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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
1996-7-18
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pubmed:abstractText |
The transcription control region of the archetype strain of the human polyomavirus JC virus (JCV(Cy)), unlike its neurotropic counterpart (JCV(Mad-1)), contains only one copy of the 98-bp enhancer/promoter repeat with the 23-bp and the 66-bp insertion blocks. Early studies by us and others have indicated that the structural organization of JCV(Mad-1) is critical for glial cell-specific transcription of the viral genome. In addition, the kappa B regulatory motif found in the JCV(Mad-1) genome, which also exists in JCV(Cy), confers inducibility to the JCV(Mad-1) early and late promoters in response to extracellular stimuli. In this study, we have investigated the regulatory role of the 23- and the 66-bp blocks and their functional relationship to the kappa B motif in stimulating transcription of the Cy early and late promoters in glial cells. We demonstrate that mutations in the kappa B motif reduce the basal activity of the Cy early promoter and decrease the levels of its induction by phorbol myristate acetate or factors derived from activated T cells. Under similar circumstances, mutation in the kappa B motif completely abrogated the basal and the induced levels of transcription of the viral late promoter. Using deletion and hybrid promoter constructs, we have demonstrated that the 23-bp block of the Cy promoter plays a critical role in the observed inactivation of Cy late promoter transcription in glial cells. Results from DNA binding studies have indicated the formation of a common nucleoprotein complex with the 23-bp sequence, mutant kappa B (kappa B(mut)), and wild-type kappa B (kappa B(wt)). Analysis of this complex by UV cross-linking has identified a 40-kDa protein which binds to the 23-bp sequence and the kappa B motif. The importance of these findings for the activation of JCV(Cy) under various physiological conditions is discussed.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-1310194,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-1310438,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-14038684,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-1477668,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-1505523,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-1649346,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-1846488,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-1850021,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-2159570,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-2550676,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-2841118,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-2981353,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-3037497,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-4292395,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-4705382,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-6086957,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-6099652,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-6302172,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-6304749,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-6309442,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-6327777,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-6960240,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-7491753,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-7969118,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-8011280,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-8452515,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8642666-9222338
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-538X
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
70
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2387-93
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8642666-Animals,
pubmed-meshheading:8642666-Binding Sites,
pubmed-meshheading:8642666-Cercopithecus aethiops,
pubmed-meshheading:8642666-DNA, Viral,
pubmed-meshheading:8642666-Gene Expression Regulation, Viral,
pubmed-meshheading:8642666-Genome, Viral,
pubmed-meshheading:8642666-Humans,
pubmed-meshheading:8642666-JC Virus,
pubmed-meshheading:8642666-Kidney,
pubmed-meshheading:8642666-Molecular Sequence Data,
pubmed-meshheading:8642666-Mutagenesis,
pubmed-meshheading:8642666-NF-kappa B,
pubmed-meshheading:8642666-Neuroglia,
pubmed-meshheading:8642666-Nuclear Proteins,
pubmed-meshheading:8642666-Promoter Regions, Genetic,
pubmed-meshheading:8642666-Transcription, Genetic,
pubmed-meshheading:8642666-Tumor Cells, Cultured
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pubmed:year |
1996
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pubmed:articleTitle |
Transcription of the JC virus archetype late genome: importance of the kappa B and the 23-base-pair motifs in late promoter activity in glial cells.
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pubmed:affiliation |
Molecular Neurovirology, Jefferson Institute of Molecular Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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