PubMed:10359895 JSONTXT

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    jnlpba-st-training

    {"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":11,"end":14},"obj":"protein"},{"id":"T2","span":{"begin":19,"end":23},"obj":"protein"},{"id":"T3","span":{"begin":76,"end":80},"obj":"protein"},{"id":"T4","span":{"begin":90,"end":97},"obj":"cell_type"},{"id":"T5","span":{"begin":111,"end":115},"obj":"protein"},{"id":"T6","span":{"begin":275,"end":279},"obj":"protein"},{"id":"T7","span":{"begin":335,"end":339},"obj":"protein"},{"id":"T8","span":{"begin":372,"end":379},"obj":"cell_type"},{"id":"T9","span":{"begin":507,"end":534},"obj":"DNA"},{"id":"T10","span":{"begin":641,"end":645},"obj":"protein"},{"id":"T11","span":{"begin":663,"end":670},"obj":"cell_type"},{"id":"T12","span":{"begin":716,"end":723},"obj":"protein"},{"id":"T13","span":{"begin":920,"end":943},"obj":"DNA"},{"id":"T14","span":{"begin":945,"end":948},"obj":"DNA"},{"id":"T15","span":{"begin":969,"end":992},"obj":"DNA"},{"id":"T16","span":{"begin":1033,"end":1036},"obj":"DNA"},{"id":"T17","span":{"begin":1064,"end":1078},"obj":"DNA"},{"id":"T18","span":{"begin":1111,"end":1114},"obj":"DNA"},{"id":"T19","span":{"begin":1119,"end":1122},"obj":"DNA"},{"id":"T20","span":{"begin":1209,"end":1213},"obj":"protein"},{"id":"T21","span":{"begin":1228,"end":1235},"obj":"cell_type"},{"id":"T22","span":{"begin":1254,"end":1257},"obj":"DNA"},{"id":"T23","span":{"begin":1284,"end":1311},"obj":"DNA"},{"id":"T24","span":{"begin":1351,"end":1365},"obj":"DNA"},{"id":"T25","span":{"begin":1379,"end":1383},"obj":"protein"},{"id":"T26","span":{"begin":1385,"end":1397},"obj":"protein"},{"id":"T27","span":{"begin":1403,"end":1422},"obj":"protein"},{"id":"T28","span":{"begin":1497,"end":1509},"obj":"DNA"},{"id":"T29","span":{"begin":1535,"end":1549},"obj":"DNA"},{"id":"T30","span":{"begin":1562,"end":1579},"obj":"cell_type"},{"id":"T31","span":{"begin":1609,"end":1613},"obj":"protein"},{"id":"T32","span":{"begin":1615,"end":1618},"obj":"protein"},{"id":"T33","span":{"begin":1624,"end":1644},"obj":"protein"},{"id":"T34","span":{"begin":1660,"end":1676},"obj":"DNA"},{"id":"T35","span":{"begin":1688,"end":1710},"obj":"DNA"},{"id":"T36","span":{"begin":1742,"end":1746},"obj":"protein"},{"id":"T37","span":{"begin":1764,"end":1771},"obj":"cell_type"}],"text":"Binding of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.\nBACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level.\nOBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells.\nMETHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis.\nRESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells.\nCONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells."}

    semrep-sample

    {"project":"semrep-sample","denotations":[{"id":"E1-ti-1","span":{"begin":11,"end":14},"obj":"entrez:7528"},{"id":"E2-ti-1","span":{"begin":19,"end":23},"obj":"cui:C1335233"},{"id":"E3-ti-1","span":{"begin":29,"end":34},"obj":"cui:C0679622"},{"id":"E4-ti-1","span":{"begin":35,"end":42},"obj":"cui:C0013879"},{"id":"E5-ti-1","span":{"begin":62,"end":72},"obj":"cui:C0185117"},{"id":"E6-ti-1","span":{"begin":76,"end":80},"obj":"cui:C0021759"},{"id":"E7-ti-1","span":{"begin":84,"end":97},"obj":"cui:C0427861"},{"id":"T1","span":{"begin":48,"end":61},"obj":"INHIBITS"},{"id":"T2","span":{"begin":48,"end":61},"obj":"INHIBITS"},{"id":"E1-ab-1","span":{"begin":111,"end":115},"obj":"cui:C0021759"},{"id":"E2-ab-1","span":{"begin":125,"end":136},"obj":"cui:C1527148"},{"id":"E3-ab-1","span":{"begin":140,"end":152},"obj":"cui:C0014457"},{"id":"E4-ab-1","span":{"begin":194,"end":206},"obj":"cui:C0699748"},{"id":"E5-ab-1","span":{"begin":210,"end":218},"obj":"cui:C0700624"},{"id":"E6-ab-1","span":{"begin":219,"end":227},"obj":"cui:C0012634"},{"id":"T3","span":{"begin":116,"end":124},"obj":"AFFECTS"},{"id":"E1-ab-2","span":{"begin":237,"end":243},"obj":"cui:C0857523"},{"id":"E2-ab-2","span":{"begin":258,"end":264},"obj":"cui:C0004096"},{"id":"E3-ab-2","span":{"begin":266,"end":274},"obj":"cui:C0205250"},{"id":"E4-ab-2","span":{"begin":275,"end":279},"obj":"cui:C0021759"},{"id":"E5-ab-2","span":{"begin":301,"end":317},"obj":"cui:C0229664"},{"id":"E6-ab-2","span":{"begin":326,"end":333},"obj":"cui:C0178987"},{"id":"E1-ab-3","span":{"begin":335,"end":339},"obj":"cui:C0021759"},{"id":"E2-ab-3","span":{"begin":362,"end":371},"obj":"cui:C1515877"},{"id":"E3-ab-3","span":{"begin":372,"end":379},"obj":"cui:C0039194"},{"id":"E4-ab-3","span":{"begin":389,"end":399},"obj":"cui:C0185117"},{"id":"E5-ab-3","span":{"begin":420,"end":435},"obj":"cui:C0040649"},{"id":"T4","span":{"begin":343,"end":351},"obj":"PRODUCES"},{"id":"T5","span":{"begin":403,"end":412},"obj":"AFFECTS"},{"id":"E1-ab-4","span":{"begin":459,"end":464},"obj":"cui:C0008972"},{"id":"E2-ab-4","span":{"begin":480,"end":499},"obj":"cui:C0558024"},{"id":"E3-ab-4","span":{"begin":507,"end":512},"obj":"cui:C0020114"},{"id":"E4-ab-4","span":{"begin":513,"end":517},"obj":"cui:C0021759"},{"id":"E5-ab-4","span":{"begin":559,"end":562},"obj":"entrez:1154"},{"id":"E6-ab-4","span":{"begin":564,"end":583},"obj":"cui:C1514827"},{"id":"E7-ab-4","span":{"begin":588,"end":609},"obj":"cui:C0040648"},{"id":"E8-ab-4","span":{"begin":626,"end":637},"obj":"cui:C0439181"},{"id":"E9-ab-4","span":{"begin":641,"end":645},"obj":"cui:C0021759"},{"id":"E10-ab-4","span":{"begin":646,"end":659},"obj":"cui:C0040649"},{"id":"E11-ab-4","span":{"begin":663,"end":670},"obj":"cui:C0039194"},{"id":"T6","span":{"begin":507,"end":517},"obj":"PART_OF"},{"id":"T7","span":{"begin":626,"end":637},"obj":"INHIBITS"},{"id":"T8","span":{"begin":660,"end":662},"obj":"LOCATION_OF"},{"id":"E1-ab-5","span":{"begin":672,"end":679},"obj":"cui:C0025663"},{"id":"E2-ab-5","span":{"begin":681,"end":688},"obj":"cui:C0025663"},{"id":"E3-ab-5","span":{"begin":702,"end":707},"obj":"cui:C0008972"},{"id":"E4-ab-5","span":{"begin":716,"end":723},"obj":"cui:C0011519"},{"id":"E5-ab-5","span":{"begin":734,"end":740},"obj":"cui:C1510438"},{"id":"E6-ab-5","span":{"begin":742,"end":779},"obj":"cui:C0949632"},{"id":"E7-ab-5","span":{"begin":785,"end":804},"obj":"cui:C0558024"},{"id":"E8-ab-5","span":{"begin":808,"end":822},"obj":"cui:C1512977"},{"id":"E9-ab-5","span":{"begin":823,"end":835},"obj":"cui:C0040669"},{"id":"E10-ab-5","span":{"begin":846,"end":854},"obj":"cui:C1442161"},{"id":"E11-ab-5","span":{"begin":855,"end":863},"obj":"cui:C0936012"},{"id":"E12-ab-5","span":{"begin":868,"end":893},"obj":"cui:C0079870"},{"id":"E1-ab-6","span":{"begin":895,"end":902},"obj":"cui:C1274040"},{"id":"E2-ab-6","span":{"begin":920,"end":935},"obj":"cui:C0033618"},{"id":"E3-ab-6","span":{"begin":936,"end":943},"obj":"cui:C0205147"},{"id":"E4-ab-6","span":{"begin":969,"end":977},"obj":"cui:C0205107"},{"id":"E5-ab-6","span":{"begin":978,"end":983},"obj":"cui:C0020114"},{"id":"E6-ab-6","span":{"begin":978,"end":983},"obj":"cui:C0021759"},{"id":"T9","span":{"begin":978,"end":983},"obj":"PART_OF"},{"id":"E1-ab-7","span":{"begin":994,"end":1013},"obj":"cui:C0558024"},{"id":"E2-ab-7","span":{"begin":1033,"end":1036},"obj":"cui:C0205147"},{"id":"E3-ab-7","span":{"begin":1053,"end":1060},"obj":"cui:C0243148"},{"id":"E4-ab-7","span":{"begin":1064,"end":1069},"obj":"cui:C0021759"},{"id":"E5-ab-7","span":{"begin":1064,"end":1087},"obj":"cui:C0020115"},{"id":"E1-ab-8","span":{"begin":1089,"end":1092},"obj":"cui:C0205448"},{"id":"E2-ab-8","span":{"begin":1102,"end":1109},"obj":"cui:C0205147"},{"id":"E3-ab-8","span":{"begin":1134,"end":1143},"obj":"cui:C0733755"},{"id":"E4-ab-8","span":{"begin":1162,"end":1165},"obj":"cui:C1518422"},{"id":"E5-ab-8","span":{"begin":1209,"end":1213},"obj":"cui:C0021759"},{"id":"E6-ab-8","span":{"begin":1214,"end":1224},"obj":"cui:C0185117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of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.\nBACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level.\nOBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells.\nMETHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis.\nRESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells.\nCONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells."}

    pubmed-sentences-benchmark

    {"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":98},"obj":"Sentence"},{"id":"S2","span":{"begin":99,"end":228},"obj":"Sentence"},{"id":"S3","span":{"begin":229,"end":334},"obj":"Sentence"},{"id":"S4","span":{"begin":335,"end":442},"obj":"Sentence"},{"id":"S5","span":{"begin":443,"end":671},"obj":"Sentence"},{"id":"S6","span":{"begin":672,"end":894},"obj":"Sentence"},{"id":"S7","span":{"begin":895,"end":993},"obj":"Sentence"},{"id":"S8","span":{"begin":994,"end":1088},"obj":"Sentence"},{"id":"S9","span":{"begin":1089,"end":1236},"obj":"Sentence"},{"id":"S10","span":{"begin":1237,"end":1423},"obj":"Sentence"},{"id":"S11","span":{"begin":1424,"end":1580},"obj":"Sentence"},{"id":"S12","span":{"begin":1581,"end":1772},"obj":"Sentence"}],"text":"Binding of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.\nBACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level.\nOBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells.\nMETHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis.\nRESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells.\nCONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells."}

    genia-medco-coref

    {"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":27,"end":42},"obj":"NP"},{"id":"C2","span":{"begin":43,"end":47},"obj":"NP"},{"id":"C3","span":{"begin":76,"end":80},"obj":"NP"},{"id":"C4","span":{"begin":84,"end":97},"obj":"NP"},{"id":"C5","span":{"begin":111,"end":115},"obj":"NP"},{"id":"C6","span":{"begin":335,"end":339},"obj":"NP"},{"id":"C7","span":{"begin":362,"end":379},"obj":"NP"},{"id":"C9","span":{"begin":385,"end":388},"obj":"NP"},{"id":"C8","span":{"begin":385,"end":399},"obj":"NP"},{"id":"C10","span":{"begin":454,"end":464},"obj":"NP"},{"id":"C11","span":{"begin":503,"end":534},"obj":"NP"},{"id":"C13","span":{"begin":663,"end":670},"obj":"NP"},{"id":"C12","span":{"begin":622,"end":670},"obj":"NP"},{"id":"C14","span":{"begin":697,"end":707},"obj":"NP"},{"id":"C16","span":{"begin":965,"end":992},"obj":"NP"},{"id":"C15","span":{"begin":918,"end":992},"obj":"NP"},{"id":"C17","span":{"begin":1029,"end":1036},"obj":"NP"},{"id":"C19","span":{"begin":1096,"end":1109},"obj":"NP"},{"id":"C18","span":{"begin":1089,"end":1109},"obj":"NP"},{"id":"C20","span":{"begin":1111,"end":1155},"obj":"NP"},{"id":"C21","span":{"begin":1209,"end":1224},"obj":"NP"},{"id":"C22","span":{"begin":1228,"end":1235},"obj":"NP"},{"id":"C23","span":{"begin":1250,"end":1266},"obj":"NP"},{"id":"C25","span":{"begin":1347,"end":1365},"obj":"NP"},{"id":"C24","span":{"begin":1276,"end":1365},"obj":"NP"},{"id":"C26","span":{"begin":1367,"end":1372},"obj":"NP"},{"id":"C27","span":{"begin":1379,"end":1422},"obj":"NP"},{"id":"C28","span":{"begin":1424,"end":1446},"obj":"NP"},{"id":"C29","span":{"begin":1448,"end":1453},"obj":"NP"},{"id":"C30","span":{"begin":1475,"end":1489},"obj":"NP"},{"id":"C31","span":{"begin":1493,"end":1509},"obj":"NP"},{"id":"C32","span":{"begin":1562,"end":1579},"obj":"NP"},{"id":"C33","span":{"begin":1684,"end":1710},"obj":"NP"},{"id":"C35","span":{"begin":1764,"end":1771},"obj":"NP"},{"id":"C34","span":{"begin":1727,"end":1771},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-relat","subj":"C2","obj":"C1"},{"id":"R2","pred":"coref-ident","subj":"C5","obj":"C3"},{"id":"R3","pred":"coref-ident","subj":"C6","obj":"C5"},{"id":"R4","pred":"coref-pron","subj":"C9","obj":"C6"},{"id":"R5","pred":"coref-ident","subj":"C13","obj":"C4"},{"id":"R6","pred":"coref-ident","subj":"C14","obj":"C10"},{"id":"R7","pred":"coref-ident","subj":"C17","obj":"C15"},{"id":"R8","pred":"coref-ident","subj":"C19","obj":"C17"},{"id":"R9","pred":"coref-appos","subj":"C20","obj":"C18"},{"id":"R10","pred":"coref-ident","subj":"C21","obj":"C8"},{"id":"R11","pred":"coref-ident","subj":"C22","obj":"C13"},{"id":"R12","pred":"coref-ident","subj":"C25","obj":"C11"},{"id":"R13","pred":"coref-relat","subj":"C26","obj":"C24"},{"id":"R14","pred":"coref-relat","subj":"C29","obj":"C28"},{"id":"R15","pred":"coref-ident","subj":"C30","obj":"C27"},{"id":"R16","pred":"coref-ident","subj":"C31","obj":"C23"},{"id":"R17","pred":"coref-ident","subj":"C32","obj":"C7"},{"id":"R18","pred":"coref-ident","subj":"C33","obj":"C16"},{"id":"R19","pred":"coref-ident","subj":"C35","obj":"C22"},{"id":"R20","pred":"coref-ident","subj":"C34","obj":"C12"}],"text":"Binding of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.\nBACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level.\nOBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells.\nMETHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis.\nRESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells.\nCONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells."}

    GENIAcorpus

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In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level.\nOBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells.\nMETHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis.\nRESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells.\nCONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells."}

    metamap-sample

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of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.\nBACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level.\nOBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells.\nMETHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis.\nRESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells.\nCONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells."}

    PubmedHPO

    {"project":"PubmedHPO","denotations":[{"id":"T2","span":{"begin":258,"end":264},"obj":"HP_0002099"},{"id":"T1","span":{"begin":140,"end":152},"obj":"HP_0001880"}],"text":"Binding of YY1 and Oct1 to a novel element that downregulates expression of IL-5 in human T cells.\nBACKGROUND: IL-5 controls development of eosinophilia and has been shown to be involved in the pathogenesis of allergic diseases. In both atopic and nonatopic asthma, elevated IL-5 has been detected in peripheral blood and the airways. IL-5 is produced mainly by activated T cells, and its expression is regulated at the transcriptional level.\nOBJECTIVE: This study focuses on the functional analysis of the human IL-5 (hIL-5) promoter and characterization of cis -regulatory elements and transcription factors involved in the suppression of IL-5 transcription in T cells.\nMETHODS: Methods used in this study include DNase I footprint assays, electrophoretic mobility shift assays, and functional analysis by mammalian cell transfection involving deletion analysis and site-directed mutagenesis.\nRESULTS: We identified 5 protein binding regions (BRs) located within the proximal hIL-5 promoter. Functional analysis indicates that the BRs are involved in control of hIL-5 promoter activity. Two of these regions, BR3 and BR4 located at positions -102 to -73, have not previously been described as regulators of IL-5 expression in T cells. We show that the BR3 sequence contains a novel negative regulatory element located at positions -90 to -79 of the hIL-5 promoter, which binds Oct1, octamer-like, and YY1 nuclear factors. Substitution mutations, which abolished binding of these proteins to the BR3 sequence, significantly increased hIL-5 promoter activity in activated T cells.\nCONCLUSION: We suggest that Oct1, YY1, and octamer-like factors binding to the -90/-79 sequence within the proximal IL-5 promoter are involved in suppression of IL-5 transcription in T cells."}