PubMed:9115242 JSONTXT

{"project":"CL-cell","denotations":[{"id":"T1","span":{"begin":61,"end":69},"obj":"Cell"},{"id":"T3","span":{"begin":281,"end":290},"obj":"Cell"},{"id":"T5","span":{"begin":919,"end":930},"obj":"Cell"},{"id":"T6","span":{"begin":1433,"end":1442},"obj":"Cell"},{"id":"T8","span":{"begin":1804,"end":1815},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000576"},{"id":"A2","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0001054"},{"id":"A3","pred":"cl_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL:0000576"},{"id":"A4","pred":"cl_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL:0001054"},{"id":"A5","pred":"cl_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CL:0000057"},{"id":"A6","pred":"cl_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CL:0000576"},{"id":"A7","pred":"cl_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CL:0001054"},{"id":"A8","pred":"cl_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/CL:0000235"},{"id":"A9","pred":"cl_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/CL:0000394"}],"text":"Transcriptional induction of collagenase-1 in differentiated monocyte-like (U937) cells is regulated by AP-1 and an upstream C/EBP-beta site.\nIn this report, we demonstrate that the AP-1 site and a distal promoter element regulate transcriptional induction of collagenase-1 during monocytic differentiation. Chloramphenicol acetyltransferase expression constructs containing regions of the human collagenase-1 promoter were stably or transiently transfected into U937 cells, and reporter activity was assessed at various times after the onset of phorbol 12-myristate 13-acetate (PMA)-mediated differentiation. Rapid and strong induction of promoter activity was lost in constructs with a mutant AP-1 element; however, at 16-96 h post-PMA, the mutant collagenase-1 promoter displayed AP-1 independent PMA-mediated transactivation. The AP-1 mutant constructs also showed delayed transcriptional activation in PMA-treated fibroblasts. Western and supershift analyses indicated that functional Jun and Fos proteins were present in nuclear extracts of PMA-differentiated U937 cells. Promoter deletion constructs demonstrated the potential role of distal promoter sequences in regulating collagenase-1 transcription. In particular, Western, supershift, and promoter deletion analyses suggested a role for CCAAT/enhancer-binding protein-beta (C/EBP-beta) binding site between -2010 and -1954 in regulating transcription of collagenase-1 in monocytic cells. Our findings suggest that distinct regulatory elements, acting somewhat independently of each other, control expression of collagenase-1. In addition, our data suggests that the rapid PMA-mediated induction of collagenase-1 transcription is controlled by a mechanism distinct from that regulating the sustained expression of this proteinase in activated macrophages."}

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":141},"obj":"Sentence"},{"id":"T2","span":{"begin":142,"end":307},"obj":"Sentence"},{"id":"T3","span":{"begin":308,"end":609},"obj":"Sentence"},{"id":"T4","span":{"begin":610,"end":829},"obj":"Sentence"},{"id":"T5","span":{"begin":830,"end":931},"obj":"Sentence"},{"id":"T6","span":{"begin":932,"end":1077},"obj":"Sentence"},{"id":"T7","span":{"begin":1078,"end":1210},"obj":"Sentence"},{"id":"T8","span":{"begin":1211,"end":1449},"obj":"Sentence"},{"id":"T9","span":{"begin":1450,"end":1587},"obj":"Sentence"},{"id":"T10","span":{"begin":1588,"end":1816},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":141},"obj":"Sentence"},{"id":"T2","span":{"begin":142,"end":307},"obj":"Sentence"},{"id":"T3","span":{"begin":308,"end":609},"obj":"Sentence"},{"id":"T4","span":{"begin":610,"end":829},"obj":"Sentence"},{"id":"T5","span":{"begin":830,"end":931},"obj":"Sentence"},{"id":"T6","span":{"begin":932,"end":1077},"obj":"Sentence"},{"id":"T7","span":{"begin":1078,"end":1210},"obj":"Sentence"},{"id":"T8","span":{"begin":1211,"end":1449},"obj":"Sentence"},{"id":"T9","span":{"begin":1450,"end":1587},"obj":"Sentence"},{"id":"T10","span":{"begin":1588,"end":1816},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Transcriptional induction of collagenase-1 in differentiated monocyte-like (U937) cells is regulated by AP-1 and an upstream C/EBP-beta site.\nIn this report, we demonstrate that the AP-1 site and a distal promoter element regulate transcriptional induction of collagenase-1 during monocytic differentiation. Chloramphenicol acetyltransferase expression constructs containing regions of the human collagenase-1 promoter were stably or transiently transfected into U937 cells, and reporter activity was assessed at various times after the onset of phorbol 12-myristate 13-acetate (PMA)-mediated differentiation. Rapid and strong induction of promoter activity was lost in constructs with a mutant AP-1 element; however, at 16-96 h post-PMA, the mutant collagenase-1 promoter displayed AP-1 independent PMA-mediated transactivation. The AP-1 mutant constructs also showed delayed transcriptional activation in PMA-treated fibroblasts. Western and supershift analyses indicated that functional Jun and Fos proteins were present in nuclear extracts of PMA-differentiated U937 cells. Promoter deletion constructs demonstrated the potential role of distal promoter sequences in regulating collagenase-1 transcription. In particular, Western, supershift, and promoter deletion analyses suggested a role for CCAAT/enhancer-binding protein-beta (C/EBP-beta) binding site between -2010 and -1954 in regulating transcription of collagenase-1 in monocytic cells. Our findings suggest that distinct regulatory elements, acting somewhat independently of each other, control expression of collagenase-1. In addition, our data suggests that the rapid PMA-mediated induction of collagenase-1 transcription is controlled by a mechanism distinct from that regulating the sustained expression of this proteinase in activated macrophages."}

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":29,"end":42},"obj":"protein"},{"id":"T2","span":{"begin":46,"end":87},"obj":"cell_line"},{"id":"T3","span":{"begin":104,"end":108},"obj":"protein"},{"id":"T4","span":{"begin":116,"end":140},"obj":"DNA"},{"id":"T5","span":{"begin":182,"end":186},"obj":"protein"},{"id":"T6","span":{"begin":198,"end":221},"obj":"DNA"},{"id":"T7","span":{"begin":260,"end":273},"obj":"protein"},{"id":"T8","span":{"begin":308,"end":363},"obj":"DNA"},{"id":"T9","span":{"begin":390,"end":418},"obj":"DNA"},{"id":"T10","span":{"begin":463,"end":473},"obj":"cell_line"},{"id":"T11","span":{"begin":688,"end":707},"obj":"DNA"},{"id":"T12","span":{"begin":743,"end":772},"obj":"DNA"},{"id":"T13","span":{"begin":783,"end":787},"obj":"protein"},{"id":"T14","span":{"begin":834,"end":856},"obj":"DNA"},{"id":"T15","span":{"begin":907,"end":930},"obj":"cell_line"},{"id":"T16","span":{"begin":979,"end":1010},"obj":"protein"},{"id":"T17","span":{"begin":1047,"end":1076},"obj":"cell_line"},{"id":"T18","span":{"begin":1142,"end":1167},"obj":"DNA"},{"id":"T19","span":{"begin":1182,"end":1195},"obj":"protein"},{"id":"T20","span":{"begin":1299,"end":1360},"obj":"DNA"},{"id":"T21","span":{"begin":1369,"end":1384},"obj":"DNA"},{"id":"T22","span":{"begin":1416,"end":1429},"obj":"protein"},{"id":"T23","span":{"begin":1433,"end":1448},"obj":"cell_type"},{"id":"T24","span":{"begin":1485,"end":1504},"obj":"DNA"},{"id":"T25","span":{"begin":1573,"end":1586},"obj":"protein"},{"id":"T26","span":{"begin":1660,"end":1673},"obj":"protein"},{"id":"T27","span":{"begin":1780,"end":1790},"obj":"protein"},{"id":"T28","span":{"begin":1794,"end":1815},"obj":"cell_type"}],"text":"Transcriptional induction of collagenase-1 in differentiated monocyte-like (U937) cells is regulated by AP-1 and an upstream C/EBP-beta site.\nIn this report, we demonstrate that the AP-1 site and a distal promoter element regulate transcriptional induction of collagenase-1 during monocytic differentiation. Chloramphenicol acetyltransferase expression constructs containing regions of the human collagenase-1 promoter were stably or transiently transfected into U937 cells, and reporter activity was assessed at various times after the onset of phorbol 12-myristate 13-acetate (PMA)-mediated differentiation. Rapid and strong induction of promoter activity was lost in constructs with a mutant AP-1 element; however, at 16-96 h post-PMA, the mutant collagenase-1 promoter displayed AP-1 independent PMA-mediated transactivation. The AP-1 mutant constructs also showed delayed transcriptional activation in PMA-treated fibroblasts. Western and supershift analyses indicated that functional Jun and Fos proteins were present in nuclear extracts of PMA-differentiated U937 cells. Promoter deletion constructs demonstrated the potential role of distal promoter sequences in regulating collagenase-1 transcription. In particular, Western, supershift, and promoter deletion analyses suggested a role for CCAAT/enhancer-binding protein-beta (C/EBP-beta) binding site between -2010 and -1954 in regulating transcription of collagenase-1 in monocytic cells. Our findings suggest that distinct regulatory elements, acting somewhat independently of each other, control expression of collagenase-1. In addition, our data suggests that the rapid PMA-mediated induction of collagenase-1 transcription is controlled by a mechanism distinct from that regulating the sustained expression of this proteinase in activated macrophages."}

{"project":"genia-medco-coref","denotations":[{"id":"C2","span":{"begin":29,"end":42},"obj":"NP"},{"id":"C1","span":{"begin":0,"end":42},"obj":"NP"},{"id":"C3","span":{"begin":113,"end":140},"obj":"NP"},{"id":"C5","span":{"begin":260,"end":273},"obj":"NP"},{"id":"C4","span":{"begin":231,"end":273},"obj":"NP"},{"id":"C6","span":{"begin":1182,"end":1209},"obj":"NP"},{"id":"C7","span":{"begin":1299,"end":1384},"obj":"NP"},{"id":"C9","span":{"begin":1416,"end":1429},"obj":"NP"},{"id":"C8","span":{"begin":1399,"end":1429},"obj":"NP"},{"id":"C10","span":{"begin":1573,"end":1586},"obj":"NP"},{"id":"C11","span":{"begin":1660,"end":1687},"obj":"NP"},{"id":"C12","span":{"begin":1705,"end":1716},"obj":"NP"},{"id":"C13","span":{"begin":1731,"end":1735},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C5","obj":"C2"},{"id":"R2","pred":"coref-ident","subj":"C4","obj":"C1"},{"id":"R3","pred":"coref-ident","subj":"C7","obj":"C3"},{"id":"R4","pred":"coref-ident","subj":"C9","obj":"C5"},{"id":"R5","pred":"coref-ident","subj":"C8","obj":"C6"},{"id":"R6","pred":"coref-ident","subj":"C10","obj":"C9"},{"id":"R7","pred":"coref-ident","subj":"C11","obj":"C8"},{"id":"R8","pred":"coref-pron","subj":"C13","obj":"C12"}],"text":"Transcriptional induction of collagenase-1 in differentiated monocyte-like (U937) cells is regulated by AP-1 and an upstream C/EBP-beta site.\nIn this report, we demonstrate that the AP-1 site and a distal promoter element regulate transcriptional induction of collagenase-1 during monocytic differentiation. Chloramphenicol acetyltransferase expression constructs containing regions of the human collagenase-1 promoter were stably or transiently transfected into U937 cells, and reporter activity was assessed at various times after the onset of phorbol 12-myristate 13-acetate (PMA)-mediated differentiation. Rapid and strong induction of promoter activity was lost in constructs with a mutant AP-1 element; however, at 16-96 h post-PMA, the mutant collagenase-1 promoter displayed AP-1 independent PMA-mediated transactivation. The AP-1 mutant constructs also showed delayed transcriptional activation in PMA-treated fibroblasts. Western and supershift analyses indicated that functional Jun and Fos proteins were present in nuclear extracts of PMA-differentiated U937 cells. Promoter deletion constructs demonstrated the potential role of distal promoter sequences in regulating collagenase-1 transcription. In particular, Western, supershift, and promoter deletion analyses suggested a role for CCAAT/enhancer-binding protein-beta (C/EBP-beta) binding site between -2010 and -1954 in regulating transcription of collagenase-1 in monocytic cells. Our findings suggest that distinct regulatory elements, acting somewhat independently of each other, control expression of collagenase-1. In addition, our data suggests that the rapid PMA-mediated induction of collagenase-1 transcription is controlled by a mechanism distinct from that regulating the sustained expression of this proteinase in activated macrophages."}

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{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":579,"end":582},"obj":"Disease"},{"id":"T3","span":{"begin":734,"end":737},"obj":"Disease"},{"id":"T5","span":{"begin":800,"end":803},"obj":"Disease"},{"id":"T7","span":{"begin":907,"end":910},"obj":"Disease"},{"id":"T9","span":{"begin":1047,"end":1050},"obj":"Disease"},{"id":"T11","span":{"begin":1634,"end":1637},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0016692"},{"id":"A2","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0018687"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0016692"},{"id":"A4","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0018687"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MONDO_0016692"},{"id":"A6","pred":"mondo_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MONDO_0018687"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MONDO_0016692"},{"id":"A8","pred":"mondo_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MONDO_0018687"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/MONDO_0016692"},{"id":"A10","pred":"mondo_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/MONDO_0018687"},{"id":"A11","pred":"mondo_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/MONDO_0016692"},{"id":"A12","pred":"mondo_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/MONDO_0018687"}],"text":"Transcriptional induction of collagenase-1 in differentiated monocyte-like (U937) cells is regulated by AP-1 and an upstream C/EBP-beta site.\nIn this report, we demonstrate that the AP-1 site and a distal promoter element regulate transcriptional induction of collagenase-1 during monocytic differentiation. Chloramphenicol acetyltransferase expression constructs containing regions of the human collagenase-1 promoter were stably or transiently transfected into U937 cells, and reporter activity was assessed at various times after the onset of phorbol 12-myristate 13-acetate (PMA)-mediated differentiation. Rapid and strong induction of promoter activity was lost in constructs with a mutant AP-1 element; however, at 16-96 h post-PMA, the mutant collagenase-1 promoter displayed AP-1 independent PMA-mediated transactivation. The AP-1 mutant constructs also showed delayed transcriptional activation in PMA-treated fibroblasts. Western and supershift analyses indicated that functional Jun and Fos proteins were present in nuclear extracts of PMA-differentiated U937 cells. Promoter deletion constructs demonstrated the potential role of distal promoter sequences in regulating collagenase-1 transcription. In particular, Western, supershift, and promoter deletion analyses suggested a role for CCAAT/enhancer-binding protein-beta (C/EBP-beta) binding site between -2010 and -1954 in regulating transcription of collagenase-1 in monocytic cells. Our findings suggest that distinct regulatory elements, acting somewhat independently of each other, control expression of collagenase-1. In addition, our data suggests that the rapid PMA-mediated induction of collagenase-1 transcription is controlled by a mechanism distinct from that regulating the sustained expression of this proteinase in activated macrophages."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":390,"end":395},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"}],"text":"Transcriptional induction of collagenase-1 in differentiated monocyte-like (U937) cells is regulated by AP-1 and an upstream C/EBP-beta site.\nIn this report, we demonstrate that the AP-1 site and a distal promoter element regulate transcriptional induction of collagenase-1 during monocytic differentiation. Chloramphenicol acetyltransferase expression constructs containing regions of the human collagenase-1 promoter were stably or transiently transfected into U937 cells, and reporter activity was assessed at various times after the onset of phorbol 12-myristate 13-acetate (PMA)-mediated differentiation. Rapid and strong induction of promoter activity was lost in constructs with a mutant AP-1 element; however, at 16-96 h post-PMA, the mutant collagenase-1 promoter displayed AP-1 independent PMA-mediated transactivation. The AP-1 mutant constructs also showed delayed transcriptional activation in PMA-treated fibroblasts. Western and supershift analyses indicated that functional Jun and Fos proteins were present in nuclear extracts of PMA-differentiated U937 cells. Promoter deletion constructs demonstrated the potential role of distal promoter sequences in regulating collagenase-1 transcription. In particular, Western, supershift, and promoter deletion analyses suggested a role for CCAAT/enhancer-binding protein-beta (C/EBP-beta) binding site between -2010 and -1954 in regulating transcription of collagenase-1 in monocytic cells. Our findings suggest that distinct regulatory elements, acting somewhat independently of each other, control expression of collagenase-1. In addition, our data suggests that the rapid PMA-mediated induction of collagenase-1 transcription is controlled by a mechanism distinct from that regulating the sustained expression of this proteinase in activated macrophages."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":61,"end":69},"obj":"Body_part"},{"id":"T3","span":{"begin":919,"end":930},"obj":"Body_part"},{"id":"T4","span":{"begin":1804,"end":1815},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL_0000576"},{"id":"A2","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL_0001054"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL_0000057"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL_0000235"}],"text":"Transcriptional induction of collagenase-1 in differentiated monocyte-like (U937) cells is regulated by AP-1 and an upstream C/EBP-beta site.\nIn this report, we demonstrate that the AP-1 site and a distal promoter element regulate transcriptional induction of collagenase-1 during monocytic differentiation. Chloramphenicol acetyltransferase expression constructs containing regions of the human collagenase-1 promoter were stably or transiently transfected into U937 cells, and reporter activity was assessed at various times after the onset of phorbol 12-myristate 13-acetate (PMA)-mediated differentiation. Rapid and strong induction of promoter activity was lost in constructs with a mutant AP-1 element; however, at 16-96 h post-PMA, the mutant collagenase-1 promoter displayed AP-1 independent PMA-mediated transactivation. The AP-1 mutant constructs also showed delayed transcriptional activation in PMA-treated fibroblasts. Western and supershift analyses indicated that functional Jun and Fos proteins were present in nuclear extracts of PMA-differentiated U937 cells. Promoter deletion constructs demonstrated the potential role of distal promoter sequences in regulating collagenase-1 transcription. In particular, Western, supershift, and promoter deletion analyses suggested a role for CCAAT/enhancer-binding protein-beta (C/EBP-beta) binding site between -2010 and -1954 in regulating transcription of collagenase-1 in monocytic cells. Our findings suggest that distinct regulatory elements, acting somewhat independently of each other, control expression of collagenase-1. In addition, our data suggests that the rapid PMA-mediated induction of collagenase-1 transcription is controlled by a mechanism distinct from that regulating the sustained expression of this proteinase in activated macrophages."}