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testone

bionlp-st-ge-2016-spacy-parsed

DLUT931

bionlp-st-ge-2016-uniprot

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T6913","span":{"begin":703,"end":708},"obj":"http://www.uniprot.org/uniprot/Q13490"},{"id":"T6908","span":{"begin":932,"end":937},"obj":"http://www.uniprot.org/uniprot/Q12933"},{"id":"T6907","span":{"begin":685,"end":690},"obj":"http://www.uniprot.org/uniprot/Q12933"},{"id":"T6894","span":{"begin":1112,"end":1116},"obj":"http://www.uniprot.org/uniprot/Q60680-2"},{"id":"T6893","span":{"begin":421,"end":425},"obj":"http://www.uniprot.org/uniprot/Q60680-2"},{"id":"T6889","span":{"begin":1112,"end":1116},"obj":"http://www.uniprot.org/uniprot/O15111"},{"id":"T6888","span":{"begin":421,"end":425},"obj":"http://www.uniprot.org/uniprot/O15111"},{"id":"T6875","span":{"begin":177,"end":180},"obj":"http://www.uniprot.org/uniprot/Q00653"},{"id":"T6936","span":{"begin":986,"end":991},"obj":"http://www.uniprot.org/uniprot/Q13114"},{"id":"T6935","span":{"begin":854,"end":859},"obj":"http://www.uniprot.org/uniprot/Q13114"},{"id":"T6934","span":{"begin":692,"end":697},"obj":"http://www.uniprot.org/uniprot/Q13114"},{"id":"T6933","span":{"begin":1091,"end":1094},"obj":"http://www.uniprot.org/uniprot/Q99558"},{"id":"T6932","span":{"begin":1039,"end":1042},"obj":"http://www.uniprot.org/uniprot/Q99558"},{"id":"T6931","span":{"begin":740,"end":743},"obj":"http://www.uniprot.org/uniprot/Q99558"},{"id":"T6930","span":{"begin":644,"end":647},"obj":"http://www.uniprot.org/uniprot/Q99558"},{"id":"T6929","span":{"begin":499,"end":502},"obj":"http://www.uniprot.org/uniprot/Q99558"},{"id":"T6928","span":{"begin":493,"end":496},"obj":"http://www.uniprot.org/uniprot/Q99558"},{"id":"T6927","span":{"begin":206,"end":210},"obj":"http://www.uniprot.org/uniprot/Q01201"},{"id":"T6921","span":{"begin":94,"end":98},"obj":"http://www.uniprot.org/uniprot/P25942"},{"id":"T6914","span":{"begin":942,"end":947},"obj":"http://www.uniprot.org/uniprot/Q13490"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

bionlp-st-ge-2016-test-proteins

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T4552","span":{"begin":1112,"end":1116},"obj":"Protein"},{"id":"T4551","span":{"begin":1091,"end":1094},"obj":"Protein"},{"id":"T4550","span":{"begin":1039,"end":1042},"obj":"Protein"},{"id":"T4549","span":{"begin":986,"end":991},"obj":"Protein"},{"id":"T4548","span":{"begin":948,"end":949},"obj":"Protein"},{"id":"T4547","span":{"begin":942,"end":947},"obj":"Protein"},{"id":"T4546","span":{"begin":932,"end":937},"obj":"Protein"},{"id":"T4545","span":{"begin":854,"end":859},"obj":"Protein"},{"id":"T4544","span":{"begin":740,"end":743},"obj":"Protein"},{"id":"T4543","span":{"begin":709,"end":710},"obj":"Protein"},{"id":"T4542","span":{"begin":703,"end":708},"obj":"Protein"},{"id":"T4541","span":{"begin":692,"end":697},"obj":"Protein"},{"id":"T4540","span":{"begin":685,"end":690},"obj":"Protein"},{"id":"T4539","span":{"begin":644,"end":647},"obj":"Protein"},{"id":"T4538","span":{"begin":499,"end":502},"obj":"Protein"},{"id":"T4537","span":{"begin":493,"end":496},"obj":"Protein"},{"id":"T4536","span":{"begin":470,"end":491},"obj":"Protein"},{"id":"T4535","span":{"begin":421,"end":425},"obj":"Protein"},{"id":"T4534","span":{"begin":206,"end":210},"obj":"Protein"},{"id":"T4533","span":{"begin":177,"end":180},"obj":"Protein"},{"id":"T4532","span":{"begin":138,"end":142},"obj":"Protein"},{"id":"T4531","span":{"begin":104,"end":108},"obj":"Protein"},{"id":"T4530","span":{"begin":94,"end":98},"obj":"Protein"},{"id":"T4529","span":{"begin":79,"end":92},"obj":"Protein"},{"id":"T4528","span":{"begin":55,"end":77},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

bionlp-st-ge-2016-coref

{"project":"bionlp-st-ge-2016-coref","denotations":[{"id":"T4460","span":{"begin":1039,"end":1042},"obj":"Antecedent"},{"id":"T4459","span":{"begin":1048,"end":1051},"obj":"Anaphor"},{"id":"T4458","span":{"begin":854,"end":859},"obj":"Antecedent"},{"id":"T4457","span":{"begin":892,"end":894},"obj":"Anaphor"},{"id":"T4456","span":{"begin":740,"end":743},"obj":"Antecedent"},{"id":"T4455","span":{"begin":756,"end":759},"obj":"Anaphor"},{"id":"T4454","span":{"begin":421,"end":425},"obj":"Antecedent"},{"id":"T4453","span":{"begin":427,"end":432},"obj":"Anaphor"}],"relations":[{"id":"R3029","pred":"boundBy","subj":"T4453","obj":"T4454"},{"id":"R3030","pred":"boundBy","subj":"T4455","obj":"T4456"},{"id":"R3031","pred":"boundBy","subj":"T4457","obj":"T4458"},{"id":"R3032","pred":"boundBy","subj":"T4459","obj":"T4460"}],"namespaces":[{"prefix":"_base","uri":"https://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

2_test

{"project":"2_test","denotations":[{"id":"21639951-21173796-4289456","span":{"begin":361,"end":363},"obj":"21173796"},{"id":"21639951-11520989-4289457","span":{"begin":1134,"end":1136},"obj":"11520989"},{"id":"21639951-15140882-4289458","span":{"begin":1137,"end":1139},"obj":"15140882"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

pmc-enju-pas

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"T4236","span":{"begin":318,"end":323},"obj":"http://purl.obolibrary.org/obo/UBERON_0000062"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

GO-BP

{"project":"GO-BP","denotations":[{"id":"T5600","span":{"begin":1091,"end":1094},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5599","span":{"begin":1039,"end":1042},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5598","span":{"begin":740,"end":743},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5597","span":{"begin":644,"end":647},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5596","span":{"begin":499,"end":502},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5595","span":{"begin":493,"end":496},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5594","span":{"begin":318,"end":335},"obj":"http://purl.obolibrary.org/obo/GO_0048513"},{"id":"T5593","span":{"begin":324,"end":335},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T5592","span":{"begin":286,"end":297},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T5591","span":{"begin":281,"end":297},"obj":"http://purl.obolibrary.org/obo/GO_0048468"},{"id":"T5590","span":{"begin":279,"end":297},"obj":"http://purl.obolibrary.org/obo/GO_0002329"},{"id":"T5589","span":{"begin":279,"end":297},"obj":"http://purl.obolibrary.org/obo/GO_0002328"},{"id":"T5526","span":{"begin":771,"end":800},"obj":"http://purl.obolibrary.org/obo/GO_1903009"},{"id":"T5524","span":{"begin":1065,"end":1076},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T5523","span":{"begin":992,"end":1003},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T5522","span":{"begin":771,"end":782},"obj":"http://purl.obolibrary.org/obo/GO_0009056"},{"id":"T5520","span":{"begin":1117,"end":1132},"obj":"http://purl.obolibrary.org/obo/GO_0016310"},{"id":"T5519","span":{"begin":451,"end":466},"obj":"http://purl.obolibrary.org/obo/GO_0016310"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

GO-MF

{"project":"GO-MF","denotations":[{"id":"T5679","span":{"begin":1091,"end":1094},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5678","span":{"begin":1039,"end":1042},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5677","span":{"begin":740,"end":743},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5676","span":{"begin":644,"end":647},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5675","span":{"begin":499,"end":502},"obj":"http://purl.obolibrary.org/obo/GO_0004704"},{"id":"T5674","span":{"begin":493,"end":496},"obj":"http://purl.obolibrary.org/obo/GO_0004704"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

GO-CC

{"project":"GO-CC","denotations":[{"id":"T5693","span":{"begin":637,"end":642},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T5692","span":{"begin":609,"end":613},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T5691","span":{"begin":281,"end":285},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T5688","span":{"begin":790,"end":800},"obj":"http://purl.obolibrary.org/obo/GO_0000502"},{"id":"T5687","span":{"begin":163,"end":173},"obj":"http://purl.obolibrary.org/obo/GO_0000502"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

sentences

{"project":"sentences","denotations":[{"id":"T4261","span":{"begin":1005,"end":1152},"obj":"Sentence"},{"id":"T4260","span":{"begin":802,"end":1004},"obj":"Sentence"},{"id":"T4259","span":{"begin":621,"end":801},"obj":"Sentence"},{"id":"T4258","span":{"begin":499,"end":620},"obj":"Sentence"},{"id":"T4257","span":{"begin":121,"end":498},"obj":"Sentence"},{"id":"T4256","span":{"begin":0,"end":120},"obj":"Sentence"},{"id":"T68","span":{"begin":0,"end":120},"obj":"Sentence"},{"id":"T69","span":{"begin":121,"end":498},"obj":"Sentence"},{"id":"T70","span":{"begin":499,"end":620},"obj":"Sentence"},{"id":"T71","span":{"begin":621,"end":801},"obj":"Sentence"},{"id":"T72","span":{"begin":802,"end":1004},"obj":"Sentence"},{"id":"T73","span":{"begin":1005,"end":1152},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

simple1

{"project":"simple1","denotations":[{"id":"T5881","span":{"begin":1112,"end":1116},"obj":"Protein"},{"id":"T5880","span":{"begin":1091,"end":1094},"obj":"Protein"},{"id":"T5879","span":{"begin":1039,"end":1042},"obj":"Protein"},{"id":"T5878","span":{"begin":986,"end":991},"obj":"Protein"},{"id":"T5877","span":{"begin":948,"end":949},"obj":"Protein"},{"id":"T5876","span":{"begin":942,"end":947},"obj":"Protein"},{"id":"T5875","span":{"begin":932,"end":937},"obj":"Protein"},{"id":"T5874","span":{"begin":854,"end":859},"obj":"Protein"},{"id":"T5873","span":{"begin":740,"end":743},"obj":"Protein"},{"id":"T5872","span":{"begin":709,"end":710},"obj":"Protein"},{"id":"T5871","span":{"begin":703,"end":708},"obj":"Protein"},{"id":"T5870","span":{"begin":692,"end":697},"obj":"Protein"},{"id":"T5869","span":{"begin":685,"end":690},"obj":"Protein"},{"id":"T5868","span":{"begin":644,"end":647},"obj":"Protein"},{"id":"T5867","span":{"begin":499,"end":502},"obj":"Protein"},{"id":"T5866","span":{"begin":493,"end":496},"obj":"Protein"},{"id":"T5865","span":{"begin":470,"end":491},"obj":"Protein"},{"id":"T5864","span":{"begin":421,"end":425},"obj":"Protein"},{"id":"T5863","span":{"begin":206,"end":210},"obj":"Protein"},{"id":"T5862","span":{"begin":177,"end":180},"obj":"Protein"},{"id":"T5861","span":{"begin":138,"end":142},"obj":"Protein"},{"id":"T5860","span":{"begin":104,"end":108},"obj":"Protein"},{"id":"T5859","span":{"begin":94,"end":98},"obj":"Protein"},{"id":"T5858","span":{"begin":79,"end":92},"obj":"Protein"},{"id":"T5857","span":{"begin":55,"end":77},"obj":"Protein"}],"text":"The noncanonical NF-κB pathway can be activated by the lymphotoxin β receptor, BAFF receptor, CD40, and RANK (Figure 2). In this pathway, p100 is processed by the proteasome to p52, which together with the RelB NF-κB subunit regulates a distinct set of target genes that control B-cell development, secondary lymphoid organ development, and osteoclastogenesis [27] The noncanonical NF-κB pathway is strictly dependent on IKK1, which is activated upon phosphorylation by NF-κB inducing kinase (NIK). NIK is predominantly regulated at the post-translational level and is present at extremely low levels in most cell types. In unstimulated cells, NIK occurs in a cytoplasmic complex with TRAF2, TRAF3, and cIAP1/2, which K48-polyubiquitinates NIK, leading to its continuous degradation by the proteasome. Receptor ligation has been shown not only to remove TRAF3 from this complex by recruiting it to the receptor, but also to attract TRAF2 and cIAP1/2, which are essential for subsequent TRAF3 degradation. All this contributes to releasing NIK from its constitutive degradation, resulting in NIK accumulation and IKK1 phosphorylation [28,29] (Figure 2)."}

BioNLP16_DUT

BioNLP16_Messiy

bionlp-st-ge-2016-test-ihmc

bionlp-st-ge-2016-test-tees

test3

PMC:3218875 / 12686-13838 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:3218875 / 12686-13838 JSON TXT