PubMed:8388998 JSONTXT

Annnotations TAB JSON ListView MergeView

    jnlpba-st-training

    {"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":35,"end":62},"obj":"DNA"},{"id":"T2","span":{"begin":66,"end":89},"obj":"protein"},{"id":"T3","span":{"begin":135,"end":151},"obj":"protein"},{"id":"T4","span":{"begin":153,"end":156},"obj":"protein"},{"id":"T5","span":{"begin":163,"end":186},"obj":"protein"},{"id":"T6","span":{"begin":188,"end":190},"obj":"protein"},{"id":"T7","span":{"begin":246,"end":249},"obj":"protein"},{"id":"T8","span":{"begin":329,"end":331},"obj":"protein"},{"id":"T9","span":{"begin":396,"end":416},"obj":"DNA"},{"id":"T10","span":{"begin":418,"end":421},"obj":"DNA"},{"id":"T11","span":{"begin":553,"end":561},"obj":"DNA"},{"id":"T12","span":{"begin":573,"end":585},"obj":"cell_line"},{"id":"T13","span":{"begin":608,"end":627},"obj":"cell_line"},{"id":"T14","span":{"begin":685,"end":706},"obj":"DNA"},{"id":"T15","span":{"begin":708,"end":711},"obj":"DNA"},{"id":"T16","span":{"begin":745,"end":761},"obj":"DNA"},{"id":"T17","span":{"begin":765,"end":795},"obj":"DNA"},{"id":"T18","span":{"begin":804,"end":838},"obj":"protein"},{"id":"T19","span":{"begin":880,"end":901},"obj":"protein"},{"id":"T20","span":{"begin":911,"end":946},"obj":"protein"},{"id":"T21","span":{"begin":997,"end":1000},"obj":"protein"},{"id":"T22","span":{"begin":1048,"end":1051},"obj":"protein"},{"id":"T23","span":{"begin":1063,"end":1068},"obj":"protein"},{"id":"T24","span":{"begin":1070,"end":1075},"obj":"protein"},{"id":"T25","span":{"begin":1081,"end":1086},"obj":"protein"},{"id":"T26","span":{"begin":1159,"end":1187},"obj":"DNA"},{"id":"T27","span":{"begin":1197,"end":1239},"obj":"DNA"},{"id":"T28","span":{"begin":1257,"end":1264},"obj":"cell_type"},{"id":"T29","span":{"begin":1341,"end":1353},"obj":"protein"},{"id":"T30","span":{"begin":1372,"end":1374},"obj":"protein"},{"id":"T31","span":{"begin":1378,"end":1385},"obj":"cell_type"},{"id":"T32","span":{"begin":1430,"end":1471},"obj":"DNA"},{"id":"T33","span":{"begin":1489,"end":1491},"obj":"protein"},{"id":"T34","span":{"begin":1528,"end":1536},"obj":"DNA"},{"id":"T35","span":{"begin":1540,"end":1543},"obj":"DNA"},{"id":"T36","span":{"begin":1557,"end":1562},"obj":"protein"},{"id":"T37","span":{"begin":1567,"end":1572},"obj":"protein"},{"id":"T38","span":{"begin":1594,"end":1596},"obj":"protein"},{"id":"T39","span":{"begin":1624,"end":1634},"obj":"cell_line"},{"id":"T40","span":{"begin":1652,"end":1657},"obj":"protein"},{"id":"T41","span":{"begin":1686,"end":1688},"obj":"protein"},{"id":"T42","span":{"begin":1776,"end":1779},"obj":"protein"},{"id":"T43","span":{"begin":1796,"end":1798},"obj":"protein"},{"id":"T44","span":{"begin":1825,"end":1830},"obj":"protein"},{"id":"T45","span":{"begin":1842,"end":1846},"obj":"protein"},{"id":"T46","span":{"begin":1905,"end":1915},"obj":"cell_line"},{"id":"T47","span":{"begin":1928,"end":1935},"obj":"cell_type"},{"id":"T48","span":{"begin":1967,"end":1982},"obj":"protein"},{"id":"T49","span":{"begin":2011,"end":2013},"obj":"protein"},{"id":"T50","span":{"begin":2043,"end":2046},"obj":"DNA"},{"id":"T51","span":{"begin":2050,"end":2057},"obj":"cell_type"},{"id":"T52","span":{"begin":2075,"end":2078},"obj":"protein"},{"id":"T53","span":{"begin":2108,"end":2110},"obj":"protein"},{"id":"T54","span":{"begin":2151,"end":2154},"obj":"DNA"},{"id":"T55","span":{"begin":2299,"end":2304},"obj":"protein"}],"text":"Cell-specific bifunctional role of Jun oncogene family members on glucocorticoid receptor-dependent transcription.\nInteraction between protein kinase C (PKC)- and glucocorticoid receptor (GR)-mediated signaling is suggested by the ability of the PKC activating phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) to inhibit GR-dependent transcription of the mouse mammary tumor virus (MMTV) long terminal repeat (LTR). Here we report that this interference is cell specific, as TPA augmented dexamethasone-induced transcriptional activation of the MMTV LTR in several T cell lines but was inhibitory in NIH-3T3 fibroblasts. TPA-GR synergism was determined to have occurred at the GR-responsive element (GRE) level by functional analysis of deletion mutants or synthetic GRE oligonucleotides driving chloramphenicol acetyl-transferase expression. Synergism required an intact GR DNA-binding domain, whereas amino- or carboxyl-terminal domains were dispensable. The effect was abrogated by the PKC inhibitor staurosporine, suggesting a role for PKC. Increased c-jun, jun-B, and jun-D expression above basal levels and increased transcriptional activity of AP-1/TPA responsive elements fused to chloramphenicol acetyl-transferase vectors were observed in T cells treated with TPA alone or in combination with dexamethasone. The ability of Jun proteins to cooperate with GR in T cells has been investigated after transfection of c-jun, jun-B, or jun-D expression vectors, which augmented GR-dependent transcription from either MMTV LTR or GRE. Conversely, c-jun and jun-B transfection blunted GR-dependent transcription in HeLa cells. The presence of c-fos had a negative influence on GR function and correlated with the cell-specific synergistic or antagonistic activity of Jun with respect to GR; high basal expression of c-fos as well as AP-1 DNA binding and transcriptional activity were observed in HeLa cells, but not in T cells. Furthermore overexpression of exogenous c-fos has an inhibitory effect on GR-dependent transcription from GRE in T cells. We propose that Jun plays a bifunctional role on GR-dependent transcriptional activation of GRE, selecting either synergistic or antagonistic activity depending on the cell-specific microenvironment. In this regard, intracellular levels of c-fos appear to be influential."}

    pubmed-sentences-benchmark

    {"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":114},"obj":"Sentence"},{"id":"S2","span":{"begin":115,"end":423},"obj":"Sentence"},{"id":"S3","span":{"begin":424,"end":628},"obj":"Sentence"},{"id":"S4","span":{"begin":629,"end":850},"obj":"Sentence"},{"id":"S5","span":{"begin":851,"end":964},"obj":"Sentence"},{"id":"S6","span":{"begin":965,"end":1052},"obj":"Sentence"},{"id":"S7","span":{"begin":1053,"end":1325},"obj":"Sentence"},{"id":"S8","span":{"begin":1326,"end":1544},"obj":"Sentence"},{"id":"S9","span":{"begin":1545,"end":1635},"obj":"Sentence"},{"id":"S10","span":{"begin":1636,"end":1936},"obj":"Sentence"},{"id":"S11","span":{"begin":1937,"end":2058},"obj":"Sentence"},{"id":"S12","span":{"begin":2059,"end":2258},"obj":"Sentence"},{"id":"S13","span":{"begin":2259,"end":2330},"obj":"Sentence"}],"text":"Cell-specific bifunctional role of Jun oncogene family members on glucocorticoid receptor-dependent transcription.\nInteraction between protein kinase C (PKC)- and glucocorticoid receptor (GR)-mediated signaling is suggested by the ability of the PKC activating phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) to inhibit GR-dependent transcription of the mouse mammary tumor virus (MMTV) long terminal repeat (LTR). Here we report that this interference is cell specific, as TPA augmented dexamethasone-induced transcriptional activation of the MMTV LTR in several T cell lines but was inhibitory in NIH-3T3 fibroblasts. TPA-GR synergism was determined to have occurred at the GR-responsive element (GRE) level by functional analysis of deletion mutants or synthetic GRE oligonucleotides driving chloramphenicol acetyl-transferase expression. Synergism required an intact GR DNA-binding domain, whereas amino- or carboxyl-terminal domains were dispensable. The effect was abrogated by the PKC inhibitor staurosporine, suggesting a role for PKC. Increased c-jun, jun-B, and jun-D expression above basal levels and increased transcriptional activity of AP-1/TPA responsive elements fused to chloramphenicol acetyl-transferase vectors were observed in T cells treated with TPA alone or in combination with dexamethasone. The ability of Jun proteins to cooperate with GR in T cells has been investigated after transfection of c-jun, jun-B, or jun-D expression vectors, which augmented GR-dependent transcription from either MMTV LTR or GRE. Conversely, c-jun and jun-B transfection blunted GR-dependent transcription in HeLa cells. The presence of c-fos had a negative influence on GR function and correlated with the cell-specific synergistic or antagonistic activity of Jun with respect to GR; high basal expression of c-fos as well as AP-1 DNA binding and transcriptional activity were observed in HeLa cells, but not in T cells. Furthermore overexpression of exogenous c-fos has an inhibitory effect on GR-dependent transcription from GRE in T cells. We propose that Jun plays a bifunctional role on GR-dependent transcriptional activation of GRE, selecting either synergistic or antagonistic activity depending on the cell-specific microenvironment. In this regard, intracellular levels of c-fos appear to be influential."}

    genia-medco-coref

    {"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":66,"end":90},"obj":"NP"},{"id":"C2","span":{"begin":135,"end":158},"obj":"NP"},{"id":"C3","span":{"begin":163,"end":192},"obj":"NP"},{"id":"C4","span":{"begin":275,"end":317},"obj":"NP"},{"id":"C5","span":{"begin":359,"end":422},"obj":"NP"},{"id":"C6","span":{"begin":483,"end":486},"obj":"NP"},{"id":"C7","span":{"begin":549,"end":561},"obj":"NP"},{"id":"C8","span":{"begin":629,"end":633},"obj":"NP"},{"id":"C9","span":{"begin":633,"end":635},"obj":"NP"},{"id":"C11","span":{"begin":685,"end":688},"obj":"NP"},{"id":"C10","span":{"begin":685,"end":712},"obj":"NP"},{"id":"C12","span":{"begin":1278,"end":1281},"obj":"NP"},{"id":"C13","span":{"begin":1372,"end":1374},"obj":"NP"},{"id":"C14","span":{"begin":1378,"end":1385},"obj":"NP"},{"id":"C15","span":{"begin":1430,"end":1471},"obj":"NP"},{"id":"C16","span":{"begin":1473,"end":1478},"obj":"NP"},{"id":"C17","span":{"begin":1489,"end":1492},"obj":"NP"},{"id":"C18","span":{"begin":1528,"end":1536},"obj":"NP"},{"id":"C19","span":{"begin":1540,"end":1543},"obj":"NP"},{"id":"C20","span":{"begin":1594,"end":1597},"obj":"NP"},{"id":"C21","span":{"begin":1624,"end":1634},"obj":"NP"},{"id":"C22","span":{"begin":1652,"end":1657},"obj":"NP"},{"id":"C23","span":{"begin":1686,"end":1688},"obj":"NP"},{"id":"C24","span":{"begin":1796,"end":1798},"obj":"NP"},{"id":"C25","span":{"begin":1825,"end":1830},"obj":"NP"},{"id":"C26","span":{"begin":1905,"end":1915},"obj":"NP"},{"id":"C27","span":{"begin":1928,"end":1935},"obj":"NP"},{"id":"C28","span":{"begin":2011,"end":2014},"obj":"NP"},{"id":"C29","span":{"begin":2050,"end":2057},"obj":"NP"},{"id":"C30","span":{"begin":2108,"end":2111},"obj":"NP"},{"id":"C31","span":{"begin":2151,"end":2154},"obj":"NP"},{"id":"C32","span":{"begin":2299,"end":2304},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C3","obj":"C1"},{"id":"R2","pred":"coref-ident","subj":"C6","obj":"C4"},{"id":"R3","pred":"coref-ident","subj":"C7","obj":"C5"},{"id":"R4","pred":"coref-ident","subj":"C8","obj":"C6"},{"id":"R5","pred":"coref-ident","subj":"C9","obj":"C3"},{"id":"R6","pred":"coref-ident","subj":"C11","obj":"C3"},{"id":"R7","pred":"coref-ident","subj":"C12","obj":"C4"},{"id":"R8","pred":"coref-ident","subj":"C13","obj":"C11"},{"id":"R9","pred":"coref-relat","subj":"C16","obj":"C15"},{"id":"R10","pred":"coref-ident","subj":"C17","obj":"C13"},{"id":"R11","pred":"coref-ident","subj":"C18","obj":"C7"},{"id":"R12","pred":"coref-ident","subj":"C19","obj":"C10"},{"id":"R13","pred":"coref-ident","subj":"C20","obj":"C17"},{"id":"R14","pred":"coref-ident","subj":"C23","obj":"C20"},{"id":"R15","pred":"coref-ident","subj":"C24","obj":"C23"},{"id":"R16","pred":"coref-ident","subj":"C25","obj":"C22"},{"id":"R17","pred":"coref-ident","subj":"C26","obj":"C21"},{"id":"R18","pred":"coref-ident","subj":"C27","obj":"C14"},{"id":"R19","pred":"coref-ident","subj":"C28","obj":"C24"},{"id":"R20","pred":"coref-ident","subj":"C29","obj":"C27"},{"id":"R21","pred":"coref-ident","subj":"C30","obj":"C28"},{"id":"R22","pred":"coref-ident","subj":"C31","obj":"C19"},{"id":"R23","pred":"coref-ident","subj":"C32","obj":"C25"}],"text":"Cell-specific bifunctional role of Jun oncogene family members on glucocorticoid receptor-dependent transcription.\nInteraction between protein kinase C (PKC)- and glucocorticoid receptor (GR)-mediated signaling is suggested by the ability of the PKC activating phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) to inhibit GR-dependent transcription of the mouse mammary tumor virus (MMTV) long terminal repeat (LTR). Here we report that this interference is cell specific, as TPA augmented dexamethasone-induced transcriptional activation of the MMTV LTR in several T cell lines but was inhibitory in NIH-3T3 fibroblasts. TPA-GR synergism was determined to have occurred at the GR-responsive element (GRE) level by functional analysis of deletion mutants or synthetic GRE oligonucleotides driving chloramphenicol acetyl-transferase expression. Synergism required an intact GR DNA-binding domain, whereas amino- or carboxyl-terminal domains were dispensable. The effect was abrogated by the PKC inhibitor staurosporine, suggesting a role for PKC. Increased c-jun, jun-B, and jun-D expression above basal levels and increased transcriptional activity of AP-1/TPA responsive elements fused to chloramphenicol acetyl-transferase vectors were observed in T cells treated with TPA alone or in combination with dexamethasone. The ability of Jun proteins to cooperate with GR in T cells has been investigated after transfection of c-jun, jun-B, or jun-D expression vectors, which augmented GR-dependent transcription from either MMTV LTR or GRE. Conversely, c-jun and jun-B transfection blunted GR-dependent transcription in HeLa cells. The presence of c-fos had a negative influence on GR function and correlated with the cell-specific synergistic or antagonistic activity of Jun with respect to GR; high basal expression of c-fos as well as AP-1 DNA binding and transcriptional activity were observed in HeLa cells, but not in T cells. Furthermore overexpression of exogenous c-fos has an inhibitory effect on GR-dependent transcription from GRE in T cells. We propose that Jun plays a bifunctional role on GR-dependent transcriptional activation of GRE, selecting either synergistic or antagonistic activity depending on the cell-specific microenvironment. In this regard, intracellular levels of c-fos appear to be influential."}

    GENIAcorpus

    {"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":35,"end":62},"obj":"DNA_family_or_group"},{"id":"T2","span":{"begin":66,"end":89},"obj":"protein_family_or_group"},{"id":"T3","span":{"begin":135,"end":151},"obj":"protein_molecule"},{"id":"T4","span":{"begin":153,"end":156},"obj":"protein_molecule"},{"id":"T5","span":{"begin":163,"end":186},"obj":"protein_family_or_group"},{"id":"T6","span":{"begin":188,"end":190},"obj":"protein_family_or_group"},{"id":"T7","span":{"begin":246,"end":249},"obj":"protein_molecule"},{"id":"T8","span":{"begin":275,"end":311},"obj":"other_organic_compound"},{"id":"T9","span":{"begin":313,"end":316},"obj":"other_organic_compound"},{"id":"T10","span":{"begin":329,"end":331},"obj":"protein_family_or_group"},{"id":"T11","span":{"begin":363,"end":388},"obj":"virus"},{"id":"T12","span":{"begin":390,"end":394},"obj":"virus"},{"id":"T13","span":{"begin":396,"end":416},"obj":"DNA_domain_or_region"},{"id":"T14","span":{"begin":418,"end":421},"obj":"DNA_domain_or_region"},{"id":"T15","span":{"begin":483,"end":486},"obj":"other_organic_compound"},{"id":"T16","span":{"begin":497,"end":510},"obj":"other_organic_compound"},{"id":"T17","span":{"begin":553,"end":561},"obj":"DNA_domain_or_region"},{"id":"T18","span":{"begin":573,"end":585},"obj":"cell_line"},{"id":"T19","span":{"begin":608,"end":627},"obj":"cell_line"},{"id":"T20","span":{"begin":629,"end":645},"obj":"other_name"},{"id":"T21","span":{"begin":685,"end":687},"obj":"protein_family_or_group"},{"id":"T22","span":{"begin":708,"end":711},"obj":"DNA_domain_or_region"},{"id":"T23","span":{"begin":745,"end":761},"obj":"DNA_family_or_group"},{"id":"T24","span":{"begin":765,"end":774},"obj":"DNA_family_or_group"},{"id":"T25","span":{"begin":775,"end":778},"obj":"DNA_domain_or_region"},{"id":"T26","span":{"begin":804,"end":838},"obj":"protein_molecule"},{"id":"T27","span":{"begin":880,"end":901},"obj":"protein_domain_or_region"},{"id":"T28","span":{"begin":997,"end":1000},"obj":"protein_molecule"},{"id":"T29","span":{"begin":1011,"end":1024},"obj":"other_organic_compound"},{"id":"T30","span":{"begin":1048,"end":1051},"obj":"protein_molecule"},{"id":"T31","span":{"begin":1063,"end":1068},"obj":"protein_molecule"},{"id":"T32","span":{"begin":1070,"end":1075},"obj":"protein_molecule"},{"id":"T33","span":{"begin":1081,"end":1086},"obj":"protein_molecule"},{"id":"T34","span":{"begin":1159,"end":1187},"obj":"DNA_domain_or_region"},{"id":"T35","span":{"begin":1197,"end":1231},"obj":"protein_molecule"},{"id":"T36","span":{"begin":1257,"end":1264},"obj":"cell_type"},{"id":"T37","span":{"begin":1278,"end":1281},"obj":"other_organic_compound"},{"id":"T38","span":{"begin":1311,"end":1324},"obj":"other_organic_compound"},{"id":"T39","span":{"begin":1341,"end":1353},"obj":"protein_family_or_group"},{"id":"T40","span":{"begin":1372,"end":1374},"obj":"protein_family_or_group"},{"id":"T41","span":{"begin":1378,"end":1385},"obj":"cell_type"},{"id":"T42","span":{"begin":1489,"end":1491},"obj":"protein_family_or_group"},{"id":"T43","span":{"begin":1528,"end":1536},"obj":"DNA_domain_or_region"},{"id":"T44","span":{"begin":1540,"end":1543},"obj":"DNA_domain_or_region"},{"id":"T45","span":{"begin":1557,"end":1562},"obj":"protein_molecule"},{"id":"T46","span":{"begin":1567,"end":1572},"obj":"protein_molecule"},{"id":"T47","span":{"begin":1594,"end":1596},"obj":"protein_family_or_group"},{"id":"T48","span":{"begin":1624,"end":1634},"obj":"cell_line"},{"id":"T49","span":{"begin":1652,"end":1657},"obj":"protein_molecule"},{"id":"T50","span":{"begin":1686,"end":1688},"obj":"protein_family_or_group"},{"id":"T51","span":{"begin":1776,"end":1779},"obj":"protein_family_or_group"},{"id":"T52","span":{"begin":1796,"end":1798},"obj":"protein_family_or_group"},{"id":"T53","span":{"begin":1825,"end":1830},"obj":"protein_molecule"},{"id":"T54","span":{"begin":1842,"end":1846},"obj":"protein_molecule"},{"id":"T55","span":{"begin":1863,"end":1887},"obj":"other_name"},{"id":"T56","span":{"begin":1905,"end":1915},"obj":"cell_line"},{"id":"T57","span":{"begin":1928,"end":1935},"obj":"cell_type"},{"id":"T58","span":{"begin":1967,"end":1976},"obj":"protein_molecule"},{"id":"T59","span":{"begin":1977,"end":1982},"obj":"protein_molecule"},{"id":"T60","span":{"begin":2011,"end":2013},"obj":"protein_family_or_group"},{"id":"T61","span":{"begin":2043,"end":2046},"obj":"DNA_domain_or_region"},{"id":"T62","span":{"begin":2050,"end":2057},"obj":"cell_type"},{"id":"T63","span":{"begin":2075,"end":2078},"obj":"protein_family_or_group"},{"id":"T64","span":{"begin":2108,"end":2110},"obj":"protein_family_or_group"},{"id":"T65","span":{"begin":2151,"end":2154},"obj":"DNA_domain_or_region"},{"id":"T66","span":{"begin":2299,"end":2304},"obj":"protein_molecule"}],"text":"Cell-specific bifunctional role of Jun oncogene family members on glucocorticoid receptor-dependent transcription.\nInteraction between protein kinase C (PKC)- and glucocorticoid receptor (GR)-mediated signaling is suggested by the ability of the PKC activating phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) to inhibit GR-dependent transcription of the mouse mammary tumor virus (MMTV) long terminal repeat (LTR). Here we report that this interference is cell specific, as TPA augmented dexamethasone-induced transcriptional activation of the MMTV LTR in several T cell lines but was inhibitory in NIH-3T3 fibroblasts. TPA-GR synergism was determined to have occurred at the GR-responsive element (GRE) level by functional analysis of deletion mutants or synthetic GRE oligonucleotides driving chloramphenicol acetyl-transferase expression. Synergism required an intact GR DNA-binding domain, whereas amino- or carboxyl-terminal domains were dispensable. The effect was abrogated by the PKC inhibitor staurosporine, suggesting a role for PKC. Increased c-jun, jun-B, and jun-D expression above basal levels and increased transcriptional activity of AP-1/TPA responsive elements fused to chloramphenicol acetyl-transferase vectors were observed in T cells treated with TPA alone or in combination with dexamethasone. The ability of Jun proteins to cooperate with GR in T cells has been investigated after transfection of c-jun, jun-B, or jun-D expression vectors, which augmented GR-dependent transcription from either MMTV LTR or GRE. Conversely, c-jun and jun-B transfection blunted GR-dependent transcription in HeLa cells. The presence of c-fos had a negative influence on GR function and correlated with the cell-specific synergistic or antagonistic activity of Jun with respect to GR; high basal expression of c-fos as well as AP-1 DNA binding and transcriptional activity were observed in HeLa cells, but not in T cells. Furthermore overexpression of exogenous c-fos has an inhibitory effect on GR-dependent transcription from GRE in T cells. We propose that Jun plays a bifunctional role on GR-dependent transcriptional activation of GRE, selecting either synergistic or antagonistic activity depending on the cell-specific microenvironment. In this regard, intracellular levels of c-fos appear to be influential."}