| pubmed-article:2249669 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2249669 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:2249669 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:2249669 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:2249669 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
| pubmed-article:2249669 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:2249669 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
| pubmed-article:2249669 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:2249669 | pubmed:dateCreated | 1991-1-11 | lld:pubmed |
| pubmed-article:2249669 | pubmed:abstractText | To examine the restriction of HIV growth in murine cells, we infected NIH 3T3 cells with HIV pseudotyped by Moloney murine leukemia virus. The virus, which carried a dominant selectable marker under the control of the HIV LTR, gave large numbers of resistant clones, showing that murine cells are permissive for HIV uncoating, reverse transcription, nuclear transport and integration. However, we found that several murine cell lines, as well as CHO cells, could not support the function of rev, the viral regulatory gene which, in human cells, induces the cytoplasmic expression of the incompletely spliced class of HIV mRNAs that encode the viral structural proteins. Transfection of the HIV-infected murine cells with a HTLV-1 rex-expressing vector failed to rescue the rev- phenotype, indicating that the block extended to rex function. Most importantly, we could complement the rev defect by fusing the infected murine with uninfected human cells. We conclude that HIV tropism is partly a consequence of a trans-acting cellular factor critical for Rev function. | lld:pubmed |
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| pubmed-article:2249669 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:2249669 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2249669 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2249669 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:2249669 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:2249669 | pubmed:author | pubmed-author:BaltimoreDD | lld:pubmed |
| pubmed-article:2249669 | pubmed:author | pubmed-author:TronoDD | lld:pubmed |
| pubmed-article:2249669 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2249669 | pubmed:volume | 9 | lld:pubmed |
| pubmed-article:2249669 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2249669 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2249669 | pubmed:pagination | 4155-60 | lld:pubmed |
| pubmed-article:2249669 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2249669 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2249669 | pubmed:articleTitle | A human cell factor is essential for HIV-1 Rev action. | lld:pubmed |
| pubmed-article:2249669 | pubmed:affiliation | Whitehead Institute for Biomedical Research, Cambridge, MA 02142. | lld:pubmed |
| pubmed-article:2249669 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2249669 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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