| pubmed-article:16403635 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16403635 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
| pubmed-article:16403635 | lifeskim:mentions | umls-concept:C0178539 | lld:lifeskim |
| pubmed-article:16403635 | lifeskim:mentions | umls-concept:C1158478 | lld:lifeskim |
| pubmed-article:16403635 | lifeskim:mentions | umls-concept:C1705422 | lld:lifeskim |
| pubmed-article:16403635 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:16403635 | pubmed:dateCreated | 2006-2-14 | lld:pubmed |
| pubmed-article:16403635 | pubmed:abstractText | To achieve productive infection, the reverse transcribed cDNA of human immunodeficiency virus type 1 (HIV-1) is inserted in the host cell genome. The main protein responsible for this reaction is the viral integrase. However, studies indicate that the virus is assisted by cellular proteins, or co-factors, to achieve integration into the infected cell. The barrier-to-autointegration factor (BAF) might prevent autointegration. Its ability to bridge DNA and the finding that the nuclear lamina-associated polypeptide-2alpha interacts with BAF suggest a role in nuclear structure organization. Integrase interactor 1 was found to directly interact with HIV-1 integrase and to activate its DNA-joining activity, and the high mobility group chromosomal protein A1 might approximate both long terminal repeat (LTR) ends and facilitate integrase binding by unwinding the LTR termini. Furthermore, the lens-epithelium-derived growth factor (LEDGF; also known as p75) seems to tether HIV-1 integrase to the chromosomes. Although a direct role in integration has only been demonstrated for LEDGF/p75, to date, each validated cellular co-factor for HIV-1 integration could constitute a promising new target for antiviral therapy. | lld:pubmed |
| pubmed-article:16403635 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16403635 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16403635 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16403635 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:16403635 | pubmed:issn | 0968-0004 | lld:pubmed |
| pubmed-article:16403635 | pubmed:author | pubmed-author:DebyserZegerZ | lld:pubmed |
| pubmed-article:16403635 | pubmed:author | pubmed-author:Van... | lld:pubmed |
| pubmed-article:16403635 | pubmed:author | pubmed-author:BusschotsKatr... | lld:pubmed |
| pubmed-article:16403635 | pubmed:author | pubmed-author:ChristFraukeF | lld:pubmed |
| pubmed-article:16403635 | pubmed:author | pubmed-author:Vandekerckhov... | lld:pubmed |
| pubmed-article:16403635 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16403635 | pubmed:volume | 31 | lld:pubmed |
| pubmed-article:16403635 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16403635 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16403635 | pubmed:pagination | 98-105 | lld:pubmed |
| pubmed-article:16403635 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:16403635 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16403635 | pubmed:articleTitle | Cellular co-factors of HIV-1 integration. | lld:pubmed |
| pubmed-article:16403635 | pubmed:affiliation | Molecular Virology and Gene Therapy, Molecular Medicine, KULAK and K.U. Leuven, Kapucijnenvoer 33 3000 Leuven, Flanders, Belgium. | lld:pubmed |
| pubmed-article:16403635 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16403635 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:16403635 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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