PubMed:2072454 JSONTXT

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    PubmedHPO

    {"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":249,"end":265},"obj":"HP_0002721"},{"id":"T2","span":{"begin":1219,"end":1235},"obj":"HP_0002721"}],"text":"Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1: distinct patterns of viral growth are determined by T-cell types.\nStarting with a replication-incompetent molecular clone of human immunodeficiency virus type 1, lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat (LTR), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation. Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element(s) was present in the LTR. For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites), a hierarchy of cellular permissivity to virus replication (peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat) was observed. Of note was the associated emergence of second-site LTR revertants which involved an alteration of the TATA box. These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present."}

    jnlpba-st-training

    {"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":16,"end":26},"obj":"protein"},{"id":"T2","span":{"begin":31,"end":49},"obj":"DNA"},{"id":"T3","span":{"begin":170,"end":182},"obj":"cell_type"},{"id":"T4","span":{"begin":296,"end":328},"obj":"DNA"},{"id":"T5","span":{"begin":344,"end":371},"obj":"DNA"},{"id":"T6","span":{"begin":373,"end":376},"obj":"DNA"},{"id":"T7","span":{"begin":401,"end":419},"obj":"DNA"},{"id":"T8","span":{"begin":455,"end":482},"obj":"DNA"},{"id":"T9","span":{"begin":700,"end":718},"obj":"cell_type"},{"id":"T10","span":{"begin":738,"end":745},"obj":"DNA"},{"id":"T11","span":{"begin":768,"end":771},"obj":"DNA"},{"id":"T12","span":{"begin":832,"end":836},"obj":"DNA"},{"id":"T13","span":{"begin":859,"end":878},"obj":"DNA"},{"id":"T14","span":{"begin":887,"end":904},"obj":"DNA"},{"id":"T15","span":{"begin":966,"end":994},"obj":"cell_type"},{"id":"T16","span":{"begin":997,"end":1000},"obj":"cell_line"},{"id":"T17","span":{"begin":1014,"end":1016},"obj":"cell_line"},{"id":"T18","span":{"begin":1030,"end":1033},"obj":"cell_line"},{"id":"T19","span":{"begin":1047,"end":1053},"obj":"cell_line"},{"id":"T20","span":{"begin":1109,"end":1124},"obj":"DNA"},{"id":"T21","span":{"begin":1172,"end":1180},"obj":"DNA"},{"id":"T22","span":{"begin":1213,"end":1252},"obj":"DNA"},{"id":"T23","span":{"begin":1330,"end":1342},"obj":"cell_type"},{"id":"T24","span":{"begin":1413,"end":1436},"obj":"protein"}],"text":"Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1: distinct patterns of viral growth are determined by T-cell types.\nStarting with a replication-incompetent molecular clone of human immunodeficiency virus type 1, lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat (LTR), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation. Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element(s) was present in the LTR. For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites), a hierarchy of cellular permissivity to virus replication (peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat) was observed. Of note was the associated emergence of second-site LTR revertants which involved an alteration of the TATA box. These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present."}

    pubmed-sentences-benchmark

    {"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":183},"obj":"Sentence"},{"id":"S2","span":{"begin":184,"end":593},"obj":"Sentence"},{"id":"S3","span":{"begin":594,"end":772},"obj":"Sentence"},{"id":"S4","span":{"begin":773,"end":1068},"obj":"Sentence"},{"id":"S5","span":{"begin":1069,"end":1181},"obj":"Sentence"},{"id":"S6","span":{"begin":1182,"end":1445},"obj":"Sentence"}],"text":"Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1: distinct patterns of viral growth are determined by T-cell types.\nStarting with a replication-incompetent molecular clone of human immunodeficiency virus type 1, lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat (LTR), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation. Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element(s) was present in the LTR. For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites), a hierarchy of cellular permissivity to virus replication (peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat) was observed. Of note was the associated emergence of second-site LTR revertants which involved an alteration of the TATA box. These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present."}

    genia-medco-coref

    {"project":"genia-medco-coref","denotations":[{"id":"C2","span":{"begin":16,"end":26},"obj":"NP"},{"id":"C3","span":{"begin":31,"end":34},"obj":"NP"},{"id":"C1","span":{"begin":16,"end":49},"obj":"NP"},{"id":"C4","span":{"begin":81,"end":116},"obj":"NP"},{"id":"C5","span":{"begin":243,"end":278},"obj":"NP"},{"id":"C7","span":{"begin":296,"end":306},"obj":"NP"},{"id":"C8","span":{"begin":311,"end":314},"obj":"NP"},{"id":"C6","span":{"begin":296,"end":328},"obj":"NP"},{"id":"C9","span":{"begin":340,"end":377},"obj":"NP"},{"id":"C10","span":{"begin":415,"end":419},"obj":"NP"},{"id":"C12","span":{"begin":455,"end":465},"obj":"NP"},{"id":"C13","span":{"begin":470,"end":473},"obj":"NP"},{"id":"C11","span":{"begin":455,"end":482},"obj":"NP"},{"id":"C14","span":{"begin":732,"end":748},"obj":"NP"},{"id":"C15","span":{"begin":764,"end":771},"obj":"NP"},{"id":"C16","span":{"begin":832,"end":836},"obj":"NP"},{"id":"C17","span":{"begin":859,"end":878},"obj":"NP"},{"id":"C18","span":{"begin":887,"end":890},"obj":"NP"},{"id":"C20","span":{"begin":1121,"end":1124},"obj":"NP"},{"id":"C19","span":{"begin":1109,"end":1135},"obj":"NP"},{"id":"C21","span":{"begin":1136,"end":1141},"obj":"NP"},{"id":"C22","span":{"begin":1209,"end":1248},"obj":"NP"},{"id":"C23","span":{"begin":1249,"end":1252},"obj":"NP"},{"id":"C24","span":{"begin":1263,"end":1284},"obj":"NP"},{"id":"C25","span":{"begin":1285,"end":1290},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C5","obj":"C4"},{"id":"R2","pred":"coref-ident","subj":"C7","obj":"C2"},{"id":"R3","pred":"coref-ident","subj":"C8","obj":"C3"},{"id":"R4","pred":"coref-other","subj":"C6","obj":"C1"},{"id":"R5","pred":"coref-ident","subj":"C10","obj":"C9"},{"id":"R6","pred":"coref-ident","subj":"C12","obj":"C7"},{"id":"R7","pred":"coref-ident","subj":"C13","obj":"C8"},{"id":"R8","pred":"coref-other","subj":"C11","obj":"C1"},{"id":"R9","pred":"coref-ident","subj":"C14","obj":"C11"},{"id":"R10","pred":"coref-ident","subj":"C15","obj":"C10"},{"id":"R11","pred":"coref-ident","subj":"C16","obj":"C15"},{"id":"R12","pred":"coref-ident","subj":"C17","obj":"C12"},{"id":"R13","pred":"coref-ident","subj":"C18","obj":"C13"},{"id":"R14","pred":"coref-ident","subj":"C20","obj":"C16"},{"id":"R15","pred":"coref-relat","subj":"C21","obj":"C19"},{"id":"R16","pred":"coref-ident","subj":"C22","obj":"C5"},{"id":"R17","pred":"coref-ident","subj":"C23","obj":"C20"},{"id":"R18","pred":"coref-relat","subj":"C25","obj":"C24"}],"text":"Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1: distinct patterns of viral growth are determined by T-cell types.\nStarting with a replication-incompetent molecular clone of human immunodeficiency virus type 1, lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat (LTR), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation. Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element(s) was present in the LTR. For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites), a hierarchy of cellular permissivity to virus replication (peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat) was observed. Of note was the associated emergence of second-site LTR revertants which involved an alteration of the TATA box. These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present."}

    GENIAcorpus

    {"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":16,"end":26},"obj":"protein_molecule"},{"id":"T2","span":{"begin":31,"end":49},"obj":"DNA_domain_or_region"},{"id":"T3","span":{"begin":81,"end":116},"obj":"virus"},{"id":"T4","span":{"begin":170,"end":182},"obj":"cell_type"},{"id":"T5","span":{"begin":200,"end":242},"obj":"virus"},{"id":"T6","span":{"begin":243,"end":278},"obj":"virus"},{"id":"T7","span":{"begin":344,"end":371},"obj":"DNA_domain_or_region"},{"id":"T8","span":{"begin":373,"end":376},"obj":"DNA_domain_or_region"},{"id":"T9","span":{"begin":379,"end":389},"obj":"virus"},{"id":"T10","span":{"begin":401,"end":419},"obj":"DNA_domain_or_region"},{"id":"T11","span":{"begin":542,"end":555},"obj":"virus"},{"id":"T12","span":{"begin":566,"end":592},"obj":"other_name"},{"id":"T13","span":{"begin":594,"end":606},"obj":"virus"},{"id":"T14","span":{"begin":700,"end":705},"obj":"cell_type"},{"id":"T15","span":{"begin":706,"end":718},"obj":"cell_type"},{"id":"T16","span":{"begin":738,"end":745},"obj":"DNA_domain_or_region"},{"id":"T17","span":{"begin":768,"end":771},"obj":"DNA_domain_or_region"},{"id":"T18","span":{"begin":811,"end":826},"obj":"virus"},{"id":"T19","span":{"begin":832,"end":836},"obj":"DNA_domain_or_region"},{"id":"T20","span":{"begin":859,"end":869},"obj":"protein_molecule"},{"id":"T21","span":{"begin":887,"end":904},"obj":"DNA_domain_or_region"},{"id":"T22","span":{"begin":922,"end":943},"obj":"other_name"},{"id":"T23","span":{"begin":947,"end":964},"obj":"other_name"},{"id":"T24","span":{"begin":966,"end":982},"obj":"cell_type"},{"id":"T25","span":{"begin":983,"end":994},"obj":"cell_type"},{"id":"T26","span":{"begin":997,"end":1000},"obj":"cell_line"},{"id":"T27","span":{"begin":1014,"end":1016},"obj":"cell_line"},{"id":"T28","span":{"begin":1030,"end":1033},"obj":"cell_line"},{"id":"T29","span":{"begin":1047,"end":1053},"obj":"cell_line"},{"id":"T30","span":{"begin":1109,"end":1124},"obj":"DNA_domain_or_region"},{"id":"T31","span":{"begin":1172,"end":1180},"obj":"DNA_domain_or_region"},{"id":"T32","span":{"begin":1213,"end":1248},"obj":"virus"},{"id":"T33","span":{"begin":1299,"end":1316},"obj":"other_name"},{"id":"T34","span":{"begin":1330,"end":1342},"obj":"cell_type"},{"id":"T35","span":{"begin":1413,"end":1436},"obj":"protein_family_or_group"}],"text":"Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1: distinct patterns of viral growth are determined by T-cell types.\nStarting with a replication-incompetent molecular clone of human immunodeficiency virus type 1, lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat (LTR), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation. Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element(s) was present in the LTR. For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites), a hierarchy of cellular permissivity to virus replication (peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat) was observed. Of note was the associated emergence of second-site LTR revertants which involved an alteration of the TATA box. These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present."}