Bcl10 activation was inhibited following long-term stimulation with PMA, which explains the inhibitory effect of PMA on NF-κB activation. β-actin was used as a loading control. (n = 3).\n\nD"}

GO-CC

{"project":"GO-CC","denotations":[{"id":"T6312","span":{"begin":159,"end":164},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6313","span":{"begin":407,"end":412},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6314","span":{"begin":496,"end":501},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T6315","span":{"begin":638,"end":643},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T16950","span":{"begin":879,"end":892},"obj":"http://purl.obolibrary.org/obo/GO_0005622"}],"text":"NF-κB inhibition due to PKC-dependent Bcl10 degradation\nWestern blot analysis revealed an up-regulation of phosphorylated-PKC after 24 h treatment of Jurkat T-cells with PMA or HK E. coli (figure 7a), while IκBβ levels remained unaffected (figure 7b). Bcl10 is a signalling protein that acts upstream of NF-κB in concert with CARMA1 and MALT1 and has been suggested to directly regulate NF-κB activity in T-cells [27]. Therefore, Bcl10 activation was evaluated in both control and PMA stimulated cells after 10 min, 1 h, 6 h, and 24 h using western blot analysis. The Bcl10 levels decreased following treatment with PMA, while in control cells, Bcl10 returned to higher levels by 24 h (figure 7c). This suggests that Bcl10 is involved in the PMA dependent inhibition of NF-κB activation.\nFigure 7 NF-κB inhibition by PMA correlated to PKC-dependent Bcl10 degradation. Levels of intracellular protein were assessed following 24 h stimulation with PMA (162 nM) or HK E. coli (5 × 107 CFU/ml). (A) Phospho-PKC increased in response to PMA and HK E. coli stimulation. (B) IκB decreased following stimulation with HK E. coli indicating NF-κB activation. (C) Bcl10 activation was inhibited following long-term stimulation with PMA, which explains the inhibitory effect of PMA on NF-κB activation. β-actin was used as a loading control. (n = 3).\n\nD"}

sentences

{"project":"sentences","denotations":[{"id":"T5994","span":{"begin":0,"end":55},"obj":"Sentence"},{"id":"T5995","span":{"begin":56,"end":251},"obj":"Sentence"},{"id":"T5996","span":{"begin":252,"end":418},"obj":"Sentence"},{"id":"T5997","span":{"begin":419,"end":563},"obj":"Sentence"},{"id":"T5998","span":{"begin":564,"end":697},"obj":"Sentence"},{"id":"T5999","span":{"begin":698,"end":787},"obj":"Sentence"},{"id":"T16732","span":{"begin":798,"end":868},"obj":"Sentence"},{"id":"T16733","span":{"begin":869,"end":1339},"obj":"Sentence"},{"id":"T111","span":{"begin":0,"end":55},"obj":"Sentence"},{"id":"T112","span":{"begin":56,"end":251},"obj":"Sentence"},{"id":"T113","span":{"begin":252,"end":418},"obj":"Sentence"},{"id":"T114","span":{"begin":419,"end":563},"obj":"Sentence"},{"id":"T115","span":{"begin":564,"end":697},"obj":"Sentence"},{"id":"T116","span":{"begin":698,"end":787},"obj":"Sentence"},{"id":"T117","span":{"begin":788,"end":868},"obj":"Sentence"},{"id":"T118","span":{"begin":869,"end":1339},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"NF-κB inhibition due to PKC-dependent Bcl10 degradation\nWestern blot analysis revealed an up-regulation of phosphorylated-PKC after 24 h treatment of Jurkat T-cells with PMA or HK E. coli (figure 7a), while IκBβ levels remained unaffected (figure 7b). Bcl10 is a signalling protein that acts upstream of NF-κB in concert with CARMA1 and MALT1 and has been suggested to directly regulate NF-κB activity in T-cells [27]. Therefore, Bcl10 activation was evaluated in both control and PMA stimulated cells after 10 min, 1 h, 6 h, and 24 h using western blot analysis. The Bcl10 levels decreased following treatment with PMA, while in control cells, Bcl10 returned to higher levels by 24 h (figure 7c). This suggests that Bcl10 is involved in the PMA dependent inhibition of NF-κB activation.\nFigure 7 NF-κB inhibition by PMA correlated to PKC-dependent Bcl10 degradation. Levels of intracellular protein were assessed following 24 h stimulation with PMA (162 nM) or HK E. coli (5 × 107 CFU/ml). (A) Phospho-PKC increased in response to PMA and HK E. coli stimulation. (B) IκB decreased following stimulation with HK E. coli indicating NF-κB activation. (C) Bcl10 activation was inhibited following long-term stimulation with PMA, which explains the inhibitory effect of PMA on NF-κB activation. β-actin was used as a loading control. (n = 3).\n\nD"}

events-check-again

{"project":"events-check-again","denotations":[{"id":"T6385","span":{"begin":28,"end":37},"obj":"Regulation"},{"id":"T6386","span":{"begin":38,"end":43},"obj":"Protein"},{"id":"T6387","span":{"begin":44,"end":55},"obj":"Protein_catabolism"},{"id":"T6388","span":{"begin":207,"end":211},"obj":"Protein"},{"id":"T6389","span":{"begin":228,"end":238},"obj":"Regulation"},{"id":"T6390","span":{"begin":252,"end":257},"obj":"Protein"},{"id":"T6391","span":{"begin":326,"end":332},"obj":"Protein"},{"id":"T6392","span":{"begin":337,"end":342},"obj":"Protein"},{"id":"T6393","span":{"begin":430,"end":435},"obj":"Protein"},{"id":"T6394","span":{"begin":436,"end":446},"obj":"Positive_regulation"},{"id":"T6395","span":{"begin":568,"end":573},"obj":"Protein"},{"id":"T6396","span":{"begin":581,"end":590},"obj":"Negative_regulation"},{"id":"T6397","span":{"begin":645,"end":650},"obj":"Protein"},{"id":"T6398","span":{"begin":651,"end":669},"obj":"Positive_regulation"},{"id":"T6399","span":{"begin":717,"end":722},"obj":"Protein"},{"id":"T16984","span":{"begin":840,"end":849},"obj":"Regulation"},{"id":"T16985","span":{"begin":850,"end":855},"obj":"Protein"},{"id":"T16986","span":{"begin":856,"end":867},"obj":"Protein_catabolism"},{"id":"T16987","span":{"begin":1154,"end":1159},"obj":"Protein"},{"id":"T16988","span":{"begin":1160,"end":1170},"obj":"Positive_regulation"},{"id":"T16989","span":{"begin":1175,"end":1184},"obj":"Negative_regulation"},{"id":"T16990","span":{"begin":1292,"end":1299},"obj":"Protein"}],"relations":[{"id":"R5132","pred":"themeOf","subj":"T6386","obj":"T6387"},{"id":"R5133","pred":"themeOf","subj":"T6387","obj":"T6385"},{"id":"R5134","pred":"themeOf","subj":"T6388","obj":"T6389"},{"id":"R5135","pred":"themeOf","subj":"T6393","obj":"T6394"},{"id":"R5136","pred":"themeOf","subj":"T6395","obj":"T6396"},{"id":"R5137","pred":"themeOf","subj":"T6397","obj":"T6398"},{"id":"R13831","pred":"themeOf","subj":"T16985","obj":"T16986"},{"id":"R13832","pred":"themeOf","subj":"T16986","obj":"T16984"},{"id":"R13833","pred":"themeOf","subj":"T16987","obj":"T16988"},{"id":"R13834","pred":"themeOf","subj":"T16988","obj":"T16989"}],"attributes":[{"id":"M115","pred":"Negation","subj":"T6389","obj":"true"},{"id":"M116","pred":"Speculation","subj":"T6394","obj":"true"}],"text":"NF-κB inhibition due to PKC-dependent Bcl10 degradation\nWestern blot analysis revealed an up-regulation of phosphorylated-PKC after 24 h treatment of Jurkat T-cells with PMA or HK E. coli (figure 7a), while IκBβ levels remained unaffected (figure 7b). Bcl10 is a signalling protein that acts upstream of NF-κB in concert with CARMA1 and MALT1 and has been suggested to directly regulate NF-κB activity in T-cells [27]. Therefore, Bcl10 activation was evaluated in both control and PMA stimulated cells after 10 min, 1 h, 6 h, and 24 h using western blot analysis. The Bcl10 levels decreased following treatment with PMA, while in control cells, Bcl10 returned to higher levels by 24 h (figure 7c). This suggests that Bcl10 is involved in the PMA dependent inhibition of NF-κB activation.\nFigure 7 NF-κB inhibition by PMA correlated to PKC-dependent Bcl10 degradation. Levels of intracellular protein were assessed following 24 h stimulation with PMA (162 nM) or HK E. coli (5 × 107 CFU/ml). (A) Phospho-PKC increased in response to PMA and HK E. coli stimulation. (B) IκB decreased following stimulation with HK E. coli indicating NF-κB activation. (C) Bcl10 activation was inhibited following long-term stimulation with PMA, which explains the inhibitory effect of PMA on NF-κB activation. β-actin was used as a loading control. (n = 3).\n\nD"}

bionlp-st-ge-2016-reference-tees

bionlp-st-ge-2016-reference

{"project":"bionlp-st-ge-2016-reference","denotations":[{"id":"T5979","span":{"begin":28,"end":37},"obj":"Regulation"},{"id":"T5980","span":{"begin":38,"end":43},"obj":"Protein"},{"id":"T5981","span":{"begin":44,"end":55},"obj":"Protein_catabolism"},{"id":"T5982","span":{"begin":207,"end":211},"obj":"Protein"},{"id":"T5983","span":{"begin":228,"end":238},"obj":"Regulation"},{"id":"T5984","span":{"begin":252,"end":257},"obj":"Protein"},{"id":"T5985","span":{"begin":326,"end":332},"obj":"Protein"},{"id":"T5986","span":{"begin":337,"end":342},"obj":"Protein"},{"id":"T5987","span":{"begin":430,"end":435},"obj":"Protein"},{"id":"T5988","span":{"begin":436,"end":446},"obj":"Positive_regulation"},{"id":"T5989","span":{"begin":568,"end":573},"obj":"Protein"},{"id":"T5990","span":{"begin":581,"end":590},"obj":"Negative_regulation"},{"id":"T5991","span":{"begin":645,"end":650},"obj":"Protein"},{"id":"T5992","span":{"begin":651,"end":669},"obj":"Positive_regulation"},{"id":"T5993","span":{"begin":717,"end":722},"obj":"Protein"},{"id":"T16725","span":{"begin":840,"end":849},"obj":"Regulation"},{"id":"T16726","span":{"begin":850,"end":855},"obj":"Protein"},{"id":"T16727","span":{"begin":856,"end":867},"obj":"Protein_catabolism"},{"id":"T16728","span":{"begin":1154,"end":1159},"obj":"Protein"},{"id":"T16729","span":{"begin":1160,"end":1170},"obj":"Positive_regulation"},{"id":"T16730","span":{"begin":1175,"end":1184},"obj":"Negative_regulation"},{"id":"T16731","span":{"begin":1292,"end":1299},"obj":"Protein"}],"relations":[{"id":"R13605","pred":"themeOf","subj":"T16726","obj":"T16727"},{"id":"R13606","pred":"themeOf","subj":"T16727","obj":"T16725"},{"id":"R13607","pred":"themeOf","subj":"T16728","obj":"T16729"},{"id":"R13608","pred":"themeOf","subj":"T16729","obj":"T16730"},{"id":"R4812","pred":"themeOf","subj":"T5980","obj":"T5981"},{"id":"R4813","pred":"themeOf","subj":"T5981","obj":"T5979"},{"id":"R4814","pred":"themeOf","subj":"T5982","obj":"T5983"},{"id":"R4815","pred":"themeOf","subj":"T5987","obj":"T5988"},{"id":"R4816","pred":"themeOf","subj":"T5989","obj":"T5990"},{"id":"R4817","pred":"themeOf","subj":"T5991","obj":"T5992"}],"attributes":[{"id":"M107","pred":"Speculation","subj":"T5988","obj":"true"},{"id":"M106","pred":"Negation","subj":"T5983","obj":"true"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"NF-κB inhibition due to PKC-dependent Bcl10 degradation\nWestern blot analysis revealed an up-regulation of phosphorylated-PKC after 24 h treatment of Jurkat T-cells with PMA or HK E. coli (figure 7a), while IκBβ levels remained unaffected (figure 7b). Bcl10 is a signalling protein that acts upstream of NF-κB in concert with CARMA1 and MALT1 and has been suggested to directly regulate NF-κB activity in T-cells [27]. Therefore, Bcl10 activation was evaluated in both control and PMA stimulated cells after 10 min, 1 h, 6 h, and 24 h using western blot analysis. The Bcl10 levels decreased following treatment with PMA, while in control cells, Bcl10 returned to higher levels by 24 h (figure 7c). This suggests that Bcl10 is involved in the PMA dependent inhibition of NF-κB activation.\nFigure 7 NF-κB inhibition by PMA correlated to PKC-dependent Bcl10 degradation. Levels of intracellular protein were assessed following 24 h stimulation with PMA (162 nM) or HK E. coli (5 × 107 CFU/ml). (A) Phospho-PKC increased in response to PMA and HK E. coli stimulation. (B) IκB decreased following stimulation with HK E. coli indicating NF-κB activation. (C) Bcl10 activation was inhibited following long-term stimulation with PMA, which explains the inhibitory effect of PMA on NF-κB activation. β-actin was used as a loading control. (n = 3).\n\nD"}

bionlp-st-ge-2016-uniprot

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T6289","span":{"begin":38,"end":43},"obj":"O95999"},{"id":"T6290","span":{"begin":207,"end":211},"obj":"Q15653"},{"id":"T6291","span":{"begin":252,"end":257},"obj":"O95999"},{"id":"T6292","span":{"begin":326,"end":332},"obj":"Q9BXL7"},{"id":"T6293","span":{"begin":337,"end":342},"obj":"Q9UDY8"},{"id":"T6294","span":{"begin":430,"end":435},"obj":"O95999"},{"id":"T6295","span":{"begin":568,"end":573},"obj":"O95999"},{"id":"T6296","span":{"begin":645,"end":650},"obj":"O95999"},{"id":"T6297","span":{"begin":717,"end":722},"obj":"O95999"},{"id":"T16937","span":{"begin":850,"end":855},"obj":"O95999"},{"id":"T16938","span":{"begin":1154,"end":1159},"obj":"O95999"},{"id":"T16939","span":{"begin":1292,"end":1299},"obj":"P60709"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"NF-κB inhibition due to PKC-dependent Bcl10 degradation\nWestern blot analysis revealed an up-regulation of phosphorylated-PKC after 24 h treatment of Jurkat T-cells with PMA or HK E. coli (figure 7a), while IκBβ levels remained unaffected (figure 7b). Bcl10 is a signalling protein that acts upstream of NF-κB in concert with CARMA1 and MALT1 and has been suggested to directly regulate NF-κB activity in T-cells [27]. Therefore, Bcl10 activation was evaluated in both control and PMA stimulated cells after 10 min, 1 h, 6 h, and 24 h using western blot analysis. The Bcl10 levels decreased following treatment with PMA, while in control cells, Bcl10 returned to higher levels by 24 h (figure 7c). This suggests that Bcl10 is involved in the PMA dependent inhibition of NF-κB activation.\nFigure 7 NF-κB inhibition by PMA correlated to PKC-dependent Bcl10 degradation. Levels of intracellular protein were assessed following 24 h stimulation with PMA (162 nM) or HK E. coli (5 × 107 CFU/ml). (A) Phospho-PKC increased in response to PMA and HK E. coli stimulation. (B) IκB decreased following stimulation with HK E. coli indicating NF-κB activation. (C) Bcl10 activation was inhibited following long-term stimulation with PMA, which explains the inhibitory effect of PMA on NF-κB activation. β-actin was used as a loading control. (n = 3).\n\nD"}

test2

{"project":"test2","denotations":[{"id":"T5963","span":{"begin":28,"end":37},"obj":"Regulation"},{"id":"T5964","span":{"begin":38,"end":43},"obj":"Protein"},{"id":"T5965","span":{"begin":44,"end":55},"obj":"Protein_catabolism"},{"id":"T5966","span":{"begin":207,"end":211},"obj":"Protein"},{"id":"T5967","span":{"begin":252,"end":257},"obj":"Protein"},{"id":"T5968","span":{"begin":326,"end":332},"obj":"Protein"},{"id":"T5969","span":{"begin":337,"end":342},"obj":"Protein"},{"id":"T5970","span":{"begin":430,"end":435},"obj":"Protein"},{"id":"T5971","span":{"begin":436,"end":446},"obj":"Positive_regulation"},{"id":"T5972","span":{"begin":568,"end":573},"obj":"Protein"},{"id":"T5973","span":{"begin":581,"end":590},"obj":"Negative_regulation"},{"id":"T5974","span":{"begin":591,"end":600},"obj":"Positive_regulation"},{"id":"T5975","span":{"begin":645,"end":650},"obj":"Protein"},{"id":"T5976","span":{"begin":651,"end":662},"obj":"Positive_regulation"},{"id":"T5977","span":{"begin":663,"end":669},"obj":"Positive_regulation"},{"id":"T5978","span":{"begin":717,"end":722},"obj":"Protein"},{"id":"T16717","span":{"begin":840,"end":849},"obj":"Regulation"},{"id":"T16718","span":{"begin":850,"end":855},"obj":"Protein"},{"id":"T16719","span":{"begin":856,"end":867},"obj":"Protein_catabolism"},{"id":"T16720","span":{"begin":1154,"end":1159},"obj":"Protein"},{"id":"T16721","span":{"begin":1160,"end":1170},"obj":"Positive_regulation"},{"id":"T16722","span":{"begin":1175,"end":1184},"obj":"Negative_regulation"},{"id":"T16723","span":{"begin":1185,"end":1194},"obj":"Positive_regulation"},{"id":"T16724","span":{"begin":1292,"end":1299},"obj":"Protein"}],"relations":[{"id":"R4807","pred":"themeOf","subj":"T5964","obj":"T5965"},{"id":"R4808","pred":"themeOf","subj":"T5965","obj":"T5963"},{"id":"R4809","pred":"themeOf","subj":"T5970","obj":"T5971"},{"id":"R4810","pred":"themeOf","subj":"T5972","obj":"T5973"},{"id":"R4811","pred":"themeOf","subj":"T5975","obj":"T5977"},{"id":"R13600","pred":"themeOf","subj":"T16718","obj":"T16719"},{"id":"R13601","pred":"themeOf","subj":"T16719","obj":"T16717"},{"id":"R13602","pred":"themeOf","subj":"T16720","obj":"T16721"},{"id":"R13603","pred":"themeOf","subj":"T16721","obj":"T16723"},{"id":"R13604","pred":"themeOf","subj":"T16721","obj":"T16722"}],"attributes":[{"id":"M105","pred":"Speculation","subj":"T5966","obj":"true"},{"id":"M104","pred":"Negation","subj":"T5965","obj":"true"}],"text":"NF-κB inhibition due to PKC-dependent Bcl10 degradation\nWestern blot analysis revealed an up-regulation of phosphorylated-PKC after 24 h treatment of Jurkat T-cells with PMA or HK E. coli (figure 7a), while IκBβ levels remained unaffected (figure 7b). Bcl10 is a signalling protein that acts upstream of NF-κB in concert with CARMA1 and MALT1 and has been suggested to directly regulate NF-κB activity in T-cells [27]. Therefore, Bcl10 activation was evaluated in both control and PMA stimulated cells after 10 min, 1 h, 6 h, and 24 h using western blot analysis. The Bcl10 levels decreased following treatment with PMA, while in control cells, Bcl10 returned to higher levels by 24 h (figure 7c). This suggests that Bcl10 is involved in the PMA dependent inhibition of NF-κB activation.\nFigure 7 NF-κB inhibition by PMA correlated to PKC-dependent Bcl10 degradation. Levels of intracellular protein were assessed following 24 h stimulation with PMA (162 nM) or HK E. coli (5 × 107 CFU/ml). (A) Phospho-PKC increased in response to PMA and HK E. coli stimulation. (B) IκB decreased following stimulation with HK E. coli indicating NF-κB activation. (C) Bcl10 activation was inhibited following long-term stimulation with PMA, which explains the inhibitory effect of PMA on NF-κB activation. β-actin was used as a loading control. (n = 3).\n\nD"}

PMC:2889865 / 14966-16308 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:2889865 / 14966-16308 JSON TXT