pubmed-article:8529100 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8529100 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
pubmed-article:8529100 | lifeskim:mentions | umls-concept:C0525021 | lld:lifeskim |
pubmed-article:8529100 | lifeskim:mentions | umls-concept:C0808232 | lld:lifeskim |
pubmed-article:8529100 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
pubmed-article:8529100 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
pubmed-article:8529100 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
pubmed-article:8529100 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:8529100 | pubmed:dateCreated | 1996-1-29 | lld:pubmed |
pubmed-article:8529100 | pubmed:abstractText | Human immunodeficiency virus type 1 (HIV-1) is a lentivirus and shares with other members of this retroviral subfamily the ability to replicate in nondividing cells, in particular, cells of the monocyte/macrophage lineage. This feature relies on the presence of a specific nuclear localization signal (NLS) within the viral matrix protein (MA p17), which to some degree can be complemented by the activity of the viral vpr gene product. The MA p17 NLS ensures efficient transportation of the viral preintegration complex into the nucleus of an infected macrophage and confers persistence of HIV-1 in quiescent T cells, and therefore presents an attractive target for therapeutic intervention. | lld:pubmed |
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pubmed-article:8529100 | pubmed:language | eng | lld:pubmed |
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pubmed-article:8529100 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:8529100 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8529100 | pubmed:month | Jan | lld:pubmed |
pubmed-article:8529100 | pubmed:issn | 1076-1551 | lld:pubmed |
pubmed-article:8529100 | pubmed:author | pubmed-author:CeramiAA | lld:pubmed |
pubmed-article:8529100 | pubmed:author | pubmed-author:UlrichPP | lld:pubmed |
pubmed-article:8529100 | pubmed:author | pubmed-author:NuovoG JGJ | lld:pubmed |
pubmed-article:8529100 | pubmed:author | pubmed-author:ManogueK RKR | lld:pubmed |
pubmed-article:8529100 | pubmed:author | pubmed-author:BukrinskyMM | lld:pubmed |
pubmed-article:8529100 | pubmed:author | pubmed-author:DubrovskyLL | lld:pubmed |
pubmed-article:8529100 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8529100 | pubmed:volume | 1 | lld:pubmed |
pubmed-article:8529100 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8529100 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8529100 | pubmed:pagination | 217-30 | lld:pubmed |
pubmed-article:8529100 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:8529100 | pubmed:year | 1995 | lld:pubmed |
pubmed-article:8529100 | pubmed:articleTitle | Nuclear localization signal of HIV-1 as a novel target for therapeutic intervention. | lld:pubmed |
pubmed-article:8529100 | pubmed:affiliation | Picower Institute for Medical Research, Manhasset, New York 11030, USA. | lld:pubmed |
pubmed-article:8529100 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8529100 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:8529100 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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