| pubmed-article:10764760 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C1444754 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C0040624 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C0005456 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C1519249 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C0023978 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C1621396 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:10764760 | lifeskim:mentions | umls-concept:C0332183 | lld:lifeskim |
| pubmed-article:10764760 | pubmed:issue | 27 | lld:pubmed |
| pubmed-article:10764760 | pubmed:dateCreated | 2000-8-16 | lld:pubmed |
| pubmed-article:10764760 | pubmed:abstractText | To study the role of MAPK cascades in the regulation of naturally occurring human immunodeficiency virus type 1 long terminal repeats (HIV-1 LTRs), we analyzed several HIV-1 LTRs from patients at different stages of disease progression. One of these naturally occurring HIV-1 LTRs contains an insertion termed the most frequent naturally occurring length polymorphism (MFNLP) and exhibited high inducibility upon T cell activation. We found that the protein kinase mixed lineage kinase 3/src-homology 3 domain-containing proline-rich kinase, a specific activator of the stress-activated protein kinase (SAPK)/JNK signaling pathway in T lymphocytes, induces high transcriptional activation of this promoter. Promoter inducibility is inhibited by the SAPK/JNK inhibitor, the JNK binding domain of the JNK interacting protein 1, and Tam-67 (N-terminal deletion mutant of c-Jun). In electrophoretic mobility shift assay, several protein complexes were found to bind to the MFNLP sequence in T cells. We identified AP-1 factors c-Fos and JunB as MFNLP-binding proteins, whose binding is abolished by introducing point mutations in the 3'-half of the MFNLP sequence. Introduction of these point mutations into the MFNLP containing HIV-1 LTR reduced src-homology 3 domain-containing proline-rich kinase -mediated transactivation. These data indicate that the AP-1-like binding site in the MFNLP sequence gives rise to a higher inducibility of natural HIV-LTRs by the SAPK/JNK signaling pathway. | lld:pubmed |
| pubmed-article:10764760 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10764760 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10764760 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10764760 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10764760 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:10764760 | pubmed:author | pubmed-author:RappU RUR | lld:pubmed |
| pubmed-article:10764760 | pubmed:author | pubmed-author:ChenPP | lld:pubmed |
| pubmed-article:10764760 | pubmed:author | pubmed-author:LudwigSS | lld:pubmed |
| pubmed-article:10764760 | pubmed:author | pubmed-author:FloroSS | lld:pubmed |
| pubmed-article:10764760 | pubmed:author | pubmed-author:KirchhoffFF | lld:pubmed |
| pubmed-article:10764760 | pubmed:author | pubmed-author:AvotsAA | lld:pubmed |
| pubmed-article:10764760 | pubmed:author | pubmed-author:JordanB WBW | lld:pubmed |
| pubmed-article:10764760 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10764760 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:10764760 | pubmed:volume | 275 | lld:pubmed |
| pubmed-article:10764760 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10764760 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10764760 | pubmed:pagination | 20382-90 | lld:pubmed |
| pubmed-article:10764760 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:10764760 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10764760 | pubmed:articleTitle | Transactivation of naturally occurring HIV-1 long terminal repeats by the JNK signaling pathway. The most frequent naturally occurring length polymorphism sequence introduces a novel binding site for AP-1 factors. | lld:pubmed |
| pubmed-article:10764760 | pubmed:affiliation | Institut für Medizinische Strahlenkunde und Zellforschung, Universität Würzburg, Versbacher Strasse 5, D-97078 Würzburg, Germany. | lld:pubmed |
| pubmed-article:10764760 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10764760 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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