PubMed:8189531
Annnotations
jnlpba-st-training
{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":0,"end":36},"obj":"cell_type"},{"id":"T2","span":{"begin":161,"end":164},"obj":"DNA"},{"id":"T3","span":{"begin":196,"end":199},"obj":"protein"},{"id":"T4","span":{"begin":205,"end":216},"obj":"protein"},{"id":"T5","span":{"begin":289,"end":309},"obj":"DNA"},{"id":"T6","span":{"begin":416,"end":437},"obj":"DNA"},{"id":"T7","span":{"begin":438,"end":441},"obj":"DNA"},{"id":"T8","span":{"begin":443,"end":465},"obj":"cell_type"},{"id":"T9","span":{"begin":474,"end":477},"obj":"DNA"},{"id":"T10","span":{"begin":565,"end":568},"obj":"protein"},{"id":"T11","span":{"begin":599,"end":613},"obj":"DNA"},{"id":"T12","span":{"begin":680,"end":700},"obj":"protein"},{"id":"T13","span":{"begin":725,"end":735},"obj":"protein"},{"id":"T14","span":{"begin":775,"end":788},"obj":"cell_type"},{"id":"T15","span":{"begin":790,"end":793},"obj":"protein"},{"id":"T16","span":{"begin":826,"end":840},"obj":"DNA"},{"id":"T17","span":{"begin":879,"end":882},"obj":"DNA"},{"id":"T18","span":{"begin":907,"end":917},"obj":"cell_type"},{"id":"T19","span":{"begin":967,"end":999},"obj":"protein"},{"id":"T20","span":{"begin":1011,"end":1033},"obj":"cell_type"},{"id":"T21","span":{"begin":1064,"end":1074},"obj":"protein"},{"id":"T22","span":{"begin":1153,"end":1156},"obj":"protein"},{"id":"T23","span":{"begin":1193,"end":1203},"obj":"protein"},{"id":"T24","span":{"begin":1209,"end":1223},"obj":"cell_line"},{"id":"T25","span":{"begin":1280,"end":1321},"obj":"protein"},{"id":"T26","span":{"begin":1352,"end":1378},"obj":"DNA"},{"id":"T27","span":{"begin":1424,"end":1438},"obj":"DNA"},{"id":"T28","span":{"begin":1450,"end":1453},"obj":"DNA"},{"id":"T29","span":{"begin":1638,"end":1677},"obj":"protein"},{"id":"T30","span":{"begin":1678,"end":1698},"obj":"protein"}],"text":"Central nervous system-derived cells express a kappa B-binding activity that enhances human immunodeficiency virus type 1 transcription in vitro and facilitates TAR-independent transactivation by Tat.\nThe Tat protein of human immunodeficiency virus type 1 (HIV-1) is a potent activator of long terminal repeat-directed transcription. While in most cell types, activation requires interaction of Tat with the unusual transcription element TAR, astrocytic glial cells support TAR-independent transactivation of HIV-1 transcription by Tat. This alternative pathway of Tat activation is mediated by the viral enhancer, a kappa B domain capable of binding the prototypical form of the transcription factor nuclear factor kappa B (NF-kappa B) present in many cell types, including T lymphocytes. Tat transactivation mediated by the kappa B domain is sufficient to allow replication of TAR-deleted mutant HIV-1 in astrocytes. The present study demonstrates the existence of kappa B-specific binding factors present in human glial astrocytes that differ from prototypical NF-kappa B. The novel astrocyte-derived kappa B-binding activity is retained on an HIV-1 Tat affinity column, while prototypical NF-kappa B from Jurkat T cells is not. In vitro transcription studies demonstrate that astrocyte-derived kappa B-binding factors activate transcription of the HIV-1 long terminal repeat and that this activation is dependent on the kappa B domain. Moreover, TAR-independent transactivation of HIV-1 transcription is reproduced in vitro in an astrocyte factor-dependent manner which correlates with kappa B-binding activity. The importance of the central nervous system-enriched kappa B transcription factor in the regulation of HIV-1 expression is discussed."}
genia-medco-coref
{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":45,"end":71},"obj":"NP"},{"id":"C2","span":{"begin":72,"end":76},"obj":"NP"},{"id":"C3","span":{"begin":86,"end":135},"obj":"NP"},{"id":"C5","span":{"begin":196,"end":199},"obj":"NP"},{"id":"C4","span":{"begin":161,"end":199},"obj":"NP"},{"id":"C6","span":{"begin":201,"end":263},"obj":"NP"},{"id":"C7","span":{"begin":289,"end":332},"obj":"NP"},{"id":"C8","span":{"begin":395,"end":398},"obj":"NP"},{"id":"C10","span":{"begin":509,"end":528},"obj":"NP"},{"id":"C11","span":{"begin":532,"end":535},"obj":"NP"},{"id":"C9","span":{"begin":474,"end":535},"obj":"NP"},{"id":"C12","span":{"begin":595,"end":613},"obj":"NP"},{"id":"C13","span":{"begin":615,"end":763},"obj":"NP"},{"id":"C14","span":{"begin":822,"end":840},"obj":"NP"},{"id":"C15","span":{"begin":1011,"end":1033},"obj":"NP"},{"id":"C16","span":{"begin":1034,"end":1038},"obj":"NP"},{"id":"C17","span":{"begin":1051,"end":1074},"obj":"NP"},{"id":"C18","span":{"begin":1180,"end":1203},"obj":"NP"},{"id":"C19","span":{"begin":1331,"end":1378},"obj":"NP"},{"id":"C20","span":{"begin":1420,"end":1438},"obj":"NP"},{"id":"C21","span":{"begin":1450,"end":1504},"obj":"NP"},{"id":"C22","span":{"begin":1531,"end":1567},"obj":"NP"},{"id":"C23","span":{"begin":1568,"end":1573},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-relat","subj":"C2","obj":"C1"},{"id":"R2","pred":"coref-ident","subj":"C6","obj":"C5"},{"id":"R3","pred":"coref-ident","subj":"C8","obj":"C5"},{"id":"R4","pred":"coref-ident","subj":"C10","obj":"C3"},{"id":"R5","pred":"coref-ident","subj":"C11","obj":"C8"},{"id":"R6","pred":"coref-ident","subj":"C9","obj":"C4"},{"id":"R7","pred":"coref-appos","subj":"C13","obj":"C12"},{"id":"R8","pred":"coref-relat","subj":"C16","obj":"C15"},{"id":"R9","pred":"coref-ident","subj":"C18","obj":"C17"},{"id":"R10","pred":"coref-ident","subj":"C19","obj":"C7"},{"id":"R11","pred":"coref-ident","subj":"C20","obj":"C14"},{"id":"R12","pred":"coref-ident","subj":"C21","obj":"C9"},{"id":"R13","pred":"coref-relat","subj":"C23","obj":"C22"}],"text":"Central nervous system-derived cells express a kappa B-binding activity that enhances human immunodeficiency virus type 1 transcription in vitro and facilitates TAR-independent transactivation by Tat.\nThe Tat protein of human immunodeficiency virus type 1 (HIV-1) is a potent activator of long terminal repeat-directed transcription. While in most cell types, activation requires interaction of Tat with the unusual transcription element TAR, astrocytic glial cells support TAR-independent transactivation of HIV-1 transcription by Tat. This alternative pathway of Tat activation is mediated by the viral enhancer, a kappa B domain capable of binding the prototypical form of the transcription factor nuclear factor kappa B (NF-kappa B) present in many cell types, including T lymphocytes. Tat transactivation mediated by the kappa B domain is sufficient to allow replication of TAR-deleted mutant HIV-1 in astrocytes. The present study demonstrates the existence of kappa B-specific binding factors present in human glial astrocytes that differ from prototypical NF-kappa B. The novel astrocyte-derived kappa B-binding activity is retained on an HIV-1 Tat affinity column, while prototypical NF-kappa B from Jurkat T cells is not. In vitro transcription studies demonstrate that astrocyte-derived kappa B-binding factors activate transcription of the HIV-1 long terminal repeat and that this activation is dependent on the kappa B domain. Moreover, TAR-independent transactivation of HIV-1 transcription is reproduced in vitro in an astrocyte factor-dependent manner which correlates with kappa B-binding activity. The importance of the central nervous system-enriched kappa B transcription factor in the regulation of HIV-1 expression is discussed."}
pubmed-sentences-benchmark
{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":200},"obj":"Sentence"},{"id":"S2","span":{"begin":201,"end":333},"obj":"Sentence"},{"id":"S3","span":{"begin":334,"end":536},"obj":"Sentence"},{"id":"S4","span":{"begin":537,"end":789},"obj":"Sentence"},{"id":"S5","span":{"begin":790,"end":918},"obj":"Sentence"},{"id":"S6","span":{"begin":919,"end":1075},"obj":"Sentence"},{"id":"S7","span":{"begin":1076,"end":1231},"obj":"Sentence"},{"id":"S8","span":{"begin":1232,"end":1439},"obj":"Sentence"},{"id":"S9","span":{"begin":1440,"end":1615},"obj":"Sentence"},{"id":"S10","span":{"begin":1616,"end":1750},"obj":"Sentence"}],"text":"Central nervous system-derived cells express a kappa B-binding activity that enhances human immunodeficiency virus type 1 transcription in vitro and facilitates TAR-independent transactivation by Tat.\nThe Tat protein of human immunodeficiency virus type 1 (HIV-1) is a potent activator of long terminal repeat-directed transcription. While in most cell types, activation requires interaction of Tat with the unusual transcription element TAR, astrocytic glial cells support TAR-independent transactivation of HIV-1 transcription by Tat. This alternative pathway of Tat activation is mediated by the viral enhancer, a kappa B domain capable of binding the prototypical form of the transcription factor nuclear factor kappa B (NF-kappa B) present in many cell types, including T lymphocytes. Tat transactivation mediated by the kappa B domain is sufficient to allow replication of TAR-deleted mutant HIV-1 in astrocytes. The present study demonstrates the existence of kappa B-specific binding factors present in human glial astrocytes that differ from prototypical NF-kappa B. The novel astrocyte-derived kappa B-binding activity is retained on an HIV-1 Tat affinity column, while prototypical NF-kappa B from Jurkat T cells is not. In vitro transcription studies demonstrate that astrocyte-derived kappa B-binding factors activate transcription of the HIV-1 long terminal repeat and that this activation is dependent on the kappa B domain. Moreover, TAR-independent transactivation of HIV-1 transcription is reproduced in vitro in an astrocyte factor-dependent manner which correlates with kappa B-binding activity. The importance of the central nervous system-enriched kappa B transcription factor in the regulation of HIV-1 expression is discussed."}
GENIAcorpus
{"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":0,"end":22},"obj":"body_part"},{"id":"T2","span":{"begin":47,"end":71},"obj":"other_name"},{"id":"T3","span":{"begin":86,"end":121},"obj":"virus"},{"id":"T4","span":{"begin":161,"end":164},"obj":"DNA_domain_or_region"},{"id":"T5","span":{"begin":196,"end":199},"obj":"protein_molecule"},{"id":"T6","span":{"begin":205,"end":216},"obj":"protein_molecule"},{"id":"T7","span":{"begin":220,"end":255},"obj":"virus"},{"id":"T8","span":{"begin":257,"end":262},"obj":"virus"},{"id":"T9","span":{"begin":289,"end":309},"obj":"DNA_domain_or_region"},{"id":"T10","span":{"begin":416,"end":437},"obj":"DNA_family_or_group"},{"id":"T11","span":{"begin":438,"end":441},"obj":"DNA_domain_or_region"},{"id":"T12","span":{"begin":443,"end":465},"obj":"cell_type"},{"id":"T13","span":{"begin":474,"end":477},"obj":"DNA_domain_or_region"},{"id":"T14","span":{"begin":509,"end":514},"obj":"virus"},{"id":"T15","span":{"begin":565,"end":568},"obj":"protein_molecule"},{"id":"T16","span":{"begin":599,"end":613},"obj":"DNA_domain_or_region"},{"id":"T17","span":{"begin":680,"end":700},"obj":"protein_family_or_group"},{"id":"T18","span":{"begin":725,"end":735},"obj":"protein_molecule"},{"id":"T19","span":{"begin":775,"end":788},"obj":"cell_type"},{"id":"T20","span":{"begin":790,"end":793},"obj":"protein_molecule"},{"id":"T21","span":{"begin":826,"end":840},"obj":"DNA_domain_or_region"},{"id":"T22","span":{"begin":879,"end":882},"obj":"DNA_domain_or_region"},{"id":"T23","span":{"begin":898,"end":903},"obj":"virus"},{"id":"T24","span":{"begin":907,"end":917},"obj":"cell_type"},{"id":"T25","span":{"begin":967,"end":999},"obj":"protein_family_or_group"},{"id":"T26","span":{"begin":1011,"end":1033},"obj":"cell_type"},{"id":"T27","span":{"begin":1064,"end":1074},"obj":"protein_molecule"},{"id":"T28","span":{"begin":1104,"end":1128},"obj":"other_name"},{"id":"T29","span":{"begin":1147,"end":1152},"obj":"virus"},{"id":"T30","span":{"begin":1153,"end":1156},"obj":"protein_molecule"},{"id":"T31","span":{"begin":1193,"end":1203},"obj":"protein_molecule"},{"id":"T32","span":{"begin":1209,"end":1223},"obj":"cell_line"},{"id":"T33","span":{"begin":1280,"end":1321},"obj":"protein_family_or_group"},{"id":"T34","span":{"begin":1352,"end":1357},"obj":"virus"},{"id":"T35","span":{"begin":1424,"end":1438},"obj":"DNA_domain_or_region"},{"id":"T36","span":{"begin":1450,"end":1453},"obj":"DNA_domain_or_region"},{"id":"T37","span":{"begin":1485,"end":1490},"obj":"virus"},{"id":"T38","span":{"begin":1534,"end":1567},"obj":"other_name"},{"id":"T39","span":{"begin":1590,"end":1614},"obj":"other_name"},{"id":"T40","span":{"begin":1638,"end":1660},"obj":"body_part"},{"id":"T41","span":{"begin":1678,"end":1698},"obj":"protein_family_or_group"},{"id":"T42","span":{"begin":1720,"end":1725},"obj":"virus"}],"text":"Central nervous system-derived cells express a kappa B-binding activity that enhances human immunodeficiency virus type 1 transcription in vitro and facilitates TAR-independent transactivation by Tat.\nThe Tat protein of human immunodeficiency virus type 1 (HIV-1) is a potent activator of long terminal repeat-directed transcription. While in most cell types, activation requires interaction of Tat with the unusual transcription element TAR, astrocytic glial cells support TAR-independent transactivation of HIV-1 transcription by Tat. This alternative pathway of Tat activation is mediated by the viral enhancer, a kappa B domain capable of binding the prototypical form of the transcription factor nuclear factor kappa B (NF-kappa B) present in many cell types, including T lymphocytes. Tat transactivation mediated by the kappa B domain is sufficient to allow replication of TAR-deleted mutant HIV-1 in astrocytes. The present study demonstrates the existence of kappa B-specific binding factors present in human glial astrocytes that differ from prototypical NF-kappa B. The novel astrocyte-derived kappa B-binding activity is retained on an HIV-1 Tat affinity column, while prototypical NF-kappa B from Jurkat T cells is not. In vitro transcription studies demonstrate that astrocyte-derived kappa B-binding factors activate transcription of the HIV-1 long terminal repeat and that this activation is dependent on the kappa B domain. Moreover, TAR-independent transactivation of HIV-1 transcription is reproduced in vitro in an astrocyte factor-dependent manner which correlates with kappa B-binding activity. The importance of the central nervous system-enriched kappa B transcription factor in the regulation of HIV-1 expression is discussed."}