| pubmed-article:1309259 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1309259 | lifeskim:mentions | umls-concept:C0014644 | lld:lifeskim |
| pubmed-article:1309259 | lifeskim:mentions | umls-concept:C1819995 | lld:lifeskim |
| pubmed-article:1309259 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:1309259 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:1309259 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:1309259 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:1309259 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1309259 | pubmed:dateCreated | 1992-1-17 | lld:pubmed |
| pubmed-article:1309259 | pubmed:abstractText | The six latent-cycle nuclear antigens (EBNAs) of Epstein-Barr virus (EBV), whose genes share 5' leader exons and two promoters (Cp and Wp), are differentially expressed by cells of the B lineage. To examine the possibility that EBNA gene expression is regulated through selective use of Cp and Wp, we monitored the activity of promoter-chloramphenicol acetyltransferase (CAT) gene constructs transfected into EBV-positive and EBV-negative B lymphocytes and Burkitt's lymphoma cells. Wp was a much stronger promoter than Cp in EBV genome-negative B-cell lines and was used exclusively in primary B cells. When B cells were infected with transforming EBV, Cp became the stronger promoter. This switch was not observed when B cells were infected with an immortalization-deficient virus, P3HR-1, which lacks the EBNA-2 open reading frame and expresses a mutant leader protein (EBNA-LP). Cp function was transactivated when EBV-negative or P3HR-1-infected B cells were cotransfected with Cp and a 12-kb fragment of DNA (BamHI-WWYH) that spanned the P3HR-1 deletion. This activity was mapped to the EBNA-2 gene within WWYH; constructs expressing EBNA-LP did not induce Cp function, and the deletion of 405 bp from the EBNA-2 open reading frame abolished transactivation. This research demonstrates host cell and EBNA-2 regulation of latent-cycle promoter activity in B lymphocytes, a mechanism with implications for persistence of EBV-infected lymphoid cells in vivo. | lld:pubmed |
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| pubmed-article:1309259 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1309259 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1309259 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1309259 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1309259 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:1309259 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:1309259 | pubmed:author | pubmed-author:AllanGG | lld:pubmed |
| pubmed-article:1309259 | pubmed:author | pubmed-author:FarrellP JPJ | lld:pubmed |
| pubmed-article:1309259 | pubmed:author | pubmed-author:RooneyC MCM | lld:pubmed |
| pubmed-article:1309259 | pubmed:author | pubmed-author:BuschleMM | lld:pubmed |
| pubmed-article:1309259 | pubmed:author | pubmed-author:KolmanJ LJL | lld:pubmed |
| pubmed-article:1309259 | pubmed:author | pubmed-author:BrimmellMM | lld:pubmed |
| pubmed-article:1309259 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1309259 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:1309259 | pubmed:geneSymbol | EBNA | lld:pubmed |
| pubmed-article:1309259 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1309259 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1309259 | pubmed:pagination | 496-504 | lld:pubmed |
| pubmed-article:1309259 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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| pubmed-article:1309259 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1309259 | pubmed:articleTitle | Host cell and EBNA-2 regulation of Epstein-Barr virus latent-cycle promoter activity in B lymphocytes. | lld:pubmed |
| pubmed-article:1309259 | pubmed:affiliation | St. Jude Children's Research Hospital, Memphis, Tennessee 38103. | lld:pubmed |
| pubmed-article:1309259 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1309259 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1309259 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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