PubMed:10770937 JSON TXT

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sentences

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":88},"obj":"Sentence"},{"id":"T2","span":{"begin":89,"end":224},"obj":"Sentence"},{"id":"T3","span":{"begin":225,"end":451},"obj":"Sentence"},{"id":"T4","span":{"begin":452,"end":658},"obj":"Sentence"},{"id":"T5","span":{"begin":659,"end":930},"obj":"Sentence"},{"id":"T6","span":{"begin":931,"end":1052},"obj":"Sentence"},{"id":"T7","span":{"begin":1053,"end":1212},"obj":"Sentence"},{"id":"T8","span":{"begin":1213,"end":1342},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Direct transactivation of the anti-apoptotic gene apolipoprotein J (clusterin) by B-MYB.\nB-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cells."}

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":384,"end":397},"obj":"HP_0003006"},{"id":"T2","span":{"begin":640,"end":645},"obj":"HP_0002664"},{"id":"T3","span":{"begin":1143,"end":1156},"obj":"HP_0003006"}],"text":"Direct transactivation of the anti-apoptotic gene apolipoprotein J (clusterin) by B-MYB.\nB-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cells."}

PennBioIE

{"project":"PennBioIE","denotations":[{"id":"T1","span":{"begin":50,"end":66},"obj":"protein"},{"id":"T2","span":{"begin":68,"end":77},"obj":"protein"},{"id":"T3","span":{"begin":82,"end":87},"obj":"protein"},{"id":"T4","span":{"begin":90,"end":94},"obj":"protein"},{"id":"T5","span":{"begin":250,"end":255},"obj":"protein"},{"id":"T6","span":{"begin":301,"end":306},"obj":"protein"},{"id":"T7","span":{"begin":384,"end":397},"obj":"protein"},{"id":"T8","span":{"begin":434,"end":439},"obj":"protein"},{"id":"T9","span":{"begin":512,"end":517},"obj":"protein"},{"id":"T10","span":{"begin":540,"end":544},"obj":"protein"},{"id":"T11","span":{"begin":545,"end":554},"obj":"protein"},{"id":"T12","span":{"begin":555,"end":560},"obj":"protein"},{"id":"T13","span":{"begin":561,"end":567},"obj":"protein"},{"id":"T14","span":{"begin":570,"end":574},"obj":"protein"},{"id":"T15","span":{"begin":575,"end":584},"obj":"protein"},{"id":"T16","span":{"begin":687,"end":691},"obj":"protein"},{"id":"T17","span":{"begin":692,"end":701},"obj":"protein"},{"id":"T18","span":{"begin":718,"end":721},"obj":"protein"},{"id":"T19","span":{"begin":807,"end":812},"obj":"protein"},{"id":"T20","span":{"begin":834,"end":839},"obj":"protein"},{"id":"T21","span":{"begin":873,"end":877},"obj":"protein"},{"id":"T22","span":{"begin":878,"end":887},"obj":"protein"},{"id":"T23","span":{"begin":942,"end":946},"obj":"protein"},{"id":"T24","span":{"begin":947,"end":956},"obj":"protein"},{"id":"T25","span":{"begin":1041,"end":1046},"obj":"protein"},{"id":"T26","span":{"begin":1074,"end":1083},"obj":"protein"},{"id":"T27","span":{"begin":1089,"end":1108},"obj":"protein"},{"id":"T28","span":{"begin":1143,"end":1156},"obj":"protein"},{"id":"T29","span":{"begin":1233,"end":1237},"obj":"protein"},{"id":"T30","span":{"begin":1238,"end":1247},"obj":"protein"},{"id":"T31","span":{"begin":1251,"end":1256},"obj":"protein"}],"text":"Direct transactivation of the anti-apoptotic gene apolipoprotein J (clusterin) by B-MYB.\nB-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cells."}

DisGeNET5_gene_disease

2015-BEL-Sample-2

{"project":"2015-BEL-Sample-2","denotations":[{"id":"BEL:20043932","span":{"begin":0,"end":1341},"obj":"p(HGNC:MYBL2) increases r(HGNC:CCNA2)"},{"id":"BEL:20043934","span":{"begin":0,"end":1211},"obj":"p(HGNC:MYBL2) increases r(HGNC:CLU)"},{"id":"BEL:20066076","span":{"begin":931,"end":1051},"obj":"tscript(p(HGNC:MYBL2)) increases r(HGNC:CLU)"}],"text":"Direct transactivation of the anti-apoptotic gene apolipoprotein J (clusterin) by B-MYB.\nB-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cells."}

HP-phenotype

{"project":"HP-phenotype","denotations":[{"id":"T1","span":{"begin":384,"end":397},"obj":"Phenotype"},{"id":"T2","span":{"begin":640,"end":645},"obj":"Phenotype"},{"id":"T3","span":{"begin":1143,"end":1156},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0003006"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0002664"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"HP:0003006"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"Direct transactivation of the anti-apoptotic gene apolipoprotein J (clusterin) by B-MYB.\nB-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cells."}

mondo_disease

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":384,"end":397},"obj":"Disease"},{"id":"T2","span":{"begin":640,"end":645},"obj":"Disease"},{"id":"T3","span":{"begin":1143,"end":1156},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0005072"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0005070"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0005072"}],"text":"Direct transactivation of the anti-apoptotic gene apolipoprotein J (clusterin) by B-MYB.\nB-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cells."}

NCBITAXON

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":681,"end":686},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"}],"text":"Direct transactivation of the anti-apoptotic gene apolipoprotein J (clusterin) by B-MYB.\nB-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cells."}

Anatomy-UBERON

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":310,"end":328},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/GO_0042995"}],"text":"Direct transactivation of the anti-apoptotic gene apolipoprotein J (clusterin) by B-MYB.\nB-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cells."}