PMC:3585731 / 45184-46281 JSONTXT

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Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T21073","span":{"begin":1001,"end":1005},"obj":"Protein"},{"id":"T21072","span":{"begin":496,"end":500},"obj":"Protein"},{"id":"T21071","span":{"begin":489,"end":490},"obj":"Protein"},{"id":"T21070","span":{"begin":483,"end":488},"obj":"Protein"},{"id":"T21069","span":{"begin":272,"end":276},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T22949","span":{"begin":483,"end":488},"obj":"http://www.uniprot.org/uniprot/Q12778"},{"id":"T22927","span":{"begin":1001,"end":1005},"obj":"http://www.uniprot.org/uniprot/Q13546"},{"id":"T22926","span":{"begin":272,"end":276},"obj":"http://www.uniprot.org/uniprot/Q13546"},{"id":"T22909","span":{"begin":955,"end":958},"obj":"http://www.uniprot.org/uniprot/Q9Y243"},{"id":"T22908","span":{"begin":759,"end":762},"obj":"http://www.uniprot.org/uniprot/Q9Y243"},{"id":"T22875","span":{"begin":955,"end":958},"obj":"http://www.uniprot.org/uniprot/P31751"},{"id":"T22874","span":{"begin":759,"end":762},"obj":"http://www.uniprot.org/uniprot/P31751"},{"id":"T22873","span":{"begin":567,"end":570},"obj":"http://www.uniprot.org/uniprot/P31751"},{"id":"T22872","span":{"begin":429,"end":432},"obj":"http://www.uniprot.org/uniprot/P31751"},{"id":"T22871","span":{"begin":356,"end":359},"obj":"http://www.uniprot.org/uniprot/P31751"},{"id":"T22870","span":{"begin":265,"end":268},"obj":"http://www.uniprot.org/uniprot/P31751"},{"id":"T22841","span":{"begin":955,"end":958},"obj":"http://www.uniprot.org/uniprot/P31749"},{"id":"T22840","span":{"begin":759,"end":762},"obj":"http://www.uniprot.org/uniprot/P31749"},{"id":"T22839","span":{"begin":567,"end":570},"obj":"http://www.uniprot.org/uniprot/P31749"},{"id":"T22838","span":{"begin":429,"end":432},"obj":"http://www.uniprot.org/uniprot/P31749"},{"id":"T22837","span":{"begin":356,"end":359},"obj":"http://www.uniprot.org/uniprot/P31749"},{"id":"T22836","span":{"begin":265,"end":268},"obj":"http://www.uniprot.org/uniprot/P31749"},{"id":"T22907","span":{"begin":567,"end":570},"obj":"http://www.uniprot.org/uniprot/Q9Y243"},{"id":"T22906","span":{"begin":429,"end":432},"obj":"http://www.uniprot.org/uniprot/Q9Y243"},{"id":"T22905","span":{"begin":356,"end":359},"obj":"http://www.uniprot.org/uniprot/Q9Y243"},{"id":"T22904","span":{"begin":265,"end":268},"obj":"http://www.uniprot.org/uniprot/Q9Y243"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"GO-BP","denotations":[{"id":"T21230","span":{"begin":736,"end":748},"obj":"http://purl.obolibrary.org/obo/GO_0043066"},{"id":"T21229","span":{"begin":592,"end":604},"obj":"http://purl.obolibrary.org/obo/GO_0043066"},{"id":"T21228","span":{"begin":476,"end":479},"obj":"http://purl.obolibrary.org/obo/GO_0050321"},{"id":"T21223","span":{"begin":233,"end":241},"obj":"http://purl.obolibrary.org/obo/GO_0070265"},{"id":"T21221","span":{"begin":233,"end":241},"obj":"http://purl.obolibrary.org/obo/GO_0019835"},{"id":"T21219","span":{"begin":233,"end":241},"obj":"http://purl.obolibrary.org/obo/GO_0001906"},{"id":"T21218","span":{"begin":821,"end":830},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T21217","span":{"begin":33,"end":42},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T21216","span":{"begin":861,"end":881},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T21215","span":{"begin":821,"end":830},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T21214","span":{"begin":33,"end":42},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T21205","span":{"begin":372,"end":382},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T21204","span":{"begin":251,"end":261},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T21186","span":{"begin":923,"end":928},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T21185","span":{"begin":876,"end":881},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T21184","span":{"begin":662,"end":667},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T21183","span":{"begin":123,"end":128},"obj":"http://purl.obolibrary.org/obo/GO_0016265"},{"id":"T21177","span":{"begin":233,"end":241},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T21171","span":{"begin":871,"end":881},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T21170","span":{"begin":657,"end":667},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T21169","span":{"begin":118,"end":128},"obj":"http://purl.obolibrary.org/obo/GO_0008219"},{"id":"T21144","span":{"begin":324,"end":335},"obj":"http://purl.obolibrary.org/obo/GO_0097528"},{"id":"T21120","span":{"begin":324,"end":335},"obj":"http://purl.obolibrary.org/obo/GO_0070266"},{"id":"T21096","span":{"begin":605,"end":614},"obj":"http://purl.obolibrary.org/obo/GO_0023052"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"GO-MF","denotations":[{"id":"T21276","span":{"begin":476,"end":479},"obj":"http://purl.obolibrary.org/obo/GO_0050321"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"GO-CC","denotations":[{"id":"T21300","span":{"begin":451,"end":457},"obj":"http://purl.obolibrary.org/obo/GO_0031931"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"sentences","denotations":[{"id":"T20962","span":{"begin":883,"end":1097},"obj":"Sentence"},{"id":"T20961","span":{"begin":669,"end":882},"obj":"Sentence"},{"id":"T20960","span":{"begin":502,"end":668},"obj":"Sentence"},{"id":"T20959","span":{"begin":285,"end":501},"obj":"Sentence"},{"id":"T20958","span":{"begin":197,"end":284},"obj":"Sentence"},{"id":"T20957","span":{"begin":0,"end":196},"obj":"Sentence"},{"id":"T282","span":{"begin":0,"end":196},"obj":"Sentence"},{"id":"T283","span":{"begin":197,"end":284},"obj":"Sentence"},{"id":"T284","span":{"begin":285,"end":501},"obj":"Sentence"},{"id":"T285","span":{"begin":502,"end":668},"obj":"Sentence"},{"id":"T286","span":{"begin":669,"end":882},"obj":"Sentence"},{"id":"T287","span":{"begin":883,"end":1097},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"simple1","denotations":[{"id":"T21325","span":{"begin":1001,"end":1005},"obj":"Protein"},{"id":"T21324","span":{"begin":496,"end":500},"obj":"Protein"},{"id":"T21323","span":{"begin":489,"end":490},"obj":"Protein"},{"id":"T21322","span":{"begin":483,"end":488},"obj":"Protein"},{"id":"T21321","span":{"begin":272,"end":276},"obj":"Protein"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"BioNLP16_DUT","denotations":[{"id":"T22802","span":{"begin":1014,"end":1024},"obj":"Gene_expression"},{"id":"T22772","span":{"begin":1001,"end":1005},"obj":"Protein"},{"id":"T22771","span":{"begin":496,"end":500},"obj":"Protein"},{"id":"T22770","span":{"begin":489,"end":490},"obj":"Protein"},{"id":"T22769","span":{"begin":483,"end":488},"obj":"Protein"},{"id":"T22768","span":{"begin":272,"end":276},"obj":"Protein"}],"relations":[{"id":"R15388","pred":"themeOf","subj":"T22772","obj":"T22802"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"BioNLP16_Messiy","denotations":[{"id":"T23103","span":{"begin":1001,"end":1005},"obj":"Protein"},{"id":"T23102","span":{"begin":496,"end":500},"obj":"Protein"},{"id":"T23101","span":{"begin":489,"end":490},"obj":"Protein"},{"id":"T23100","span":{"begin":483,"end":488},"obj":"Protein"},{"id":"T23099","span":{"begin":272,"end":276},"obj":"Protein"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

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role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T23257","span":{"begin":1001,"end":1012},"obj":"Protein"},{"id":"T23256","span":{"begin":955,"end":958},"obj":"Protein"},{"id":"T23255","span":{"begin":759,"end":762},"obj":"Protein"},{"id":"T23254","span":{"begin":553,"end":563},"obj":"Positive_regulation"},{"id":"T23253","span":{"begin":567,"end":570},"obj":"Protein"},{"id":"T23252","span":{"begin":496,"end":500},"obj":"Protein"},{"id":"T23251","span":{"begin":451,"end":457},"obj":"Protein"},{"id":"T23250","span":{"begin":356,"end":359},"obj":"Protein"},{"id":"T23249","span":{"begin":251,"end":261},"obj":"Regulation"},{"id":"T23248","span":{"begin":251,"end":261},"obj":"Regulation"},{"id":"T23247","span":{"begin":272,"end":283},"obj":"Protein"},{"id":"T23246","span":{"begin":265,"end":268},"obj":"Protein"},{"id":"T23245","span":{"begin":0,"end":3},"obj":"Protein"}],"relations":[{"id":"R15533","pred":"themeOf","subj":"T23246","obj":"T23248"},{"id":"R15534","pred":"themeOf","subj":"T23247","obj":"T23249"},{"id":"R15535","pred":"themeOf","subj":"T23253","obj":"T23254"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}

{"project":"test3","denotations":[{"id":"T20896","span":{"begin":1001,"end":1005},"obj":"Protein"},{"id":"T20895","span":{"begin":553,"end":563},"obj":"Positive_regulation"},{"id":"T20894","span":{"begin":496,"end":500},"obj":"Protein"},{"id":"T20893","span":{"begin":489,"end":490},"obj":"Protein"},{"id":"T20892","span":{"begin":483,"end":488},"obj":"Protein"},{"id":"T20891","span":{"begin":433,"end":440},"obj":"Binding"},{"id":"T20890","span":{"begin":372,"end":382},"obj":"Regulation"},{"id":"T20889","span":{"begin":345,"end":352},"obj":"Binding"},{"id":"T20888","span":{"begin":272,"end":276},"obj":"Protein"},{"id":"T20887","span":{"begin":251,"end":261},"obj":"Regulation"},{"id":"T20828","span":{"begin":1001,"end":1005},"obj":"Protein"},{"id":"T20827","span":{"begin":496,"end":500},"obj":"Protein"},{"id":"T20826","span":{"begin":489,"end":490},"obj":"Protein"},{"id":"T20825","span":{"begin":483,"end":488},"obj":"Protein"},{"id":"T20824","span":{"begin":272,"end":276},"obj":"Protein"}],"relations":[{"id":"R13946","pred":"themeOf","subj":"T20894","obj":"T20891"}],"text":"Akt’s role as a key inhibitor of apoptosis is well documented, however, evidence of its contribution as a mediator of cell death under various circumstances has begun to emerge as well [45], [47]. Our data demonstrates a new mode of necrosis-specific regulation of Akt by RIP1 kinase. Importantly, while it is possible that necroptosis-specific targets of Akt exist, this regulation clearly involves a number of well established Akt targets including mTORC1, and potentially, GSK-3, FoxO1/4, and MDM2. Therefore, it may no longer be safe to assume that activation of Akt universally reflects pro-survival signaling nor that its inhibition will lead to more cell death. It is tempting to speculate that rather than serving a universally pro-survival role, the Akt pathway may function to promote cell fates alternative to apoptosis, ranging from survival to non-apoptotic cell death. The final decision between survival and death may depend on additional, Akt-independent inputs, such as the status of RIP1 kinase, expression of particular oncogenic factors [45] or excessive metabolic stress [47]."}