PMC:3585731 / 36021-37013 JSONTXT

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{"project":"2_test","denotations":[{"id":"23469174-17210696-90505453","span":{"begin":162,"end":164},"obj":"17210696"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

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Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T16892","span":{"begin":793,"end":797},"obj":"Protein"},{"id":"T16891","span":{"begin":639,"end":643},"obj":"Protein"},{"id":"T16890","span":{"begin":624,"end":628},"obj":"Protein"},{"id":"T16889","span":{"begin":570,"end":574},"obj":"Protein"},{"id":"T16888","span":{"begin":520,"end":524},"obj":"Protein"},{"id":"T16887","span":{"begin":512,"end":516},"obj":"Protein"},{"id":"T16886","span":{"begin":350,"end":354},"obj":"Protein"},{"id":"T16885","span":{"begin":314,"end":318},"obj":"Protein"},{"id":"T16884","span":{"begin":222,"end":226},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

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{"project":"UBERON-AE","denotations":[{"id":"T16825","span":{"begin":473,"end":477},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T16824","span":{"begin":65,"end":69},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

{"project":"GO-BP","denotations":[{"id":"T16925","span":{"begin":184,"end":202},"obj":"http://purl.obolibrary.org/obo/GO_0071888"},{"id":"T16924","span":{"begin":184,"end":202},"obj":"http://purl.obolibrary.org/obo/GO_0043276"},{"id":"T16923","span":{"begin":798,"end":807},"obj":"http://purl.obolibrary.org/obo/GO_0009058"},{"id":"T16919","span":{"begin":44,"end":55},"obj":"http://purl.obolibrary.org/obo/GO_0097528"},{"id":"T16914","span":{"begin":44,"end":55},"obj":"http://purl.obolibrary.org/obo/GO_0070266"},{"id":"T16909","span":{"begin":979,"end":984},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T16908","span":{"begin":849,"end":854},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T16907","span":{"begin":407,"end":412},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T16906","span":{"begin":189,"end":194},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T16901","span":{"begin":974,"end":984},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T16900","span":{"begin":844,"end":854},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T16899","span":{"begin":402,"end":412},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T16898","span":{"begin":184,"end":194},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T16895","span":{"begin":931,"end":940},"obj":"http://purl.obolibrary.org/obo/GO_0023052"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

{"project":"GO-CC","denotations":[{"id":"T16933","span":{"begin":974,"end":978},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T16932","span":{"begin":844,"end":848},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T16931","span":{"begin":402,"end":406},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T16930","span":{"begin":299,"end":304},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

{"project":"sentences","denotations":[{"id":"T16837","span":{"begin":711,"end":992},"obj":"Sentence"},{"id":"T16836","span":{"begin":425,"end":710},"obj":"Sentence"},{"id":"T16835","span":{"begin":241,"end":424},"obj":"Sentence"},{"id":"T16834","span":{"begin":83,"end":240},"obj":"Sentence"},{"id":"T16833","span":{"begin":0,"end":82},"obj":"Sentence"},{"id":"T223","span":{"begin":0,"end":82},"obj":"Sentence"},{"id":"T224","span":{"begin":83,"end":240},"obj":"Sentence"},{"id":"T225","span":{"begin":241,"end":424},"obj":"Sentence"},{"id":"T226","span":{"begin":425,"end":710},"obj":"Sentence"},{"id":"T227","span":{"begin":711,"end":992},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

{"project":"simple1","denotations":[{"id":"T16952","span":{"begin":793,"end":797},"obj":"Protein"},{"id":"T16951","span":{"begin":639,"end":643},"obj":"Protein"},{"id":"T16950","span":{"begin":624,"end":628},"obj":"Protein"},{"id":"T16949","span":{"begin":570,"end":574},"obj":"Protein"},{"id":"T16948","span":{"begin":520,"end":524},"obj":"Protein"},{"id":"T16947","span":{"begin":512,"end":516},"obj":"Protein"},{"id":"T16946","span":{"begin":350,"end":354},"obj":"Protein"},{"id":"T16945","span":{"begin":314,"end":318},"obj":"Protein"},{"id":"T16944","span":{"begin":222,"end":226},"obj":"Protein"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

{"project":"BioNLP16_DUT","denotations":[{"id":"T17372","span":{"begin":798,"end":807},"obj":"Gene_expression"},{"id":"T17371","span":{"begin":629,"end":638},"obj":"Positive_regulation"},{"id":"T17370","span":{"begin":490,"end":500},"obj":"Gene_expression"},{"id":"T17369","span":{"begin":649,"end":661},"obj":"Positive_regulation"},{"id":"T17368","span":{"begin":324,"end":334},"obj":"Transcription"},{"id":"T17367","span":{"begin":305,"end":313},"obj":"Positive_regulation"},{"id":"T17358","span":{"begin":793,"end":797},"obj":"Protein"},{"id":"T17357","span":{"begin":639,"end":643},"obj":"Protein"},{"id":"T17356","span":{"begin":624,"end":628},"obj":"Protein"},{"id":"T17355","span":{"begin":570,"end":574},"obj":"Protein"},{"id":"T17354","span":{"begin":520,"end":524},"obj":"Protein"},{"id":"T17353","span":{"begin":512,"end":516},"obj":"Protein"},{"id":"T17352","span":{"begin":350,"end":354},"obj":"Protein"},{"id":"T17351","span":{"begin":314,"end":318},"obj":"Protein"},{"id":"T17350","span":{"begin":222,"end":226},"obj":"Protein"}],"relations":[{"id":"R11572","pred":"themeOf","subj":"T17351","obj":"T17368"},{"id":"R11573","pred":"themeOf","subj":"T17353","obj":"T17370"},{"id":"R11574","pred":"themeOf","subj":"T17354","obj":"T17370"},{"id":"R11575","pred":"themeOf","subj":"T17357","obj":"T17369"},{"id":"R11576","pred":"themeOf","subj":"T17358","obj":"T17372"},{"id":"R11579","pred":"themeOf","subj":"T17368","obj":"T17367"},{"id":"R11580","pred":"themeOf","subj":"T17369","obj":"T17371"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

{"project":"BioNLP16_Messiy","denotations":[{"id":"T17906","span":{"begin":798,"end":807},"obj":"Gene_expression"},{"id":"T17905","span":{"begin":770,"end":778},"obj":"Positive_regulation"},{"id":"T17904","span":{"begin":649,"end":661},"obj":"Positive_regulation"},{"id":"T17903","span":{"begin":629,"end":638},"obj":"Positive_regulation"},{"id":"T17902","span":{"begin":490,"end":500},"obj":"Gene_expression"},{"id":"T17901","span":{"begin":305,"end":313},"obj":"Negative_regulation"},{"id":"T17900","span":{"begin":359,"end":367},"obj":"Negative_regulation"},{"id":"T17899","span":{"begin":324,"end":334},"obj":"Transcription"},{"id":"T17891","span":{"begin":793,"end":797},"obj":"Protein"},{"id":"T17890","span":{"begin":639,"end":643},"obj":"Protein"},{"id":"T17889","span":{"begin":624,"end":628},"obj":"Protein"},{"id":"T17888","span":{"begin":570,"end":574},"obj":"Protein"},{"id":"T17887","span":{"begin":520,"end":524},"obj":"Protein"},{"id":"T17886","span":{"begin":512,"end":516},"obj":"Protein"},{"id":"T17885","span":{"begin":350,"end":354},"obj":"Protein"},{"id":"T17884","span":{"begin":314,"end":318},"obj":"Protein"},{"id":"T17883","span":{"begin":222,"end":226},"obj":"Protein"}],"relations":[{"id":"R12001","pred":"themeOf","subj":"T17884","obj":"T17899"},{"id":"R12002","pred":"themeOf","subj":"T17885","obj":"T17900"},{"id":"R12003","pred":"themeOf","subj":"T17886","obj":"T17902"},{"id":"R12004","pred":"themeOf","subj":"T17887","obj":"T17902"},{"id":"R12005","pred":"causeOf","subj":"T17889","obj":"T17903"},{"id":"R12006","pred":"themeOf","subj":"T17890","obj":"T17904"},{"id":"R12007","pred":"themeOf","subj":"T17891","obj":"T17906"},{"id":"R12010","pred":"themeOf","subj":"T17899","obj":"T17901"},{"id":"R12011","pred":"themeOf","subj":"T17904","obj":"T17903"},{"id":"R12012","pred":"themeOf","subj":"T17906","obj":"T17905"}],"text":"We next chose to look at the role of Akt in necroptosis in mouse lung fibroblasts. Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

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Lung fibroblasts selected to survive after deletion of all three Akt isoforms [40] were resistant to cell death induced by the addition of TNFα and zVAD.fmk. Expression of catalytically active Akt (Myr-Akt) in these cells restored TNFα mRNA production in response to TNFα and zVAD.fmk (Fig. 8G) without re-establishing cell death (Fig. S9D). Consistent with our earlier Akt knockdown data, lung fibroblasts expressing endogenous Akt1 or Akt2 were phosphorylated on Thr308 in response to TNFα and zVAD.fmk (Fig. S9E) and in both cases robust RIP1-dependent TNFα mRNA upregulation occurred under necroptotic conditions (Fig. 8H). These data further support the notion that Akt activity is critical for autocrine TNFα synthesis, even in the absence of necroptotic cell death, indicating an unexpected differentiation between Akt-mediated inflammatory signaling under necroptotic conditions and cell death per se."}

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