PMC:3317373 / 18096-19483 JSON TXT

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2_test

{"project":"2_test","denotations":[{"id":"22529521-15856023-67992103","span":{"begin":352,"end":354},"obj":"15856023"},{"id":"22529521-15139523-67992104","span":{"begin":494,"end":496},"obj":"15139523"},{"id":"22529521-18715849-67992105","span":{"begin":671,"end":672},"obj":"18715849"},{"id":"22529521-19125683-67992106","span":{"begin":674,"end":675},"obj":"19125683"},{"id":"22529521-19394962-67992107","span":{"begin":677,"end":679},"obj":"19394962"},{"id":"22529521-16585964-67992108","span":{"begin":947,"end":949},"obj":"16585964"},{"id":"22529521-18241676-67992109","span":{"begin":1202,"end":1204},"obj":"18241676"},{"id":"22529521-20486765-67992110","span":{"begin":1383,"end":1385},"obj":"20486765"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

pmc-enju-pas

bionlp-st-ge-2016-test-proteins

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T7332","span":{"begin":1042,"end":1045},"obj":"Protein"},{"id":"T7331","span":{"begin":269,"end":272},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

bionlp-st-ge-2016-uniprot

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T8392","span":{"begin":1164,"end":1167},"obj":"http://www.uniprot.org/uniprot/Q92793"},{"id":"T8391","span":{"begin":1042,"end":1045},"obj":"http://www.uniprot.org/uniprot/P21579"},{"id":"T8390","span":{"begin":269,"end":272},"obj":"http://www.uniprot.org/uniprot/P21579"},{"id":"T8389","span":{"begin":1042,"end":1045},"obj":"http://www.uniprot.org/uniprot/Q04206"},{"id":"T8388","span":{"begin":269,"end":272},"obj":"http://www.uniprot.org/uniprot/Q04206"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"T7210","span":{"begin":650,"end":659},"obj":"http://purl.obolibrary.org/obo/UBERON_0000160"},{"id":"T7209","span":{"begin":846,"end":850},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T7208","span":{"begin":633,"end":637},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T7200","span":{"begin":639,"end":644},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

GO-BP

{"project":"GO-BP","denotations":[{"id":"T7365","span":{"begin":1341,"end":1365},"obj":"http://purl.obolibrary.org/obo/GO_0032111"},{"id":"T7364","span":{"begin":1341,"end":1365},"obj":"http://purl.obolibrary.org/obo/GO_0030295"},{"id":"T7363","span":{"begin":1341,"end":1365},"obj":"http://purl.obolibrary.org/obo/GO_0032147"},{"id":"T7362","span":{"begin":1341,"end":1365},"obj":"http://purl.obolibrary.org/obo/GO_0034199"},{"id":"T7361","span":{"begin":249,"end":264},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T7360","span":{"begin":241,"end":244},"obj":"http://purl.obolibrary.org/obo/GO_0008384"},{"id":"T7359","span":{"begin":341,"end":350},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T7358","span":{"begin":177,"end":186},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T7357","span":{"begin":335,"end":350},"obj":"http://purl.obolibrary.org/obo/GO_0038061"},{"id":"T7356","span":{"begin":171,"end":186},"obj":"http://purl.obolibrary.org/obo/GO_0038061"},{"id":"T7350","span":{"begin":608,"end":629},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T7344","span":{"begin":804,"end":823},"obj":"http://purl.obolibrary.org/obo/GO_0051092"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

GO-MF

{"project":"GO-MF","denotations":[{"id":"T8295","span":{"begin":1341,"end":1365},"obj":"http://purl.obolibrary.org/obo/GO_0030295"},{"id":"T8294","span":{"begin":1164,"end":1167},"obj":"http://purl.obolibrary.org/obo/GO_0008140"},{"id":"T8293","span":{"begin":241,"end":244},"obj":"http://purl.obolibrary.org/obo/GO_0008384"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

sentences

{"project":"sentences","denotations":[{"id":"T7238","span":{"begin":1207,"end":1387},"obj":"Sentence"},{"id":"T7237","span":{"begin":1036,"end":1206},"obj":"Sentence"},{"id":"T7236","span":{"begin":952,"end":1035},"obj":"Sentence"},{"id":"T7235","span":{"begin":795,"end":951},"obj":"Sentence"},{"id":"T7234","span":{"begin":682,"end":794},"obj":"Sentence"},{"id":"T7233","span":{"begin":499,"end":681},"obj":"Sentence"},{"id":"T7232","span":{"begin":357,"end":498},"obj":"Sentence"},{"id":"T7231","span":{"begin":188,"end":356},"obj":"Sentence"},{"id":"T7230","span":{"begin":0,"end":187},"obj":"Sentence"},{"id":"T176","span":{"begin":0,"end":187},"obj":"Sentence"},{"id":"T177","span":{"begin":188,"end":356},"obj":"Sentence"},{"id":"T178","span":{"begin":357,"end":498},"obj":"Sentence"},{"id":"T179","span":{"begin":499,"end":681},"obj":"Sentence"},{"id":"T180","span":{"begin":682,"end":794},"obj":"Sentence"},{"id":"T181","span":{"begin":795,"end":951},"obj":"Sentence"},{"id":"T182","span":{"begin":952,"end":1035},"obj":"Sentence"},{"id":"T183","span":{"begin":1036,"end":1206},"obj":"Sentence"},{"id":"T184","span":{"begin":1207,"end":1387},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

ICD10

{"project":"ICD10","denotations":[{"id":"T8274","span":{"begin":787,"end":793},"obj":"http://purl.bioontology.org/ontology/ICD10/T14.9"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

simple1

{"project":"simple1","denotations":[{"id":"T8347","span":{"begin":1042,"end":1045},"obj":"Protein"},{"id":"T8346","span":{"begin":269,"end":272},"obj":"Protein"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

BioNLP16_DUT

{"project":"BioNLP16_DUT","denotations":[{"id":"T9931","span":{"begin":1054,"end":1063},"obj":"Negative_regulation"},{"id":"T9930","span":{"begin":233,"end":240},"obj":"Negative_regulation"},{"id":"T9929","span":{"begin":295,"end":308},"obj":"Localization"},{"id":"T9906","span":{"begin":1042,"end":1045},"obj":"Protein"},{"id":"T9905","span":{"begin":269,"end":272},"obj":"Protein"}],"relations":[{"id":"R8149","pred":"themeOf","subj":"T9905","obj":"T9929"},{"id":"R8151","pred":"themeOf","subj":"T9906","obj":"T9931"},{"id":"R8193","pred":"themeOf","subj":"T9929","obj":"T9930"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

BioNLP16_Messiy

{"project":"BioNLP16_Messiy","denotations":[{"id":"T8487","span":{"begin":1125,"end":1136},"obj":"Binding"},{"id":"T8486","span":{"begin":1054,"end":1063},"obj":"Negative_regulation"},{"id":"T8485","span":{"begin":233,"end":240},"obj":"Negative_regulation"},{"id":"T8484","span":{"begin":295,"end":308},"obj":"Localization"},{"id":"T8462","span":{"begin":1042,"end":1045},"obj":"Protein"},{"id":"T8461","span":{"begin":269,"end":272},"obj":"Protein"}],"relations":[{"id":"R6883","pred":"themeOf","subj":"T8461","obj":"T8484"},{"id":"R6884","pred":"themeOf","subj":"T8462","obj":"T8487"},{"id":"R6885","pred":"themeOf","subj":"T8462","obj":"T8486"},{"id":"R6905","pred":"themeOf","subj":"T8484","obj":"T8485"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

DLUT931

{"project":"DLUT931","denotations":[{"id":"T8437","span":{"begin":1054,"end":1063},"obj":"Negative_regulation"},{"id":"T8436","span":{"begin":1125,"end":1136},"obj":"Binding"},{"id":"T8435","span":{"begin":233,"end":240},"obj":"Negative_regulation"},{"id":"T8434","span":{"begin":295,"end":308},"obj":"Localization"},{"id":"T8411","span":{"begin":1042,"end":1045},"obj":"Protein"},{"id":"T8410","span":{"begin":269,"end":272},"obj":"Protein"}],"relations":[{"id":"R6832","pred":"themeOf","subj":"T8411","obj":"T8436"},{"id":"R6860","pred":"themeOf","subj":"T8434","obj":"T8435"},{"id":"R6861","pred":"themeOf","subj":"T8436","obj":"T8437"},{"id":"R6831","pred":"themeOf","subj":"T8410","obj":"T8434"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

bionlp-st-ge-2016-test-ihmc

bionlp-st-ge-2016-spacy-parsed

bionlp-st-ge-2016-test-tees

testone

{"project":"testone","denotations":[{"id":"T7099","span":{"begin":1307,"end":1316},"obj":"Regulation"},{"id":"T7098","span":{"begin":1154,"end":1160},"obj":"Entity"},{"id":"T7097","span":{"begin":1125,"end":1136},"obj":"Binding"},{"id":"T7096","span":{"begin":1054,"end":1063},"obj":"Negative_regulation"},{"id":"T7095","span":{"begin":997,"end":1004},"obj":"Negative_regulation"},{"id":"T7094","span":{"begin":905,"end":914},"obj":"Negative_regulation"},{"id":"T7093","span":{"begin":547,"end":556},"obj":"Negative_regulation"},{"id":"T7092","span":{"begin":423,"end":433},"obj":"Negative_regulation"},{"id":"T7091","span":{"begin":295,"end":308},"obj":"Localization"},{"id":"T7090","span":{"begin":287,"end":294},"obj":"Entity"},{"id":"T7089","span":{"begin":249,"end":264},"obj":"Phosphorylation"},{"id":"T7088","span":{"begin":233,"end":240},"obj":"Negative_regulation"},{"id":"T7070","span":{"begin":1042,"end":1045},"obj":"Protein"},{"id":"T7069","span":{"begin":269,"end":272},"obj":"Protein"}],"relations":[{"id":"R5817","pred":"themeOf","subj":"T7069","obj":"T7091"},{"id":"R5818","pred":"themeOf","subj":"T7070","obj":"T7097"},{"id":"R5828","pred":"themeOf","subj":"T7089","obj":"T7088"},{"id":"R5829","pred":"locationOf","subj":"T7090","obj":"T7091"},{"id":"R5830","pred":"themeOf","subj":"T7091","obj":"T7088"},{"id":"R5831","pred":"causeOf","subj":"T7097","obj":"T7096"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

test3

{"project":"test3","denotations":[{"id":"T7176","span":{"begin":1307,"end":1316},"obj":"Regulation"},{"id":"T7175","span":{"begin":1146,"end":1153},"obj":"Entity"},{"id":"T7174","span":{"begin":1125,"end":1136},"obj":"Binding"},{"id":"T7173","span":{"begin":1042,"end":1045},"obj":"Protein"},{"id":"T7172","span":{"begin":997,"end":1004},"obj":"Negative_regulation"},{"id":"T7171","span":{"begin":905,"end":914},"obj":"Negative_regulation"},{"id":"T7170","span":{"begin":295,"end":308},"obj":"Localization"},{"id":"T7169","span":{"begin":287,"end":294},"obj":"Entity"},{"id":"T7168","span":{"begin":269,"end":272},"obj":"Protein"},{"id":"T7167","span":{"begin":249,"end":264},"obj":"Phosphorylation"},{"id":"T7166","span":{"begin":233,"end":240},"obj":"Negative_regulation"},{"id":"T7165","span":{"begin":75,"end":81},"obj":"Regulation"},{"id":"T7126","span":{"begin":1042,"end":1045},"obj":"Protein"},{"id":"T7125","span":{"begin":269,"end":272},"obj":"Protein"}],"relations":[{"id":"R5852","pred":"themeOf","subj":"T7167","obj":"T7166"},{"id":"R5853","pred":"themeOf","subj":"T7168","obj":"T7170"},{"id":"R5854","pred":"locationOf","subj":"T7169","obj":"T7170"},{"id":"R5855","pred":"themeOf","subj":"T7170","obj":"T7166"},{"id":"R5856","pred":"themeOf","subj":"T7173","obj":"T7174"},{"id":"R5857","pred":"themeOf","subj":"T7175","obj":"T7174"}],"text":"Data obtained from animal studies suggest the possibility that antioxidant effect of Nrf2 may be achieved by suppression of proinflammatory pathways which are mediated by NF-κB signaling. Administration of SFN is found to be able to inhibit IKK/IκB phosphorylation and p65 NF-κB subunit nuclear translocation, consequently alleviating NF-κB signaling [21]. And NF-κB activation induced by lipopolysaccharide (LPS) could be attenuated by diverse Nrf2 activators, such as SFN and curcumin (CUR) [22]. Furthermore, our previous studies indicate that depletion of Nrf2 induces augmentation of NF-κB activity and inflammatory response in lung, brain, and intestine after TBI [4, 5, 23]. Results from this study further confirmed such relationship existed in cultured astrocytes after scratch injury. Enhanced activation of NF-κB is also discovered in lung, macrophages, and mouse embryonic fibroblasts of Nrf2-deficient mice after experimental sepsis [24]. Interestingly, it is reported that NF-κB can inhibit Nrf2 at transcriptional level. NF-κB p65 subunit repressed the Nrf2-ARE pathway at transcriptional level by competitive interaction with the CH1-KIX domain of CBP or local histone hypoacetylation [25]. All these findings indicate the potential complicate crosstalk between NF-κB and Nrf2, which may be regulated by the upstream mitogen-activated protein kinase (MAPKs) pathway [26]."}

PMC:3317373 / 18096-19483 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:3317373 / 18096-19483 JSON TXT