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{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T367","span":{"begin":615,"end":618},"obj":"Protein"},{"id":"T366","span":{"begin":512,"end":543},"obj":"Protein"},{"id":"T365","span":{"begin":481,"end":498},"obj":"Protein"},{"id":"T364","span":{"begin":475,"end":479},"obj":"Protein"},{"id":"T363","span":{"begin":464,"end":467},"obj":"Protein"},{"id":"T362","span":{"begin":338,"end":343},"obj":"Protein"},{"id":"T361","span":{"begin":332,"end":336},"obj":"Protein"},{"id":"T360","span":{"begin":326,"end":330},"obj":"Protein"},{"id":"T359","span":{"begin":319,"end":322},"obj":"Protein"},{"id":"T358","span":{"begin":311,"end":317},"obj":"Protein"},{"id":"T357","span":{"begin":303,"end":307},"obj":"Protein"},{"id":"T356","span":{"begin":295,"end":301},"obj":"Protein"},{"id":"T355","span":{"begin":287,"end":291},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"The aetiology of RA is still not understood, but it is well accepted that activation of NF-κB-dependent gene expression plays a key role in the development of RA and many other autoimmune diseases. NF-κB represents a family of structurally related and evolutionarily conserved proteins (p100 or NF-κB2, p105 or NF-κB1, p65 or RelA, RelB, c-Rel) that function as homodimers or heterodimers [1], and that regulate the expression of a large number of genes - such as TNF, IL-1, IL-6, cyclo-oxygenase-2, chemokines, inducible nitric oxide synthase, and matrix metalloproteinases - that are involved in RA. In addition, TNF and IL-1 are themselves very potent activators of NF-κB (reviewed in [2,3])."}

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aetiology of RA is still not understood, but it is well accepted that activation of NF-κB-dependent gene expression plays a key role in the development of RA and many other autoimmune diseases. NF-κB represents a family of structurally related and evolutionarily conserved proteins (p100 or NF-κB2, p105 or NF-κB1, p65 or RelA, RelB, c-Rel) that function as homodimers or heterodimers [1], and that regulate the expression of a large number of genes - such as TNF, IL-1, IL-6, cyclo-oxygenase-2, chemokines, inducible nitric oxide synthase, and matrix metalloproteinases - that are involved in RA. In addition, TNF and IL-1 are themselves very potent activators of NF-κB (reviewed in [2,3])."}

{"project":"GO-BP","denotations":[{"id":"T794","span":{"begin":522,"end":543},"obj":"http://purl.obolibrary.org/obo/GO_0051001"},{"id":"T793","span":{"begin":522,"end":543},"obj":"http://purl.obolibrary.org/obo/GO_0050999"},{"id":"T792","span":{"begin":522,"end":543},"obj":"http://purl.obolibrary.org/obo/GO_0051000"},{"id":"T791","span":{"begin":522,"end":543},"obj":"http://purl.obolibrary.org/obo/GO_0004517"},{"id":"T790","span":{"begin":487,"end":496},"obj":"http://purl.obolibrary.org/obo/GO_0016701"},{"id":"T788","span":{"begin":144,"end":155},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T786","span":{"begin":104,"end":119},"obj":"http://purl.obolibrary.org/obo/GO_0010467"},{"id":"T782","span":{"begin":655,"end":674},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T781","span":{"begin":74,"end":93},"obj":"http://purl.obolibrary.org/obo/GO_0051092"}],"text":"The aetiology of RA is still not understood, but it is well accepted that activation of NF-κB-dependent gene expression plays a key role in the development of RA and many other autoimmune diseases. NF-κB represents a family of structurally related and evolutionarily conserved proteins (p100 or NF-κB2, p105 or NF-κB1, p65 or RelA, RelB, c-Rel) that function as homodimers or heterodimers [1], and that regulate the expression of a large number of genes - such as TNF, IL-1, IL-6, cyclo-oxygenase-2, chemokines, inducible nitric oxide synthase, and matrix metalloproteinases - that are involved in RA. In addition, TNF and IL-1 are themselves very potent activators of NF-κB (reviewed in [2,3])."}

{"project":"GO-MF","denotations":[{"id":"T809","span":{"begin":522,"end":543},"obj":"http://purl.obolibrary.org/obo/GO_0050998"},{"id":"T808","span":{"begin":522,"end":543},"obj":"http://purl.obolibrary.org/obo/GO_0004517"},{"id":"T807","span":{"begin":487,"end":496},"obj":"http://purl.obolibrary.org/obo/GO_0016701"},{"id":"T806","span":{"begin":475,"end":479},"obj":"http://purl.obolibrary.org/obo/GO_0005138"},{"id":"T805","span":{"begin":623,"end":627},"obj":"http://purl.obolibrary.org/obo/GO_0005149"},{"id":"T804","span":{"begin":469,"end":473},"obj":"http://purl.obolibrary.org/obo/GO_0005149"}],"text":"The aetiology of RA is still not understood, but it is well accepted that activation of NF-κB-dependent gene expression plays a key role in the development of RA and many other autoimmune diseases. NF-κB represents a family of structurally related and evolutionarily conserved proteins (p100 or NF-κB2, p105 or NF-κB1, p65 or RelA, RelB, c-Rel) that function as homodimers or heterodimers [1], and that regulate the expression of a large number of genes - such as TNF, IL-1, IL-6, cyclo-oxygenase-2, chemokines, inducible nitric oxide synthase, and matrix metalloproteinases - that are involved in RA. In addition, TNF and IL-1 are themselves very potent activators of NF-κB (reviewed in [2,3])."}

{"project":"sentences","denotations":[{"id":"T330","span":{"begin":602,"end":695},"obj":"Sentence"},{"id":"T329","span":{"begin":198,"end":601},"obj":"Sentence"},{"id":"T328","span":{"begin":0,"end":197},"obj":"Sentence"},{"id":"T11","span":{"begin":0,"end":197},"obj":"Sentence"},{"id":"T12","span":{"begin":198,"end":601},"obj":"Sentence"},{"id":"T13","span":{"begin":602,"end":695},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"The aetiology of RA is still not understood, but it is well accepted that activation of NF-κB-dependent gene expression plays a key role in the development of RA and many other autoimmune diseases. NF-κB represents a family of structurally related and evolutionarily conserved proteins (p100 or NF-κB2, p105 or NF-κB1, p65 or RelA, RelB, c-Rel) that function as homodimers or heterodimers [1], and that regulate the expression of a large number of genes - such as TNF, IL-1, IL-6, cyclo-oxygenase-2, chemokines, inducible nitric oxide synthase, and matrix metalloproteinases - that are involved in RA. In addition, TNF and IL-1 are themselves very potent activators of NF-κB (reviewed in [2,3])."}

{"project":"simple1","denotations":[{"id":"T825","span":{"begin":615,"end":618},"obj":"Protein"},{"id":"T824","span":{"begin":512,"end":543},"obj":"Protein"},{"id":"T823","span":{"begin":481,"end":498},"obj":"Protein"},{"id":"T822","span":{"begin":475,"end":479},"obj":"Protein"},{"id":"T821","span":{"begin":464,"end":467},"obj":"Protein"},{"id":"T820","span":{"begin":338,"end":343},"obj":"Protein"},{"id":"T819","span":{"begin":332,"end":336},"obj":"Protein"},{"id":"T818","span":{"begin":326,"end":330},"obj":"Protein"},{"id":"T817","span":{"begin":319,"end":322},"obj":"Protein"},{"id":"T816","span":{"begin":311,"end":317},"obj":"Protein"},{"id":"T815","span":{"begin":303,"end":307},"obj":"Protein"},{"id":"T814","span":{"begin":295,"end":301},"obj":"Protein"},{"id":"T813","span":{"begin":287,"end":291},"obj":"Protein"}],"text":"The aetiology of RA is still not understood, but it is well accepted that activation of NF-κB-dependent gene expression plays a key role in the development of RA and many other autoimmune diseases. NF-κB represents a family of structurally related and evolutionarily conserved proteins (p100 or NF-κB2, p105 or NF-κB1, p65 or RelA, RelB, c-Rel) that function as homodimers or heterodimers [1], and that regulate the expression of a large number of genes - such as TNF, IL-1, IL-6, cyclo-oxygenase-2, chemokines, inducible nitric oxide synthase, and matrix metalloproteinases - that are involved in RA. In addition, TNF and IL-1 are themselves very potent activators of NF-κB (reviewed in [2,3])."}

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