| pubmed-article:16237100 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16237100 | lifeskim:mentions | umls-concept:C1171348 | lld:lifeskim |
| pubmed-article:16237100 | lifeskim:mentions | umls-concept:C0034790 | lld:lifeskim |
| pubmed-article:16237100 | lifeskim:mentions | umls-concept:C1155065 | lld:lifeskim |
| pubmed-article:16237100 | lifeskim:mentions | umls-concept:C0425152 | lld:lifeskim |
| pubmed-article:16237100 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:16237100 | pubmed:dateCreated | 2005-10-20 | lld:pubmed |
| pubmed-article:16237100 | pubmed:abstractText | The HIV-1 protein Nef enhances viral pathogenicity and accelerates disease progression in vivo. Nef potentiates T cell activation by an unknown mechanism, probably by optimizing the intracellular environment for HIV replication. Using a new T cell reporter system, we have found that Nef more than doubles the number of cells expressing the transcription factors NF-kappaB and NFAT after TCR stimulation. This Nef-induced priming of TCR signaling pathways occurred independently of calcium signaling and involved a very proximal step before protein kinase C activation. Engagement of the TCR by MHC-bound Ag triggers the formation of the immunological synapse by recruiting detergent-resistant membrane microdomains, termed lipid rafts. Approximately 5-10% of the total cellular pool of Nef is localized within lipid rafts. Using confocal and real-time microscopy, we found that Nef in lipid rafts was recruited into the immunological synapse within minutes after Ab engagement of the TCR/CD3 and CD28 receptors. This recruitment was dependent on the N-terminal domain of Nef encompassing its myristoylation. Nef did not increase the number of cell surface lipid rafts or immunological synapses. Recently, studies have shown a specific interaction of Nef with an active subpopulation of p21-activated kinase-2 found only in the lipid rafts. Thus, the corecruitment of Nef and key cellular partners (e.g., activated p21-activated kinase-2) into the immunological synapse may underlie the increased frequency of cells expressing transcriptionally active forms of NF-kappaB and NFAT and the resultant changes in T cell activation. | lld:pubmed |
| pubmed-article:16237100 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16237100 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:16237100 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16237100 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:16237100 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:16237100 | pubmed:author | pubmed-author:GreeneWarner... | lld:pubmed |
| pubmed-article:16237100 | pubmed:author | pubmed-author:CavroisMariel... | lld:pubmed |
| pubmed-article:16237100 | pubmed:author | pubmed-author:WilliamsSamue... | lld:pubmed |
| pubmed-article:16237100 | pubmed:author | pubmed-author:YonemotoWesW | lld:pubmed |
| pubmed-article:16237100 | pubmed:author | pubmed-author:de... | lld:pubmed |
| pubmed-article:16237100 | pubmed:author | pubmed-author:FenardDavidD | lld:pubmed |
| pubmed-article:16237100 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16237100 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:16237100 | pubmed:volume | 175 | lld:pubmed |
| pubmed-article:16237100 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16237100 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16237100 | pubmed:pagination | 6050-7 | lld:pubmed |
| pubmed-article:16237100 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:16237100 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16237100 | pubmed:articleTitle | Nef is physically recruited into the immunological synapse and potentiates T cell activation early after TCR engagement. | lld:pubmed |
| pubmed-article:16237100 | pubmed:affiliation | Gladstone Institute of Virology and Immunology, University of California, 94158, USA. | lld:pubmed |
| pubmed-article:16237100 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16237100 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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