PubMed:10381501 JSONTXT

Annnotations TAB JSON ListView MergeView

    jnlpba-st-training

    {"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":0,"end":6},"obj":"protein"},{"id":"T2","span":{"begin":11,"end":25},"obj":"protein"},{"id":"T3","span":{"begin":85,"end":91},"obj":"protein"},{"id":"T4","span":{"begin":108,"end":128},"obj":"protein"},{"id":"T5","span":{"begin":129,"end":135},"obj":"protein"},{"id":"T6","span":{"begin":192,"end":233},"obj":"cell_line"},{"id":"T7","span":{"begin":279,"end":285},"obj":"protein"},{"id":"T8","span":{"begin":287,"end":317},"obj":"cell_line"},{"id":"T9","span":{"begin":401,"end":407},"obj":"protein"},{"id":"T10","span":{"begin":467,"end":482},"obj":"cell_type"},{"id":"T11","span":{"begin":484,"end":490},"obj":"protein"},{"id":"T12","span":{"begin":530,"end":552},"obj":"protein"},{"id":"T13","span":{"begin":553,"end":559},"obj":"protein"},{"id":"T14","span":{"begin":590,"end":595},"obj":"protein"},{"id":"T15","span":{"begin":600,"end":605},"obj":"protein"},{"id":"T16","span":{"begin":634,"end":640},"obj":"protein"},{"id":"T17","span":{"begin":654,"end":660},"obj":"protein"},{"id":"T18","span":{"begin":697,"end":748},"obj":"cell_line"},{"id":"T19","span":{"begin":791,"end":806},"obj":"cell_type"},{"id":"T20","span":{"begin":839,"end":850},"obj":"DNA"},{"id":"T21","span":{"begin":889,"end":903},"obj":"protein"},{"id":"T22","span":{"begin":973,"end":979},"obj":"protein"},{"id":"T23","span":{"begin":993,"end":999},"obj":"protein"},{"id":"T24","span":{"begin":1114,"end":1120},"obj":"protein"},{"id":"T25","span":{"begin":1211,"end":1217},"obj":"protein"},{"id":"T26","span":{"begin":1255,"end":1261},"obj":"protein"},{"id":"T27","span":{"begin":1266,"end":1280},"obj":"protein"}],"text":"GATA-1 and erythropoietin cooperate to promote erythroid cell survival by regulating bcl-xL expression.\nThe transcription factor GATA-1 is essential for normal erythropoiesis. By examining in vitro-differentiated embryonic stem cells, we showed previously that in the absence of GATA-1, committed erythroid precursors fail to complete maturation and instead undergo apoptosis. The mechanisms by which GATA-1 controls cell survival are unknown. Here we report that in erythroid cells, GATA-1 strongly induces the expression of the anti-apoptotic protein bcl-xL, but not the related proteins bcl-2 and mcl-1. Consistent with a role for bcl-xL in mediating GATA-1-induced erythroid cell survival, in vitro-differentiated bcl-xL-/- embryonic stem cells fail to generate viable mature definitive erythroid cells, a phenotype resembling that of GATA-1 gene disruption. In addition, we show that erythropoietin, which is also required for erythroid cell survival, cooperates with GATA-1 to stimulate bcl-xL gene expression and to maintain erythroid cell viability during terminal maturation. Together, our data show that bcl-xL is essential for normal erythroid development and suggest a regulatory hierarchy in which bcl-xL is a critical downstream effector of GATA-1 and erythropoietin-mediated signals."}

    pubmed-sentences-benchmark

    {"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":103},"obj":"Sentence"},{"id":"S2","span":{"begin":104,"end":175},"obj":"Sentence"},{"id":"S3","span":{"begin":176,"end":376},"obj":"Sentence"},{"id":"S4","span":{"begin":377,"end":443},"obj":"Sentence"},{"id":"S5","span":{"begin":444,"end":606},"obj":"Sentence"},{"id":"S6","span":{"begin":607,"end":862},"obj":"Sentence"},{"id":"S7","span":{"begin":863,"end":1084},"obj":"Sentence"},{"id":"S8","span":{"begin":1085,"end":1298},"obj":"Sentence"}],"text":"GATA-1 and erythropoietin cooperate to promote erythroid cell survival by regulating bcl-xL expression.\nThe transcription factor GATA-1 is essential for normal erythropoiesis. By examining in vitro-differentiated embryonic stem cells, we showed previously that in the absence of GATA-1, committed erythroid precursors fail to complete maturation and instead undergo apoptosis. The mechanisms by which GATA-1 controls cell survival are unknown. Here we report that in erythroid cells, GATA-1 strongly induces the expression of the anti-apoptotic protein bcl-xL, but not the related proteins bcl-2 and mcl-1. Consistent with a role for bcl-xL in mediating GATA-1-induced erythroid cell survival, in vitro-differentiated bcl-xL-/- embryonic stem cells fail to generate viable mature definitive erythroid cells, a phenotype resembling that of GATA-1 gene disruption. In addition, we show that erythropoietin, which is also required for erythroid cell survival, cooperates with GATA-1 to stimulate bcl-xL gene expression and to maintain erythroid cell viability during terminal maturation. Together, our data show that bcl-xL is essential for normal erythroid development and suggest a regulatory hierarchy in which bcl-xL is a critical downstream effector of GATA-1 and erythropoietin-mediated signals."}

    genia-medco-coref

    {"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":0,"end":6},"obj":"NP"},{"id":"C2","span":{"begin":11,"end":25},"obj":"NP"},{"id":"C3","span":{"begin":47,"end":70},"obj":"NP"},{"id":"C4","span":{"begin":85,"end":102},"obj":"NP"},{"id":"C5","span":{"begin":104,"end":135},"obj":"NP"},{"id":"C6","span":{"begin":279,"end":285},"obj":"NP"},{"id":"C7","span":{"begin":377,"end":391},"obj":"NP"},{"id":"C8","span":{"begin":395,"end":400},"obj":"NP"},{"id":"C9","span":{"begin":401,"end":407},"obj":"NP"},{"id":"C10","span":{"begin":484,"end":490},"obj":"NP"},{"id":"C12","span":{"begin":526,"end":559},"obj":"NP"},{"id":"C11","span":{"begin":508,"end":559},"obj":"NP"},{"id":"C13","span":{"begin":634,"end":640},"obj":"NP"},{"id":"C14","span":{"begin":766,"end":806},"obj":"NP"},{"id":"C16","span":{"begin":808,"end":819},"obj":"NP"},{"id":"C17","span":{"begin":831,"end":835},"obj":"NP"},{"id":"C15","span":{"begin":808,"end":861},"obj":"NP"},{"id":"C18","span":{"begin":889,"end":903},"obj":"NP"},{"id":"C19","span":{"begin":905,"end":910},"obj":"NP"},{"id":"C20","span":{"begin":932,"end":955},"obj":"NP"},{"id":"C21","span":{"begin":973,"end":979},"obj":"NP"},{"id":"C22","span":{"begin":1114,"end":1120},"obj":"NP"},{"id":"C23","span":{"begin":1179,"end":1201},"obj":"NP"},{"id":"C24","span":{"begin":1205,"end":1210},"obj":"NP"},{"id":"C25","span":{"begin":1211,"end":1217},"obj":"NP"},{"id":"C26","span":{"begin":1255,"end":1261},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C5","obj":"C1"},{"id":"R2","pred":"coref-ident","subj":"C6","obj":"C5"},{"id":"R3","pred":"coref-relat","subj":"C8","obj":"C7"},{"id":"R4","pred":"coref-ident","subj":"C9","obj":"C6"},{"id":"R5","pred":"coref-ident","subj":"C10","obj":"C9"},{"id":"R6","pred":"coref-ident","subj":"C11","obj":"C4"},{"id":"R7","pred":"coref-ident","subj":"C13","obj":"C12"},{"id":"R8","pred":"coref-pron","subj":"C17","obj":"C16"},{"id":"R9","pred":"coref-appos","subj":"C15","obj":"C14"},{"id":"R10","pred":"coref-ident","subj":"C18","obj":"C2"},{"id":"R11","pred":"coref-relat","subj":"C19","obj":"C18"},{"id":"R12","pred":"coref-ident","subj":"C20","obj":"C3"},{"id":"R13","pred":"coref-ident","subj":"C21","obj":"C10"},{"id":"R14","pred":"coref-ident","subj":"C22","obj":"C13"},{"id":"R15","pred":"coref-relat","subj":"C24","obj":"C23"},{"id":"R16","pred":"coref-ident","subj":"C25","obj":"C22"},{"id":"R17","pred":"coref-ident","subj":"C26","obj":"C21"}],"text":"GATA-1 and erythropoietin cooperate to promote erythroid cell survival by regulating bcl-xL expression.\nThe transcription factor GATA-1 is essential for normal erythropoiesis. By examining in vitro-differentiated embryonic stem cells, we showed previously that in the absence of GATA-1, committed erythroid precursors fail to complete maturation and instead undergo apoptosis. The mechanisms by which GATA-1 controls cell survival are unknown. Here we report that in erythroid cells, GATA-1 strongly induces the expression of the anti-apoptotic protein bcl-xL, but not the related proteins bcl-2 and mcl-1. Consistent with a role for bcl-xL in mediating GATA-1-induced erythroid cell survival, in vitro-differentiated bcl-xL-/- embryonic stem cells fail to generate viable mature definitive erythroid cells, a phenotype resembling that of GATA-1 gene disruption. In addition, we show that erythropoietin, which is also required for erythroid cell survival, cooperates with GATA-1 to stimulate bcl-xL gene expression and to maintain erythroid cell viability during terminal maturation. Together, our data show that bcl-xL is essential for normal erythroid development and suggest a regulatory hierarchy in which bcl-xL is a critical downstream effector of GATA-1 and erythropoietin-mediated signals."}

    GENIAcorpus

    {"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":0,"end":6},"obj":"protein_molecule"},{"id":"T2","span":{"begin":11,"end":25},"obj":"protein_family_or_group"},{"id":"T3","span":{"begin":47,"end":70},"obj":"other_name"},{"id":"T4","span":{"begin":85,"end":91},"obj":"protein_molecule"},{"id":"T5","span":{"begin":108,"end":128},"obj":"protein_family_or_group"},{"id":"T6","span":{"begin":129,"end":135},"obj":"protein_molecule"},{"id":"T7","span":{"begin":192,"end":233},"obj":"cell_line"},{"id":"T8","span":{"begin":279,"end":285},"obj":"protein_molecule"},{"id":"T9","span":{"begin":287,"end":317},"obj":"cell_line"},{"id":"T10","span":{"begin":366,"end":375},"obj":"other_name"},{"id":"T11","span":{"begin":401,"end":407},"obj":"protein_molecule"},{"id":"T12","span":{"begin":417,"end":430},"obj":"other_name"},{"id":"T13","span":{"begin":467,"end":482},"obj":"cell_type"},{"id":"T14","span":{"begin":484,"end":490},"obj":"protein_molecule"},{"id":"T15","span":{"begin":530,"end":552},"obj":"protein_family_or_group"},{"id":"T16","span":{"begin":553,"end":559},"obj":"protein_molecule"},{"id":"T17","span":{"begin":590,"end":595},"obj":"protein_molecule"},{"id":"T18","span":{"begin":600,"end":605},"obj":"protein_molecule"},{"id":"T19","span":{"begin":634,"end":640},"obj":"protein_molecule"},{"id":"T20","span":{"begin":654,"end":660},"obj":"protein_molecule"},{"id":"T21","span":{"begin":669,"end":678},"obj":"other_name"},{"id":"T22","span":{"begin":679,"end":692},"obj":"other_name"},{"id":"T23","span":{"begin":697,"end":717},"obj":"cell_line"},{"id":"T24","span":{"begin":718,"end":724},"obj":"protein_molecule"},{"id":"T25","span":{"begin":791,"end":806},"obj":"cell_type"},{"id":"T26","span":{"begin":839,"end":850},"obj":"DNA_domain_or_region"},{"id":"T27","span":{"begin":889,"end":903},"obj":"protein_family_or_group"},{"id":"T28","span":{"begin":932,"end":941},"obj":"other_name"},{"id":"T29","span":{"begin":942,"end":955},"obj":"other_name"},{"id":"T30","span":{"begin":973,"end":979},"obj":"protein_molecule"},{"id":"T31","span":{"begin":993,"end":999},"obj":"protein_molecule"},{"id":"T32","span":{"begin":1064,"end":1083},"obj":"other_name"},{"id":"T33","span":{"begin":1114,"end":1120},"obj":"protein_molecule"},{"id":"T34","span":{"begin":1181,"end":1201},"obj":"other_name"},{"id":"T35","span":{"begin":1211,"end":1217},"obj":"protein_molecule"},{"id":"T36","span":{"begin":1255,"end":1261},"obj":"protein_molecule"},{"id":"T37","span":{"begin":1266,"end":1280},"obj":"protein_family_or_group"}],"text":"GATA-1 and erythropoietin cooperate to promote erythroid cell survival by regulating bcl-xL expression.\nThe transcription factor GATA-1 is essential for normal erythropoiesis. By examining in vitro-differentiated embryonic stem cells, we showed previously that in the absence of GATA-1, committed erythroid precursors fail to complete maturation and instead undergo apoptosis. The mechanisms by which GATA-1 controls cell survival are unknown. Here we report that in erythroid cells, GATA-1 strongly induces the expression of the anti-apoptotic protein bcl-xL, but not the related proteins bcl-2 and mcl-1. Consistent with a role for bcl-xL in mediating GATA-1-induced erythroid cell survival, in vitro-differentiated bcl-xL-/- embryonic stem cells fail to generate viable mature definitive erythroid cells, a phenotype resembling that of GATA-1 gene disruption. In addition, we show that erythropoietin, which is also required for erythroid cell survival, cooperates with GATA-1 to stimulate bcl-xL gene expression and to maintain erythroid cell viability during terminal maturation. Together, our data show that bcl-xL is essential for normal erythroid development and suggest a regulatory hierarchy in which bcl-xL is a critical downstream effector of GATA-1 and erythropoietin-mediated signals."}