PubMed:9261181 JSONTXT

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{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":0,"end":27},"obj":"protein"},{"id":"T2","span":{"begin":59,"end":83},"obj":"cell_line"},{"id":"T3","span":{"begin":128,"end":146},"obj":"DNA"},{"id":"T4","span":{"begin":148,"end":161},"obj":"protein"},{"id":"T5","span":{"begin":163,"end":167},"obj":"protein"},{"id":"T6","span":{"begin":191,"end":220},"obj":"cell_type"},{"id":"T7","span":{"begin":233,"end":242},"obj":"cell_type"},{"id":"T8","span":{"begin":418,"end":439},"obj":"cell_type"},{"id":"T9","span":{"begin":441,"end":444},"obj":"cell_type"},{"id":"T10","span":{"begin":449,"end":452},"obj":"cell_type"},{"id":"T11","span":{"begin":592,"end":612},"obj":"protein"},{"id":"T12","span":{"begin":613,"end":619},"obj":"protein"},{"id":"T13","span":{"begin":623,"end":636},"obj":"DNA"},{"id":"T14","span":{"begin":651,"end":661},"obj":"cell_line"},{"id":"T15","span":{"begin":682,"end":709},"obj":"protein"},{"id":"T16","span":{"begin":754,"end":760},"obj":"protein"},{"id":"T17","span":{"begin":795,"end":799},"obj":"protein"},{"id":"T18","span":{"begin":808,"end":827},"obj":"cell_type"},{"id":"T19","span":{"begin":854,"end":860},"obj":"protein"},{"id":"T20","span":{"begin":965,"end":971},"obj":"protein"},{"id":"T21","span":{"begin":975,"end":984},"obj":"cell_type"},{"id":"T22","span":{"begin":993,"end":1035},"obj":"cell_line"},{"id":"T23","span":{"begin":1050,"end":1063},"obj":"DNA"},{"id":"T24","span":{"begin":1095,"end":1115},"obj":"cell_type"},{"id":"T25","span":{"begin":1163,"end":1169},"obj":"protein"},{"id":"T26","span":{"begin":1217,"end":1226},"obj":"cell_type"},{"id":"T27","span":{"begin":1254,"end":1263},"obj":"cell_type"},{"id":"T28","span":{"begin":1269,"end":1305},"obj":"cell_type"},{"id":"T29","span":{"begin":1315,"end":1324},"obj":"cell_type"},{"id":"T30","span":{"begin":1340,"end":1354},"obj":"protein"},{"id":"T31","span":{"begin":1362,"end":1368},"obj":"protein"},{"id":"T32","span":{"begin":1419,"end":1422},"obj":"cell_type"},{"id":"T33","span":{"begin":1427,"end":1438},"obj":"cell_type"},{"id":"T34","span":{"begin":1474,"end":1480},"obj":"protein"}],"text":"Transcription factor GATA-3 is differentially expressed in murine Th1 and Th2 cells and controls Th2-specific expression of the interleukin-5 gene.\nInterleukin-5 (IL-5), which is produced by CD4(+) T helper 2 (Th2) cells, but not by Th1 cells, plays a key role in the development of eosinophilia in asthma. Despite increasing evidence that the outcome of many diseases is determined by the ratio of the two subsets of CD4(+) T helper cells, Th1 and Th2, the molecular basis for Th1- and Th2-specific gene expression remains to be elucidated. We previously established a critical role for the transcription factor GATA-3 in IL-5 promoter activation in EL-4 cells, which express both Th1- and Th2-type cytokines. Our studies reported here demonstrate that GATA-3 is critical for expression of the IL-5 gene in bona fide Th2 cells. Whereas mutations in the GATA-3 site abolished antigen- or cAMP-stimulated IL-5 promoter activation in Th2 cells, ectopic expression of GATA-3 in Th1 cells or in a non-lymphoid, non-IL-5-producing cell line activated the IL-5 promoter. During the differentiation of naive CD4(+) T cells isolated from T cell receptor transgenic mice, GATA-3 gene expression was up-regulated in developing Th2 cells, but was down-regulated in Th1 cells, and antigen- or cAMP-activated Th2 cells (but not Th1 cells) expressed the GATA-3 protein. Thus, GATA-3 may play an important role in the balance between Th1 and Th2 subsets in immune responses. Inhibition of GATA-3 activity has therapeutic potential in the treatment of asthma and other hypereosinophilic diseases."}

{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":0,"end":27},"obj":"NP"},{"id":"C2","span":{"begin":148,"end":168},"obj":"NP"},{"id":"C3","span":{"begin":170,"end":175},"obj":"NP"},{"id":"C4","span":{"begin":233,"end":242},"obj":"NP"},{"id":"C5","span":{"begin":299,"end":305},"obj":"NP"},{"id":"C6","span":{"begin":326,"end":334},"obj":"NP"},{"id":"C7","span":{"begin":335,"end":339},"obj":"NP"},{"id":"C8","span":{"begin":399,"end":439},"obj":"NP"},{"id":"C9","span":{"begin":441,"end":452},"obj":"NP"},{"id":"C10","span":{"begin":651,"end":661},"obj":"NP"},{"id":"C11","span":{"begin":663,"end":668},"obj":"NP"},{"id":"C12","span":{"begin":754,"end":760},"obj":"NP"},{"id":"C13","span":{"begin":1254,"end":1263},"obj":"NP"},{"id":"C14","span":{"begin":1362,"end":1368},"obj":"NP"},{"id":"C15","span":{"begin":1536,"end":1542},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-relat","subj":"C3","obj":"C2"},{"id":"R2","pred":"coref-relat","subj":"C7","obj":"C6"},{"id":"R3","pred":"coref-appos","subj":"C9","obj":"C8"},{"id":"R4","pred":"coref-relat","subj":"C11","obj":"C10"},{"id":"R5","pred":"coref-ident","subj":"C12","obj":"C1"},{"id":"R6","pred":"coref-ident","subj":"C13","obj":"C4"},{"id":"R7","pred":"coref-ident","subj":"C14","obj":"C12"},{"id":"R8","pred":"coref-ident","subj":"C15","obj":"C5"}],"text":"Transcription factor GATA-3 is differentially expressed in murine Th1 and Th2 cells and controls Th2-specific expression of the interleukin-5 gene.\nInterleukin-5 (IL-5), which is produced by CD4(+) T helper 2 (Th2) cells, but not by Th1 cells, plays a key role in the development of eosinophilia in asthma. Despite increasing evidence that the outcome of many diseases is determined by the ratio of the two subsets of CD4(+) T helper cells, Th1 and Th2, the molecular basis for Th1- and Th2-specific gene expression remains to be elucidated. We previously established a critical role for the transcription factor GATA-3 in IL-5 promoter activation in EL-4 cells, which express both Th1- and Th2-type cytokines. Our studies reported here demonstrate that GATA-3 is critical for expression of the IL-5 gene in bona fide Th2 cells. Whereas mutations in the GATA-3 site abolished antigen- or cAMP-stimulated IL-5 promoter activation in Th2 cells, ectopic expression of GATA-3 in Th1 cells or in a non-lymphoid, non-IL-5-producing cell line activated the IL-5 promoter. During the differentiation of naive CD4(+) T cells isolated from T cell receptor transgenic mice, GATA-3 gene expression was up-regulated in developing Th2 cells, but was down-regulated in Th1 cells, and antigen- or cAMP-activated Th2 cells (but not Th1 cells) expressed the GATA-3 protein. Thus, GATA-3 may play an important role in the balance between Th1 and Th2 subsets in immune responses. Inhibition of GATA-3 activity has therapeutic potential in the treatment of asthma and other hypereosinophilic diseases."}

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":147},"obj":"Sentence"},{"id":"S2","span":{"begin":148,"end":306},"obj":"Sentence"},{"id":"S3","span":{"begin":307,"end":541},"obj":"Sentence"},{"id":"S4","span":{"begin":542,"end":710},"obj":"Sentence"},{"id":"S5","span":{"begin":711,"end":828},"obj":"Sentence"},{"id":"S6","span":{"begin":829,"end":1064},"obj":"Sentence"},{"id":"S7","span":{"begin":1065,"end":1355},"obj":"Sentence"},{"id":"S8","span":{"begin":1356,"end":1459},"obj":"Sentence"},{"id":"S9","span":{"begin":1460,"end":1580},"obj":"Sentence"}],"text":"Transcription factor GATA-3 is differentially expressed in murine Th1 and Th2 cells and controls Th2-specific expression of the interleukin-5 gene.\nInterleukin-5 (IL-5), which is produced by CD4(+) T helper 2 (Th2) cells, but not by Th1 cells, plays a key role in the development of eosinophilia in asthma. Despite increasing evidence that the outcome of many diseases is determined by the ratio of the two subsets of CD4(+) T helper cells, Th1 and Th2, the molecular basis for Th1- and Th2-specific gene expression remains to be elucidated. We previously established a critical role for the transcription factor GATA-3 in IL-5 promoter activation in EL-4 cells, which express both Th1- and Th2-type cytokines. Our studies reported here demonstrate that GATA-3 is critical for expression of the IL-5 gene in bona fide Th2 cells. Whereas mutations in the GATA-3 site abolished antigen- or cAMP-stimulated IL-5 promoter activation in Th2 cells, ectopic expression of GATA-3 in Th1 cells or in a non-lymphoid, non-IL-5-producing cell line activated the IL-5 promoter. During the differentiation of naive CD4(+) T cells isolated from T cell receptor transgenic mice, GATA-3 gene expression was up-regulated in developing Th2 cells, but was down-regulated in Th1 cells, and antigen- or cAMP-activated Th2 cells (but not Th1 cells) expressed the GATA-3 protein. Thus, GATA-3 may play an important role in the balance between Th1 and Th2 subsets in immune responses. Inhibition of GATA-3 activity has therapeutic potential in the treatment of asthma and other hypereosinophilic diseases."}

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{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":283,"end":295},"obj":"Disease"},{"id":"T2","span":{"begin":299,"end":305},"obj":"Disease"},{"id":"T3","span":{"begin":1536,"end":1542},"obj":"Disease"},{"id":"T4","span":{"begin":1553,"end":1579},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0015691"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0004979"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0004979"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MONDO_0015691"}],"text":"Transcription factor GATA-3 is differentially expressed in murine Th1 and Th2 cells and controls Th2-specific expression of the interleukin-5 gene.\nInterleukin-5 (IL-5), which is produced by CD4(+) T helper 2 (Th2) cells, but not by Th1 cells, plays a key role in the development of eosinophilia in asthma. Despite increasing evidence that the outcome of many diseases is determined by the ratio of the two subsets of CD4(+) T helper cells, Th1 and Th2, the molecular basis for Th1- and Th2-specific gene expression remains to be elucidated. We previously established a critical role for the transcription factor GATA-3 in IL-5 promoter activation in EL-4 cells, which express both Th1- and Th2-type cytokines. Our studies reported here demonstrate that GATA-3 is critical for expression of the IL-5 gene in bona fide Th2 cells. Whereas mutations in the GATA-3 site abolished antigen- or cAMP-stimulated IL-5 promoter activation in Th2 cells, ectopic expression of GATA-3 in Th1 cells or in a non-lymphoid, non-IL-5-producing cell line activated the IL-5 promoter. During the differentiation of naive CD4(+) T cells isolated from T cell receptor transgenic mice, GATA-3 gene expression was up-regulated in developing Th2 cells, but was down-regulated in Th1 cells, and antigen- or cAMP-activated Th2 cells (but not Th1 cells) expressed the GATA-3 protein. Thus, GATA-3 may play an important role in the balance between Th1 and Th2 subsets in immune responses. Inhibition of GATA-3 activity has therapeutic potential in the treatment of asthma and other hypereosinophilic diseases."}

{"project":"HP-phenotype","denotations":[{"id":"T1","span":{"begin":283,"end":295},"obj":"Phenotype"},{"id":"T2","span":{"begin":299,"end":305},"obj":"Phenotype"},{"id":"T3","span":{"begin":1536,"end":1542},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0001880"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0002099"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"HP:0002099"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"Transcription factor GATA-3 is differentially expressed in murine Th1 and Th2 cells and controls Th2-specific expression of the interleukin-5 gene.\nInterleukin-5 (IL-5), which is produced by CD4(+) T helper 2 (Th2) cells, but not by Th1 cells, plays a key role in the development of eosinophilia in asthma. Despite increasing evidence that the outcome of many diseases is determined by the ratio of the two subsets of CD4(+) T helper cells, Th1 and Th2, the molecular basis for Th1- and Th2-specific gene expression remains to be elucidated. We previously established a critical role for the transcription factor GATA-3 in IL-5 promoter activation in EL-4 cells, which express both Th1- and Th2-type cytokines. Our studies reported here demonstrate that GATA-3 is critical for expression of the IL-5 gene in bona fide Th2 cells. Whereas mutations in the GATA-3 site abolished antigen- or cAMP-stimulated IL-5 promoter activation in Th2 cells, ectopic expression of GATA-3 in Th1 cells or in a non-lymphoid, non-IL-5-producing cell line activated the IL-5 promoter. During the differentiation of naive CD4(+) T cells isolated from T cell receptor transgenic mice, GATA-3 gene expression was up-regulated in developing Th2 cells, but was down-regulated in Th1 cells, and antigen- or cAMP-activated Th2 cells (but not Th1 cells) expressed the GATA-3 protein. Thus, GATA-3 may play an important role in the balance between Th1 and Th2 subsets in immune responses. Inhibition of GATA-3 activity has therapeutic potential in the treatment of asthma and other hypereosinophilic diseases."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":1157,"end":1161},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"10088"}],"text":"Transcription factor GATA-3 is differentially expressed in murine Th1 and Th2 cells and controls Th2-specific expression of the interleukin-5 gene.\nInterleukin-5 (IL-5), which is produced by CD4(+) T helper 2 (Th2) cells, but not by Th1 cells, plays a key role in the development of eosinophilia in asthma. Despite increasing evidence that the outcome of many diseases is determined by the ratio of the two subsets of CD4(+) T helper cells, Th1 and Th2, the molecular basis for Th1- and Th2-specific gene expression remains to be elucidated. We previously established a critical role for the transcription factor GATA-3 in IL-5 promoter activation in EL-4 cells, which express both Th1- and Th2-type cytokines. Our studies reported here demonstrate that GATA-3 is critical for expression of the IL-5 gene in bona fide Th2 cells. Whereas mutations in the GATA-3 site abolished antigen- or cAMP-stimulated IL-5 promoter activation in Th2 cells, ectopic expression of GATA-3 in Th1 cells or in a non-lymphoid, non-IL-5-producing cell line activated the IL-5 promoter. During the differentiation of naive CD4(+) T cells isolated from T cell receptor transgenic mice, GATA-3 gene expression was up-regulated in developing Th2 cells, but was down-regulated in Th1 cells, and antigen- or cAMP-activated Th2 cells (but not Th1 cells) expressed the GATA-3 protein. Thus, GATA-3 may play an important role in the balance between Th1 and Th2 subsets in immune responses. Inhibition of GATA-3 activity has therapeutic potential in the treatment of asthma and other hypereosinophilic diseases."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":1130,"end":1136},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL_0000084"}],"text":"Transcription factor GATA-3 is differentially expressed in murine Th1 and Th2 cells and controls Th2-specific expression of the interleukin-5 gene.\nInterleukin-5 (IL-5), which is produced by CD4(+) T helper 2 (Th2) cells, but not by Th1 cells, plays a key role in the development of eosinophilia in asthma. Despite increasing evidence that the outcome of many diseases is determined by the ratio of the two subsets of CD4(+) T helper cells, Th1 and Th2, the molecular basis for Th1- and Th2-specific gene expression remains to be elucidated. We previously established a critical role for the transcription factor GATA-3 in IL-5 promoter activation in EL-4 cells, which express both Th1- and Th2-type cytokines. Our studies reported here demonstrate that GATA-3 is critical for expression of the IL-5 gene in bona fide Th2 cells. Whereas mutations in the GATA-3 site abolished antigen- or cAMP-stimulated IL-5 promoter activation in Th2 cells, ectopic expression of GATA-3 in Th1 cells or in a non-lymphoid, non-IL-5-producing cell line activated the IL-5 promoter. During the differentiation of naive CD4(+) T cells isolated from T cell receptor transgenic mice, GATA-3 gene expression was up-regulated in developing Th2 cells, but was down-regulated in Th1 cells, and antigen- or cAMP-activated Th2 cells (but not Th1 cells) expressed the GATA-3 protein. Thus, GATA-3 may play an important role in the balance between Th1 and Th2 subsets in immune responses. Inhibition of GATA-3 activity has therapeutic potential in the treatment of asthma and other hypereosinophilic diseases."}