PMC:3585731 / 23422-24387 JSONTXT

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{"project":"2_test","denotations":[{"id":"23469174-19109899-90505442","span":{"begin":107,"end":109},"obj":"19109899"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

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{"project":"bionlp-st-ge-2016-coref","denotations":[{"id":"T9195","span":{"begin":744,"end":756},"obj":"Antecedent"},{"id":"T9194","span":{"begin":771,"end":776},"obj":"Anaphor"}],"relations":[{"id":"R5907","pred":"boundBy","subj":"T9194","obj":"T9195"}],"namespaces":[{"prefix":"_base","uri":"https://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T9233","span":{"begin":949,"end":953},"obj":"Protein"},{"id":"T9232","span":{"begin":760,"end":764},"obj":"Protein"},{"id":"T9231","span":{"begin":591,"end":595},"obj":"Protein"},{"id":"T9230","span":{"begin":552,"end":556},"obj":"Protein"},{"id":"T9229","span":{"begin":507,"end":511},"obj":"Protein"},{"id":"T9228","span":{"begin":442,"end":446},"obj":"Protein"},{"id":"T9227","span":{"begin":400,"end":404},"obj":"Protein"},{"id":"T9226","span":{"begin":373,"end":377},"obj":"Protein"},{"id":"T9225","span":{"begin":339,"end":343},"obj":"Protein"},{"id":"T9224","span":{"begin":236,"end":240},"obj":"Protein"},{"id":"T9223","span":{"begin":61,"end":65},"obj":"Protein"},{"id":"T9222","span":{"begin":0,"end":4},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T10313","span":{"begin":552,"end":556},"obj":"http://www.uniprot.org/uniprot/Q788Q8"},{"id":"T10308","span":{"begin":949,"end":953},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10307","span":{"begin":760,"end":764},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10306","span":{"begin":591,"end":595},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10305","span":{"begin":442,"end":446},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10271","span":{"begin":303,"end":306},"obj":"http://www.uniprot.org/uniprot/P31751"},{"id":"T10270","span":{"begin":13,"end":16},"obj":"http://www.uniprot.org/uniprot/P31751"},{"id":"T10257","span":{"begin":303,"end":306},"obj":"http://www.uniprot.org/uniprot/P31749"},{"id":"T10256","span":{"begin":13,"end":16},"obj":"http://www.uniprot.org/uniprot/P31749"},{"id":"T10292","span":{"begin":507,"end":511},"obj":"http://www.uniprot.org/uniprot/Q13546"},{"id":"T10291","span":{"begin":373,"end":377},"obj":"http://www.uniprot.org/uniprot/Q13546"},{"id":"T10290","span":{"begin":0,"end":4},"obj":"http://www.uniprot.org/uniprot/Q13546"},{"id":"T10285","span":{"begin":303,"end":306},"obj":"http://www.uniprot.org/uniprot/Q9Y243"},{"id":"T10284","span":{"begin":13,"end":16},"obj":"http://www.uniprot.org/uniprot/Q9Y243"},{"id":"T10304","span":{"begin":400,"end":404},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10303","span":{"begin":339,"end":343},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10302","span":{"begin":236,"end":240},"obj":"http://www.uniprot.org/uniprot/P01375"},{"id":"T10301","span":{"begin":61,"end":65},"obj":"http://www.uniprot.org/uniprot/P01375"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

{"project":"UBERON-AE","denotations":[{"id":"T9084","span":{"begin":529,"end":534},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

{"project":"GO-BP","denotations":[{"id":"T9311","span":{"begin":954,"end":963},"obj":"http://purl.obolibrary.org/obo/GO_0009058"},{"id":"T9310","span":{"begin":344,"end":353},"obj":"http://purl.obolibrary.org/obo/GO_0009058"},{"id":"T9309","span":{"begin":223,"end":232},"obj":"http://purl.obolibrary.org/obo/GO_0009058"},{"id":"T9308","span":{"begin":29,"end":32},"obj":"http://purl.obolibrary.org/obo/GO_0004705"},{"id":"T9299","span":{"begin":265,"end":270},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T9296","span":{"begin":260,"end":270},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T9280","span":{"begin":875,"end":886},"obj":"http://purl.obolibrary.org/obo/GO_0097528"},{"id":"T9279","span":{"begin":476,"end":487},"obj":"http://purl.obolibrary.org/obo/GO_0097528"},{"id":"T9278","span":{"begin":156,"end":167},"obj":"http://purl.obolibrary.org/obo/GO_0097528"},{"id":"T9277","span":{"begin":79,"end":90},"obj":"http://purl.obolibrary.org/obo/GO_0097528"},{"id":"T9262","span":{"begin":861,"end":886},"obj":"http://purl.obolibrary.org/obo/GO_0070266"},{"id":"T9261","span":{"begin":143,"end":167},"obj":"http://purl.obolibrary.org/obo/GO_0070266"},{"id":"T9259","span":{"begin":875,"end":886},"obj":"http://purl.obolibrary.org/obo/GO_0070266"},{"id":"T9258","span":{"begin":476,"end":487},"obj":"http://purl.obolibrary.org/obo/GO_0070266"},{"id":"T9257","span":{"begin":156,"end":167},"obj":"http://purl.obolibrary.org/obo/GO_0070266"},{"id":"T9256","span":{"begin":79,"end":90},"obj":"http://purl.obolibrary.org/obo/GO_0070266"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

{"project":"GO-MF","denotations":[{"id":"T9321","span":{"begin":723,"end":727},"obj":"http://purl.obolibrary.org/obo/GO_0005161"},{"id":"T9320","span":{"begin":29,"end":32},"obj":"http://purl.obolibrary.org/obo/GO_0004705"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

{"project":"GO-CC","denotations":[{"id":"T9333","span":{"begin":188,"end":207},"obj":"http://purl.obolibrary.org/obo/GO_0009986"},{"id":"T9331","span":{"begin":18,"end":24},"obj":"http://purl.obolibrary.org/obo/GO_0031931"},{"id":"T9324","span":{"begin":496,"end":501},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T9323","span":{"begin":260,"end":264},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

{"project":"sentences","denotations":[{"id":"T9109","span":{"begin":711,"end":964},"obj":"Sentence"},{"id":"T9108","span":{"begin":523,"end":710},"obj":"Sentence"},{"id":"T9107","span":{"begin":355,"end":522},"obj":"Sentence"},{"id":"T9106","span":{"begin":272,"end":354},"obj":"Sentence"},{"id":"T9105","span":{"begin":92,"end":271},"obj":"Sentence"},{"id":"T9104","span":{"begin":0,"end":91},"obj":"Sentence"},{"id":"T150","span":{"begin":0,"end":91},"obj":"Sentence"},{"id":"T151","span":{"begin":92,"end":271},"obj":"Sentence"},{"id":"T152","span":{"begin":272,"end":354},"obj":"Sentence"},{"id":"T153","span":{"begin":355,"end":522},"obj":"Sentence"},{"id":"T154","span":{"begin":523,"end":710},"obj":"Sentence"},{"id":"T155","span":{"begin":711,"end":964},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

{"project":"simple1","denotations":[{"id":"T9369","span":{"begin":949,"end":953},"obj":"Protein"},{"id":"T9368","span":{"begin":760,"end":764},"obj":"Protein"},{"id":"T9367","span":{"begin":591,"end":595},"obj":"Protein"},{"id":"T9366","span":{"begin":552,"end":556},"obj":"Protein"},{"id":"T9365","span":{"begin":507,"end":511},"obj":"Protein"},{"id":"T9364","span":{"begin":442,"end":446},"obj":"Protein"},{"id":"T9363","span":{"begin":400,"end":404},"obj":"Protein"},{"id":"T9362","span":{"begin":373,"end":377},"obj":"Protein"},{"id":"T9361","span":{"begin":339,"end":343},"obj":"Protein"},{"id":"T9360","span":{"begin":236,"end":240},"obj":"Protein"},{"id":"T9359","span":{"begin":61,"end":65},"obj":"Protein"},{"id":"T9358","span":{"begin":0,"end":4},"obj":"Protein"}],"text":"RIP1 kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

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kinase, Akt, mTORC1 and JNK control the upregulation of TNFα accompanying necroptosis. Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

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Hitomi et al. [10] have recently reported that the induction of necroptosis by zVAD.fmk in L929 cells is associated with increased synthesis of TNFα, which potentiates cell death. Therefore, we examined whether Akt and its effectors contribute to TNFα synthesis. Consistent with a RIP1-dependent increase in TNFα protein (Fig. S6A, B), we found that TNFα mRNA levels increased during necroptosis in L929 cells in a RIP1 (Fig. S6C. Under serum free conditions, bFGF alone triggered some induction of TNFα mRNA, while its combination with zVAD.fmk (but not zVAD.fmk alone) caused a pronounced further increase (Fig. 6A). Conversely, PDGF caused a modest upregulation of TNFα mRNA, which was not further increased in the presence of zVAD.fmk (Fig. 6A), demonstrating that activation of necroptosis is specifically accompanied by a marked increase in autocrine TNFα synthesis.\n"}

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