PubMed:7585505 JSONTXT

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":1023,"end":1026},"obj":"gene:3565"},{"id":"T1","span":{"begin":1114,"end":1128},"obj":"disease:C0149678"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"The normal cell cycle activation program is exploited during the infection of quiescent B lymphocytes by Epstein-Barr virus.\nB lymphocytes in the peripheral circulation are maintained in a non-proliferative state. Antigen recognition stimulates limited proliferation, whereas infection with Epstein-Barr virus (EBV) results in continual proliferation and the outgrowth of immortal cell lines. Because it is not clear at which point in cell cycle the peripheral B lymphocytes are arrested, we characterized the expression of several cell cycle-associated genes in quiescent and stimulated cells. We show that the expression of four cell genes, cdc-2, cyclin E, CD23, and cyclin D2, are up-regulated approximately 100-fold as a result of EBV-mediated immortalization. Because these genes play a positive role in cell proliferation, we suggest that this regulatory switch contributes to controlling entry into the cell cycle. Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40, anti-IgM, and IL4, or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation."}

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":78,"end":101},"obj":"cell_type"},{"id":"T2","span":{"begin":125,"end":138},"obj":"cell_type"},{"id":"T3","span":{"begin":372,"end":391},"obj":"cell_line"},{"id":"T4","span":{"begin":450,"end":474},"obj":"cell_type"},{"id":"T5","span":{"begin":532,"end":559},"obj":"DNA"},{"id":"T6","span":{"begin":563,"end":593},"obj":"cell_type"},{"id":"T7","span":{"begin":631,"end":641},"obj":"DNA"},{"id":"T8","span":{"begin":643,"end":648},"obj":"DNA"},{"id":"T9","span":{"begin":650,"end":658},"obj":"DNA"},{"id":"T10","span":{"begin":660,"end":664},"obj":"DNA"},{"id":"T11","span":{"begin":670,"end":679},"obj":"DNA"},{"id":"T12","span":{"begin":948,"end":971},"obj":"cell_type"},{"id":"T13","span":{"begin":998,"end":1007},"obj":"protein"},{"id":"T14","span":{"begin":1009,"end":1017},"obj":"protein"},{"id":"T15","span":{"begin":1023,"end":1026},"obj":"protein"},{"id":"T16","span":{"begin":1160,"end":1172},"obj":"cell_type"}],"text":"The normal cell cycle activation program is exploited during the infection of quiescent B lymphocytes by Epstein-Barr virus.\nB lymphocytes in the peripheral circulation are maintained in a non-proliferative state. Antigen recognition stimulates limited proliferation, whereas infection with Epstein-Barr virus (EBV) results in continual proliferation and the outgrowth of immortal cell lines. Because it is not clear at which point in cell cycle the peripheral B lymphocytes are arrested, we characterized the expression of several cell cycle-associated genes in quiescent and stimulated cells. We show that the expression of four cell genes, cdc-2, cyclin E, CD23, and cyclin D2, are up-regulated approximately 100-fold as a result of EBV-mediated immortalization. Because these genes play a positive role in cell proliferation, we suggest that this regulatory switch contributes to controlling entry into the cell cycle. Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40, anti-IgM, and IL4, or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"7585505-6#100#103#gene3565","span":{"begin":1023,"end":1026},"obj":"gene3565"},{"id":"7585505-6#191#205#diseaseC0149678","span":{"begin":1114,"end":1128},"obj":"diseaseC0149678"}],"relations":[{"id":"100#103#gene3565191#205#diseaseC0149678","pred":"associated_with","subj":"7585505-6#100#103#gene3565","obj":"7585505-6#191#205#diseaseC0149678"}],"text":"The normal cell cycle activation program is exploited during the infection of quiescent B lymphocytes by Epstein-Barr virus.\nB lymphocytes in the peripheral circulation are maintained in a non-proliferative state. Antigen recognition stimulates limited proliferation, whereas infection with Epstein-Barr virus (EBV) results in continual proliferation and the outgrowth of immortal cell lines. Because it is not clear at which point in cell cycle the peripheral B lymphocytes are arrested, we characterized the expression of several cell cycle-associated genes in quiescent and stimulated cells. We show that the expression of four cell genes, cdc-2, cyclin E, CD23, and cyclin D2, are up-regulated approximately 100-fold as a result of EBV-mediated immortalization. Because these genes play a positive role in cell proliferation, we suggest that this regulatory switch contributes to controlling entry into the cell cycle. Transient stimulation of quiescent B lymphocytes with either a cocktail of anti-CD40, anti-IgM, and IL4, or EBV results in the rapid expression of the same four genes, suggesting that, after infection, EBV exploits the normal program of B-lymphocyte cell cycle activation."}

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