| pubmed-article:3530501 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3530501 | lifeskim:mentions | umls-concept:C0019682 | lld:lifeskim |
| pubmed-article:3530501 | lifeskim:mentions | umls-concept:C1709305 | lld:lifeskim |
| pubmed-article:3530501 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:3530501 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:3530501 | pubmed:dateCreated | 1986-11-7 | lld:pubmed |
| pubmed-article:3530501 | pubmed:abstractText | A novel, highly quantitative transient expression assay based on the human interleukin-2 (IL-2) gene was used to examine the trans-activation of the Human Immunodeficiency Virus (HIV/HTLV-III/LAV/ARV) long terminal repeat (LTR) in a range of eukaryotic cell lines. In the absence of the trans-activating viral gene product, tat-III, IL-2 transcripts specific for the HIV LTR were present in low abundance in transfected cells and showed a low translational efficiency, when compared with IL-2 mRNAs transcribed from other viral promoters. Coexpression of tat-III resulted in a marked increase in the steady state level of IL-2 mRNAs transcribed from the HIV LTR, and these mRNAs also demonstrated a specific enhancement of their translational efficiency. These results suggest a bimodal mechanism of action for tat-III in the trans-activation of HIV-specific gene expression. | lld:pubmed |
| pubmed-article:3530501 | pubmed:language | eng | lld:pubmed |
| pubmed-article:3530501 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3530501 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:3530501 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:3530501 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:3530501 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3530501 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:3530501 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:3530501 | pubmed:author | pubmed-author:CullenB RBR | lld:pubmed |
| pubmed-article:3530501 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3530501 | pubmed:day | 26 | lld:pubmed |
| pubmed-article:3530501 | pubmed:volume | 46 | lld:pubmed |
| pubmed-article:3530501 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3530501 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3530501 | pubmed:pagination | 973-82 | lld:pubmed |
| pubmed-article:3530501 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:3530501 | pubmed:meshHeading | pubmed-meshheading:3530501-... | lld:pubmed |
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| pubmed-article:3530501 | pubmed:meshHeading | pubmed-meshheading:3530501-... | lld:pubmed |
| pubmed-article:3530501 | pubmed:meshHeading | pubmed-meshheading:3530501-... | lld:pubmed |
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| pubmed-article:3530501 | pubmed:meshHeading | pubmed-meshheading:3530501-... | lld:pubmed |
| pubmed-article:3530501 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:3530501 | pubmed:articleTitle | Trans-activation of human immunodeficiency virus occurs via a bimodal mechanism. | lld:pubmed |
| pubmed-article:3530501 | pubmed:publicationType | Journal Article | lld:pubmed |
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