PubMed:8383844 JSONTXT

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":186},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":187,"end":338},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":339,"end":575},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":576,"end":743},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":744,"end":920},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":921,"end":1067},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":1068,"end":1172},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":1173,"end":1321},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":1322,"end":1403},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":1404,"end":1503},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":1504,"end":1654},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":186},"obj":"Sentence"},{"id":"T2","span":{"begin":187,"end":338},"obj":"Sentence"},{"id":"T3","span":{"begin":339,"end":575},"obj":"Sentence"},{"id":"T4","span":{"begin":576,"end":743},"obj":"Sentence"},{"id":"T5","span":{"begin":744,"end":920},"obj":"Sentence"},{"id":"T6","span":{"begin":921,"end":1067},"obj":"Sentence"},{"id":"T7","span":{"begin":1068,"end":1172},"obj":"Sentence"},{"id":"T8","span":{"begin":1173,"end":1321},"obj":"Sentence"},{"id":"T9","span":{"begin":1322,"end":1403},"obj":"Sentence"},{"id":"T10","span":{"begin":1404,"end":1503},"obj":"Sentence"},{"id":"T11","span":{"begin":1504,"end":1654},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Competition between transcription factors HNF1 and HNF3, and alternative cell-specific activation by DBP and C/EBP contribute to the regulation of the liver-specific aldolase B promoter.\nThe aldolase B proximal promoter is controlled by at least five elements spanning from -190 to -103 bp with respect to the start site of transcription. From 5' to 3', we found: a negative DE element, an activating C/EBP-DBP binding site, a CCAAT box binding NFY that seems to play a negative role, and an activating element consisting of two overlapping binding sites for HNF-1 and HNF-3. Contransfection experiments of aldolase B/CAT constructs and of expression vectors for different transcription factors were carried out in human hepatoma Hep G2 cells. We found that DBP and HNF-1 are strong transactivators of the aldolase B promoter while C/EBP and vHNF-1 are only weak activators and HNF-3 alone does not modify such activity. Deletion of the distal negative element results in a similar transactivation by C/EBP and DBP, enhanced for the former and reduced for the latter. In hepatocytes in primary culture, the strong transactivator is C/EBP while DBP is essentially inactive. This tissue-specificity of C/EBP and DBP action could depend on interaction with tissue-specific proteins bound to a neighbouring site, probably DE. Finally, HNF3 behaves as a very strong anti-activator of the aldolase B promoter. It competitively antagonizes transactivation by HNF-1 and non-competitively transactivation by DBP. This negative effect of HNF-3 and tissue-specificity of the transactivation potential of DBP and C/EBP are unique features of the aldolase B promoter."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":618,"end":621},"obj":"gene:847"},{"id":"T1","span":{"begin":721,"end":729},"obj":"disease:C0023903"},{"id":"T2","span":{"begin":618,"end":621},"obj":"gene:847"},{"id":"T3","span":{"begin":721,"end":729},"obj":"disease:C2239176"},{"id":"T4","span":{"begin":618,"end":621},"obj":"gene:1384"},{"id":"T5","span":{"begin":721,"end":729},"obj":"disease:C0023903"},{"id":"T6","span":{"begin":618,"end":621},"obj":"gene:1384"},{"id":"T7","span":{"begin":721,"end":729},"obj":"disease:C2239176"},{"id":"T8","span":{"begin":618,"end":621},"obj":"gene:10249"},{"id":"T9","span":{"begin":721,"end":729},"obj":"disease:C0023903"},{"id":"T10","span":{"begin":618,"end":621},"obj":"gene:10249"},{"id":"T11","span":{"begin":721,"end":729},"obj":"disease:C2239176"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"},{"id":"R4","pred":"associated_with","subj":"T6","obj":"T7"},{"id":"R5","pred":"associated_with","subj":"T8","obj":"T9"},{"id":"R6","pred":"associated_with","subj":"T10","obj":"T11"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Competition between transcription factors HNF1 and HNF3, and alternative cell-specific activation by DBP and C/EBP contribute to the regulation of the liver-specific aldolase B promoter.\nThe aldolase B proximal promoter is controlled by at least five elements spanning from -190 to -103 bp with respect to the start site of transcription. From 5' to 3', we found: a negative DE element, an activating C/EBP-DBP binding site, a CCAAT box binding NFY that seems to play a negative role, and an activating element consisting of two overlapping binding sites for HNF-1 and HNF-3. Contransfection experiments of aldolase B/CAT constructs and of expression vectors for different transcription factors were carried out in human hepatoma Hep G2 cells. We found that DBP and HNF-1 are strong transactivators of the aldolase B promoter while C/EBP and vHNF-1 are only weak activators and HNF-3 alone does not modify such activity. Deletion of the distal negative element results in a similar transactivation by C/EBP and DBP, enhanced for the former and reduced for the latter. In hepatocytes in primary culture, the strong transactivator is C/EBP while DBP is essentially inactive. This tissue-specificity of C/EBP and DBP action could depend on interaction with tissue-specific proteins bound to a neighbouring site, probably DE. Finally, HNF3 behaves as a very strong anti-activator of the aldolase B promoter. It competitively antagonizes transactivation by HNF-1 and non-competitively transactivation by DBP. This negative effect of HNF-3 and tissue-specificity of the transactivation potential of DBP and C/EBP are unique features of the aldolase B promoter."}

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T810","span":{"begin":618,"end":621},"obj":"gene:847"},{"id":"T811","span":{"begin":721,"end":729},"obj":"disease:C0023903"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T810","obj":"T811"},{"id":"R2","pred":"associated_with","subj":"T810","obj":"T811"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Competition between transcription factors HNF1 and HNF3, and alternative cell-specific activation by DBP and C/EBP contribute to the regulation of the liver-specific aldolase B promoter.\nThe aldolase B proximal promoter is controlled by at least five elements spanning from -190 to -103 bp with respect to the start site of transcription. From 5' to 3', we found: a negative DE element, an activating C/EBP-DBP binding site, a CCAAT box binding NFY that seems to play a negative role, and an activating element consisting of two overlapping binding sites for HNF-1 and HNF-3. Contransfection experiments of aldolase B/CAT constructs and of expression vectors for different transcription factors were carried out in human hepatoma Hep G2 cells. We found that DBP and HNF-1 are strong transactivators of the aldolase B promoter while C/EBP and vHNF-1 are only weak activators and HNF-3 alone does not modify such activity. Deletion of the distal negative element results in a similar transactivation by C/EBP and DBP, enhanced for the former and reduced for the latter. In hepatocytes in primary culture, the strong transactivator is C/EBP while DBP is essentially inactive. This tissue-specificity of C/EBP and DBP action could depend on interaction with tissue-specific proteins bound to a neighbouring site, probably DE. Finally, HNF3 behaves as a very strong anti-activator of the aldolase B promoter. It competitively antagonizes transactivation by HNF-1 and non-competitively transactivation by DBP. This negative effect of HNF-3 and tissue-specificity of the transactivation potential of DBP and C/EBP are unique features of the aldolase B promoter."}

{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":151,"end":156},"obj":"http://purl.obolibrary.org/obo/UBERON_0002107"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1178,"end":1184},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":1254,"end":1260},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1538,"end":1544},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"Competition between transcription factors HNF1 and HNF3, and alternative cell-specific activation by DBP and C/EBP contribute to the regulation of the liver-specific aldolase B promoter.\nThe aldolase B proximal promoter is controlled by at least five elements spanning from -190 to -103 bp with respect to the start site of transcription. From 5' to 3', we found: a negative DE element, an activating C/EBP-DBP binding site, a CCAAT box binding NFY that seems to play a negative role, and an activating element consisting of two overlapping binding sites for HNF-1 and HNF-3. Contransfection experiments of aldolase B/CAT constructs and of expression vectors for different transcription factors were carried out in human hepatoma Hep G2 cells. We found that DBP and HNF-1 are strong transactivators of the aldolase B promoter while C/EBP and vHNF-1 are only weak activators and HNF-3 alone does not modify such activity. Deletion of the distal negative element results in a similar transactivation by C/EBP and DBP, enhanced for the former and reduced for the latter. In hepatocytes in primary culture, the strong transactivator is C/EBP while DBP is essentially inactive. This tissue-specificity of C/EBP and DBP action could depend on interaction with tissue-specific proteins bound to a neighbouring site, probably DE. Finally, HNF3 behaves as a very strong anti-activator of the aldolase B promoter. It competitively antagonizes transactivation by HNF-1 and non-competitively transactivation by DBP. This negative effect of HNF-3 and tissue-specificity of the transactivation potential of DBP and C/EBP are unique features of the aldolase B promoter."}

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":1178,"end":1184},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1254,"end":1260},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":1538,"end":1544},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":151,"end":156},"obj":"http://purl.obolibrary.org/obo/UBERON_0002107"}],"text":"Competition between transcription factors HNF1 and HNF3, and alternative cell-specific activation by DBP and C/EBP contribute to the regulation of the liver-specific aldolase B promoter.\nThe aldolase B proximal promoter is controlled by at least five elements spanning from -190 to -103 bp with respect to the start site of transcription. From 5' to 3', we found: a negative DE element, an activating C/EBP-DBP binding site, a CCAAT box binding NFY that seems to play a negative role, and an activating element consisting of two overlapping binding sites for HNF-1 and HNF-3. Contransfection experiments of aldolase B/CAT constructs and of expression vectors for different transcription factors were carried out in human hepatoma Hep G2 cells. We found that DBP and HNF-1 are strong transactivators of the aldolase B promoter while C/EBP and vHNF-1 are only weak activators and HNF-3 alone does not modify such activity. Deletion of the distal negative element results in a similar transactivation by C/EBP and DBP, enhanced for the former and reduced for the latter. In hepatocytes in primary culture, the strong transactivator is C/EBP while DBP is essentially inactive. This tissue-specificity of C/EBP and DBP action could depend on interaction with tissue-specific proteins bound to a neighbouring site, probably DE. Finally, HNF3 behaves as a very strong anti-activator of the aldolase B promoter. It competitively antagonizes transactivation by HNF-1 and non-competitively transactivation by DBP. This negative effect of HNF-3 and tissue-specificity of the transactivation potential of DBP and C/EBP are unique features of the aldolase B promoter."}