| pubmed-article:2760991 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2760991 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:2760991 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:2760991 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:2760991 | lifeskim:mentions | umls-concept:C0598312 | lld:lifeskim |
| pubmed-article:2760991 | lifeskim:mentions | umls-concept:C0023978 | lld:lifeskim |
| pubmed-article:2760991 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:2760991 | pubmed:dateCreated | 1989-9-12 | lld:pubmed |
| pubmed-article:2760991 | pubmed:abstractText | The effects of deletions within three functional regions of the long terminal repeat of human immunodeficiency virus type 1 upon the ability of the long terminal repeat to direct production of the chloramphenicol acetyltransferase gene product and upon the ability of viruses that carry the mutations to replicate in human cell lines was investigated. The results show that the enhancer and TATAA sequences were required for efficient virus replication. Deletion of the negative regulatory element (NRE) yielded a virus that replicated more rapidly than did an otherwise isogeneic NRE-positive virus. The suppressive effect of the NRE did not depend upon the negative regulatory gene (nef), as both NRE-positive and NRE-negative viruses were defective for nef. We conclude that factors specified by the cell interact with the NRE sequences to retard human immunodeficiency virus type 1 replication. | lld:pubmed |
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| pubmed-article:2760991 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:2760991 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2760991 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2760991 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:2760991 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:2760991 | pubmed:author | pubmed-author:HaseltineW... | lld:pubmed |
| pubmed-article:2760991 | pubmed:author | pubmed-author:StenzelMM | lld:pubmed |
| pubmed-article:2760991 | pubmed:author | pubmed-author:LoSS | lld:pubmed |
| pubmed-article:2760991 | pubmed:author | pubmed-author:SodroskiJ GJG | lld:pubmed |
| pubmed-article:2760991 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2760991 | pubmed:volume | 63 | lld:pubmed |
| pubmed-article:2760991 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2760991 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2760991 | pubmed:pagination | 4115-9 | lld:pubmed |
| pubmed-article:2760991 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2760991 | pubmed:meshHeading | pubmed-meshheading:2760991-... | lld:pubmed |
| pubmed-article:2760991 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2760991 | pubmed:articleTitle | Effects of long terminal repeat mutations on human immunodeficiency virus type 1 replication. | lld:pubmed |
| pubmed-article:2760991 | pubmed:affiliation | Dana-Farber Cancer Institute, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115. | lld:pubmed |
| pubmed-article:2760991 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2760991 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2760991 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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