PubMed:7727787 JSONTXT

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":116,"end":127},"obj":"gene:3050"},{"id":"T1","span":{"begin":272,"end":287},"obj":"disease:C0023440"},{"id":"T2","span":{"begin":167,"end":178},"obj":"gene:3050"},{"id":"T3","span":{"begin":272,"end":287},"obj":"disease:C0023440"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Identification of a major positive regulatory element located 5' to the human zeta-globin gene.\nThe function of the zeta-globin promoter was studied using a series of zeta-globin promoter deletion constructs to drive luciferase expression in transiently transfected human erythroleukemia cells. The promoters were used without enhancers, or with enhancers derived from the beta-globin locus control region and the alpha-globin HS-40 enhancer. When transfected into K562 cells, which express zeta-globin, comparable amounts of activity were obtained from the -557 and -417 zeta-luciferase constructs and the alpha-luciferase constructs when no enhancers or the alpha-globin locus enhancers were used. When the constructs were transfected into OCIM1 cells, which do not express zeta-globin, the zeta-globin promoters were at best 20% as active as the alpha-globin promoters. When sequences from -417 to -207 5' to the zeta-globin mRNA cap site were deleted, up to 95% of the zeta-globin promoter activity was lost in K562 cells. Reinsertion of these sequences into zeta-luciferase constructs missing the -417 to -207 region showed that the sequences lack classical enhancer activity. Point mutation of a GATA-1 site at -230 reduced promoter activity by 37%. Point mutation of a CCACC site at -240 had no effect. Electrophoretic mobility shift assays indicated that the -230 GATA-1 site has a relatively low affinity for GATA-1. These experiments show the presence of a strong positive-acting element, located between -417 and -207 bp 5' to the zeta-globin mRNA cap site, is necessary for high-level promoter activity in K562 cells. This element requires GATA-1 and additional unknown factors for maximal activity."}

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{"project":"DisGeNET5_gene_disease","denotations":[{"id":"7727787-1#20#31#gene3050","span":{"begin":116,"end":127},"obj":"gene3050"},{"id":"7727787-1#71#82#gene3050","span":{"begin":167,"end":178},"obj":"gene3050"},{"id":"7727787-1#176#191#diseaseC0023440","span":{"begin":272,"end":287},"obj":"diseaseC0023440"}],"relations":[{"id":"20#31#gene3050176#191#diseaseC0023440","pred":"associated_with","subj":"7727787-1#20#31#gene3050","obj":"7727787-1#176#191#diseaseC0023440"},{"id":"71#82#gene3050176#191#diseaseC0023440","pred":"associated_with","subj":"7727787-1#71#82#gene3050","obj":"7727787-1#176#191#diseaseC0023440"}],"text":"Identification of a major positive regulatory element located 5' to the human zeta-globin gene.\nThe function of the zeta-globin promoter was studied using a series of zeta-globin promoter deletion constructs to drive luciferase expression in transiently transfected human erythroleukemia cells. The promoters were used without enhancers, or with enhancers derived from the beta-globin locus control region and the alpha-globin HS-40 enhancer. When transfected into K562 cells, which express zeta-globin, comparable amounts of activity were obtained from the -557 and -417 zeta-luciferase constructs and the alpha-luciferase constructs when no enhancers or the alpha-globin locus enhancers were used. When the constructs were transfected into OCIM1 cells, which do not express zeta-globin, the zeta-globin promoters were at best 20% as active as the alpha-globin promoters. When sequences from -417 to -207 5' to the zeta-globin mRNA cap site were deleted, up to 95% of the zeta-globin promoter activity was lost in K562 cells. Reinsertion of these sequences into zeta-luciferase constructs missing the -417 to -207 region showed that the sequences lack classical enhancer activity. Point mutation of a GATA-1 site at -230 reduced promoter activity by 37%. Point mutation of a CCACC site at -240 had no effect. Electrophoretic mobility shift assays indicated that the -230 GATA-1 site has a relatively low affinity for GATA-1. These experiments show the presence of a strong positive-acting element, located between -417 and -207 bp 5' to the zeta-globin mRNA cap site, is necessary for high-level promoter activity in K562 cells. This element requires GATA-1 and additional unknown factors for maximal activity."}

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{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":95},"obj":"Sentence"},{"id":"S2","span":{"begin":96,"end":294},"obj":"Sentence"},{"id":"S3","span":{"begin":295,"end":442},"obj":"Sentence"},{"id":"S4","span":{"begin":443,"end":699},"obj":"Sentence"},{"id":"S5","span":{"begin":700,"end":872},"obj":"Sentence"},{"id":"S6","span":{"begin":873,"end":1026},"obj":"Sentence"},{"id":"S7","span":{"begin":1027,"end":1181},"obj":"Sentence"},{"id":"S8","span":{"begin":1182,"end":1255},"obj":"Sentence"},{"id":"S9","span":{"begin":1256,"end":1309},"obj":"Sentence"},{"id":"S10","span":{"begin":1310,"end":1425},"obj":"Sentence"},{"id":"S11","span":{"begin":1426,"end":1629},"obj":"Sentence"},{"id":"S12","span":{"begin":1630,"end":1711},"obj":"Sentence"}],"text":"Identification of a major positive regulatory element located 5' to the human zeta-globin gene.\nThe function of the zeta-globin promoter was studied using a series of zeta-globin promoter deletion constructs to drive luciferase expression in transiently transfected human erythroleukemia cells. The promoters were used without enhancers, or with enhancers derived from the beta-globin locus control region and the alpha-globin HS-40 enhancer. When transfected into K562 cells, which express zeta-globin, comparable amounts of activity were obtained from the -557 and -417 zeta-luciferase constructs and the alpha-luciferase constructs when no enhancers or the alpha-globin locus enhancers were used. When the constructs were transfected into OCIM1 cells, which do not express zeta-globin, the zeta-globin promoters were at best 20% as active as the alpha-globin promoters. When sequences from -417 to -207 5' to the zeta-globin mRNA cap site were deleted, up to 95% of the zeta-globin promoter activity was lost in K562 cells. Reinsertion of these sequences into zeta-luciferase constructs missing the -417 to -207 region showed that the sequences lack classical enhancer activity. Point mutation of a GATA-1 site at -230 reduced promoter activity by 37%. Point mutation of a CCACC site at -240 had no effect. Electrophoretic mobility shift assays indicated that the -230 GATA-1 site has a relatively low affinity for GATA-1. These experiments show the presence of a strong positive-acting element, located between -417 and -207 bp 5' to the zeta-globin mRNA cap site, is necessary for high-level promoter activity in K562 cells. This element requires GATA-1 and additional unknown factors for maximal activity."}

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Point mutation of a CCACC site at -240 had no effect. Electrophoretic mobility shift assays indicated that the -230 GATA-1 site has a relatively low affinity for GATA-1. These experiments show the presence of a strong positive-acting element, located between -417 and -207 bp 5' to the zeta-globin mRNA cap site, is necessary for high-level promoter activity in K562 cells. This element requires GATA-1 and additional unknown factors for maximal activity."}