PubMed:8449904 JSONTXT

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":78},"obj":"Sentence"},{"id":"T2","span":{"begin":79,"end":128},"obj":"Sentence"},{"id":"T3","span":{"begin":129,"end":241},"obj":"Sentence"},{"id":"T4","span":{"begin":242,"end":385},"obj":"Sentence"},{"id":"T5","span":{"begin":386,"end":507},"obj":"Sentence"},{"id":"T6","span":{"begin":508,"end":647},"obj":"Sentence"},{"id":"T7","span":{"begin":648,"end":772},"obj":"Sentence"},{"id":"T8","span":{"begin":773,"end":880},"obj":"Sentence"},{"id":"T9","span":{"begin":881,"end":1004},"obj":"Sentence"},{"id":"T10","span":{"begin":1005,"end":1195},"obj":"Sentence"},{"id":"T11","span":{"begin":1196,"end":1334},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":78},"obj":"Sentence"},{"id":"T2","span":{"begin":79,"end":128},"obj":"Sentence"},{"id":"T3","span":{"begin":129,"end":241},"obj":"Sentence"},{"id":"T4","span":{"begin":242,"end":385},"obj":"Sentence"},{"id":"T5","span":{"begin":386,"end":507},"obj":"Sentence"},{"id":"T6","span":{"begin":508,"end":647},"obj":"Sentence"},{"id":"T7","span":{"begin":648,"end":772},"obj":"Sentence"},{"id":"T8","span":{"begin":773,"end":880},"obj":"Sentence"},{"id":"T9","span":{"begin":881,"end":1004},"obj":"Sentence"},{"id":"T10","span":{"begin":1005,"end":1195},"obj":"Sentence"},{"id":"T11","span":{"begin":1196,"end":1334},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Transcriptional regulation of the pyruvate kinase erythroid-specific promoter.\nMammal pyruvate kinases are encoded by two genes. The L gene produces the erythroid (R-PK) or the hepatic (L-PK) isozymes by the alternative use of two promoters. We report the characterization of the cis- and trans-acting elements involved in the tissue-specific activity of the L gene erythroid promoter. A R-PK DNA fragment extending from -870 to +54 relative to the cap site confers erythroid specificity to a reporter gene. Within this region, we define a minimal promoter (-62 to +54) that displays erythroid-specific activity and contains two DNA binding sites. One, located at -50, binds members of the CCACC/Sp1 family and the other, located at -20, binds the erythroid factor GATA-1. Although the -20 GATA binding site (AGATAA) is also a potential TFIID binding site, it does not bind TFIID. Furthermore, the substitution of this GATA binding site by a canonical TFIID binding site suppresses the promoter activity. Mutations and deletions of both sites indicate that only the association of CCACC/Sp1 and GATA binding sites can drive efficient and tissue-specific expression of this R-PK minimal promoter. Finally, by co-transfection experiments, we study the elements involved in the hGATA-1 transactivation of the R-PK promoter in HeLa cells."}

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":34,"end":77},"obj":"DNA"},{"id":"T2","span":{"begin":79,"end":102},"obj":"protein"},{"id":"T3","span":{"begin":133,"end":139},"obj":"DNA"},{"id":"T4","span":{"begin":153,"end":162},"obj":"protein"},{"id":"T5","span":{"begin":164,"end":168},"obj":"protein"},{"id":"T6","span":{"begin":177,"end":200},"obj":"protein"},{"id":"T7","span":{"begin":231,"end":240},"obj":"DNA"},{"id":"T8","span":{"begin":280,"end":310},"obj":"DNA"},{"id":"T9","span":{"begin":359,"end":384},"obj":"DNA"},{"id":"T10","span":{"begin":388,"end":405},"obj":"DNA"},{"id":"T11","span":{"begin":449,"end":457},"obj":"DNA"},{"id":"T12","span":{"begin":493,"end":506},"obj":"DNA"},{"id":"T13","span":{"begin":540,"end":556},"obj":"DNA"},{"id":"T14","span":{"begin":690,"end":706},"obj":"protein"},{"id":"T15","span":{"begin":748,"end":771},"obj":"protein"},{"id":"T16","span":{"begin":790,"end":807},"obj":"DNA"},{"id":"T17","span":{"begin":837,"end":855},"obj":"DNA"},{"id":"T18","span":{"begin":874,"end":879},"obj":"protein"},{"id":"T19","span":{"begin":919,"end":936},"obj":"DNA"},{"id":"T20","span":{"begin":952,"end":970},"obj":"DNA"},{"id":"T21","span":{"begin":1081,"end":1090},"obj":"protein"},{"id":"T22","span":{"begin":1095,"end":1113},"obj":"DNA"},{"id":"T23","span":{"begin":1173,"end":1177},"obj":"protein"},{"id":"T24","span":{"begin":1178,"end":1194},"obj":"DNA"},{"id":"T25","span":{"begin":1306,"end":1319},"obj":"DNA"},{"id":"T26","span":{"begin":1323,"end":1333},"obj":"cell_line"}],"text":"Transcriptional regulation of the pyruvate kinase erythroid-specific promoter.\nMammal pyruvate kinases are encoded by two genes. The L gene produces the erythroid (R-PK) or the hepatic (L-PK) isozymes by the alternative use of two promoters. We report the characterization of the cis- and trans-acting elements involved in the tissue-specific activity of the L gene erythroid promoter. A R-PK DNA fragment extending from -870 to +54 relative to the cap site confers erythroid specificity to a reporter gene. Within this region, we define a minimal promoter (-62 to +54) that displays erythroid-specific activity and contains two DNA binding sites. One, located at -50, binds members of the CCACC/Sp1 family and the other, located at -20, binds the erythroid factor GATA-1. Although the -20 GATA binding site (AGATAA) is also a potential TFIID binding site, it does not bind TFIID. Furthermore, the substitution of this GATA binding site by a canonical TFIID binding site suppresses the promoter activity. Mutations and deletions of both sites indicate that only the association of CCACC/Sp1 and GATA binding sites can drive efficient and tissue-specific expression of this R-PK minimal promoter. Finally, by co-transfection experiments, we study the elements involved in the hGATA-1 transactivation of the R-PK promoter in HeLa cells."}

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":78},"obj":"Sentence"},{"id":"S2","span":{"begin":79,"end":128},"obj":"Sentence"},{"id":"S3","span":{"begin":129,"end":241},"obj":"Sentence"},{"id":"S4","span":{"begin":242,"end":385},"obj":"Sentence"},{"id":"S5","span":{"begin":386,"end":507},"obj":"Sentence"},{"id":"S6","span":{"begin":508,"end":647},"obj":"Sentence"},{"id":"S7","span":{"begin":648,"end":772},"obj":"Sentence"},{"id":"S8","span":{"begin":773,"end":880},"obj":"Sentence"},{"id":"S9","span":{"begin":881,"end":1004},"obj":"Sentence"},{"id":"S10","span":{"begin":1005,"end":1195},"obj":"Sentence"},{"id":"S11","span":{"begin":1196,"end":1334},"obj":"Sentence"}],"text":"Transcriptional regulation of the pyruvate kinase erythroid-specific promoter.\nMammal pyruvate kinases are encoded by two genes. The L gene produces the erythroid (R-PK) or the hepatic (L-PK) isozymes by the alternative use of two promoters. We report the characterization of the cis- and trans-acting elements involved in the tissue-specific activity of the L gene erythroid promoter. A R-PK DNA fragment extending from -870 to +54 relative to the cap site confers erythroid specificity to a reporter gene. Within this region, we define a minimal promoter (-62 to +54) that displays erythroid-specific activity and contains two DNA binding sites. One, located at -50, binds members of the CCACC/Sp1 family and the other, located at -20, binds the erythroid factor GATA-1. Although the -20 GATA binding site (AGATAA) is also a potential TFIID binding site, it does not bind TFIID. Furthermore, the substitution of this GATA binding site by a canonical TFIID binding site suppresses the promoter activity. Mutations and deletions of both sites indicate that only the association of CCACC/Sp1 and GATA binding sites can drive efficient and tissue-specific expression of this R-PK minimal promoter. Finally, by co-transfection experiments, we study the elements involved in the hGATA-1 transactivation of the R-PK promoter in HeLa cells."}

{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":538,"end":569},"obj":"NP"},{"id":"C2","span":{"begin":570,"end":574},"obj":"NP"},{"id":"C3","span":{"begin":686,"end":706},"obj":"NP"},{"id":"C4","span":{"begin":782,"end":816},"obj":"NP"},{"id":"C5","span":{"begin":857,"end":859},"obj":"NP"},{"id":"C6","span":{"begin":914,"end":936},"obj":"NP"},{"id":"C7","span":{"begin":1081,"end":1090},"obj":"NP"},{"id":"C8","span":{"begin":1168,"end":1194},"obj":"NP"},{"id":"C9","span":{"begin":1302,"end":1319},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-relat","subj":"C2","obj":"C1"},{"id":"R2","pred":"coref-pron","subj":"C5","obj":"C4"},{"id":"R3","pred":"coref-ident","subj":"C6","obj":"C4"},{"id":"R4","pred":"coref-ident","subj":"C7","obj":"C3"},{"id":"R5","pred":"coref-ident","subj":"C8","obj":"C1"},{"id":"R6","pred":"coref-ident","subj":"C9","obj":"C8"}],"text":"Transcriptional regulation of the pyruvate kinase erythroid-specific promoter.\nMammal pyruvate kinases are encoded by two genes. The L gene produces the erythroid (R-PK) or the hepatic (L-PK) isozymes by the alternative use of two promoters. We report the characterization of the cis- and trans-acting elements involved in the tissue-specific activity of the L gene erythroid promoter. A R-PK DNA fragment extending from -870 to +54 relative to the cap site confers erythroid specificity to a reporter gene. Within this region, we define a minimal promoter (-62 to +54) that displays erythroid-specific activity and contains two DNA binding sites. One, located at -50, binds members of the CCACC/Sp1 family and the other, located at -20, binds the erythroid factor GATA-1. Although the -20 GATA binding site (AGATAA) is also a potential TFIID binding site, it does not bind TFIID. Furthermore, the substitution of this GATA binding site by a canonical TFIID binding site suppresses the promoter activity. Mutations and deletions of both sites indicate that only the association of CCACC/Sp1 and GATA binding sites can drive efficient and tissue-specific expression of this R-PK minimal promoter. Finally, by co-transfection experiments, we study the elements involved in the hGATA-1 transactivation of the R-PK promoter in HeLa cells."}

{"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":0,"end":26},"obj":"other_name"},{"id":"T2","span":{"begin":34,"end":77},"obj":"DNA_domain_or_region"},{"id":"T3","span":{"begin":79,"end":102},"obj":"protein_family_or_group"},{"id":"T4","span":{"begin":133,"end":139},"obj":"DNA_domain_or_region"},{"id":"T5","span":{"begin":153,"end":162},"obj":"protein_molecule"},{"id":"T6","span":{"begin":164,"end":168},"obj":"protein_molecule"},{"id":"T7","span":{"begin":177,"end":186},"obj":"protein_molecule"},{"id":"T8","span":{"begin":186,"end":190},"obj":"protein_molecule"},{"id":"T9","span":{"begin":231,"end":240},"obj":"DNA_domain_or_region"},{"id":"T10","span":{"begin":359,"end":384},"obj":"DNA_domain_or_region"},{"id":"T11","span":{"begin":388,"end":405},"obj":"DNA_molecule"},{"id":"T12","span":{"begin":449,"end":457},"obj":"DNA_domain_or_region"},{"id":"T13","span":{"begin":493,"end":506},"obj":"DNA_family_or_group"},{"id":"T14","span":{"begin":540,"end":556},"obj":"DNA_domain_or_region"},{"id":"T15","span":{"begin":584,"end":611},"obj":"other_name"},{"id":"T16","span":{"begin":690,"end":706},"obj":"protein_family_or_group"},{"id":"T17","span":{"begin":748,"end":771},"obj":"protein_molecule"},{"id":"T18","span":{"begin":790,"end":807},"obj":"DNA_domain_or_region"},{"id":"T19","span":{"begin":809,"end":815},"obj":"polynucleotide"},{"id":"T20","span":{"begin":837,"end":855},"obj":"DNA_domain_or_region"},{"id":"T21","span":{"begin":874,"end":879},"obj":"protein_molecule"},{"id":"T22","span":{"begin":919,"end":936},"obj":"DNA_domain_or_region"},{"id":"T23","span":{"begin":952,"end":957},"obj":"protein_molecule"},{"id":"T24","span":{"begin":1081,"end":1090},"obj":"protein_molecule"},{"id":"T25","span":{"begin":1095,"end":1113},"obj":"DNA_domain_or_region"},{"id":"T26","span":{"begin":1173,"end":1177},"obj":"protein_molecule"},{"id":"T27","span":{"begin":1178,"end":1194},"obj":"DNA_domain_or_region"},{"id":"T28","span":{"begin":1208,"end":1235},"obj":"other_name"},{"id":"T29","span":{"begin":1275,"end":1298},"obj":"other_name"},{"id":"T30","span":{"begin":1306,"end":1319},"obj":"DNA_domain_or_region"},{"id":"T31","span":{"begin":1323,"end":1333},"obj":"cell_line"}],"text":"Transcriptional regulation of the pyruvate kinase erythroid-specific promoter.\nMammal pyruvate kinases are encoded by two genes. The L gene produces the erythroid (R-PK) or the hepatic (L-PK) isozymes by the alternative use of two promoters. We report the characterization of the cis- and trans-acting elements involved in the tissue-specific activity of the L gene erythroid promoter. A R-PK DNA fragment extending from -870 to +54 relative to the cap site confers erythroid specificity to a reporter gene. Within this region, we define a minimal promoter (-62 to +54) that displays erythroid-specific activity and contains two DNA binding sites. One, located at -50, binds members of the CCACC/Sp1 family and the other, located at -20, binds the erythroid factor GATA-1. Although the -20 GATA binding site (AGATAA) is also a potential TFIID binding site, it does not bind TFIID. Furthermore, the substitution of this GATA binding site by a canonical TFIID binding site suppresses the promoter activity. Mutations and deletions of both sites indicate that only the association of CCACC/Sp1 and GATA binding sites can drive efficient and tissue-specific expression of this R-PK minimal promoter. Finally, by co-transfection experiments, we study the elements involved in the hGATA-1 transactivation of the R-PK promoter in HeLa cells."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":327,"end":333},"obj":"Body_part"},{"id":"T2","span":{"begin":1138,"end":1144},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"Transcriptional regulation of the pyruvate kinase erythroid-specific promoter.\nMammal pyruvate kinases are encoded by two genes. The L gene produces the erythroid (R-PK) or the hepatic (L-PK) isozymes by the alternative use of two promoters. We report the characterization of the cis- and trans-acting elements involved in the tissue-specific activity of the L gene erythroid promoter. A R-PK DNA fragment extending from -870 to +54 relative to the cap site confers erythroid specificity to a reporter gene. Within this region, we define a minimal promoter (-62 to +54) that displays erythroid-specific activity and contains two DNA binding sites. One, located at -50, binds members of the CCACC/Sp1 family and the other, located at -20, binds the erythroid factor GATA-1. Although the -20 GATA binding site (AGATAA) is also a potential TFIID binding site, it does not bind TFIID. Furthermore, the substitution of this GATA binding site by a canonical TFIID binding site suppresses the promoter activity. Mutations and deletions of both sites indicate that only the association of CCACC/Sp1 and GATA binding sites can drive efficient and tissue-specific expression of this R-PK minimal promoter. Finally, by co-transfection experiments, we study the elements involved in the hGATA-1 transactivation of the R-PK promoter in HeLa cells."}