ArticleJournal of immunology (Baltimore, Md. : 1950)2008
The Src kinase Lck facilitates assembly of HIV-1 at the plasma membrane.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Identification of novel HIV-1 dependency factors in primary CCR4(+)CCR6(+)Th17 cells via a genome-wide transcriptional approach.Retrovirology · 2015Pooled it
- Incorporation of genome-bound cellular proteins into HIV-1 particles regulates viral infection.Cell reports · 2026Article
- Involvement of Human Cellular Proteins and Structures in Realization of the HIV Life Cycle: A Comprehensive Review, 2024.Viruses · 2024Review
- Effect of Src tyrosine kinase on a rat model of asthma.Experimental and therapeutic medicine · 2022Article
- Subtype Differences in the Interaction of HIV-1 Matrix with Calmodulin: Implications for Biological Functions.Biomolecules · 2021Article
- Post-Translational Modifications of Retroviral HIV-1 Gag Precursors: An Overview of Their Biological Role.International journal of molecular sciences · 2021Review
- CD71mBio · 2019Article
- Mechanisms of HIV-1 cell-to-cell transmission and the establishment of the latent reservoir.Virus research · 2019Review
- CD4AIDS research and human retroviruses · 2018Review
- Reconstructing the temporal progression of HIV-1 immune response pathways.Bioinformatics (Oxford, England) · 2016Article
- A Conserved GPG-Motif in the HIV-1 Nef Core Is Required for Principal Nef-Activities.PloS one · 2015Article
- Ezrin is a component of the HIV-1 virological presynapse and contributes to the inhibition of cell-cell fusion.Journal of virology · 2014Article
- Solution structure of calmodulin bound to the binding domain of the HIV-1 matrix protein.The Journal of biological chemistry · 2014Article
- Article
- Role of the HIV-1 Matrix Protein in Gag Intracellular Trafficking and Targeting to the Plasma Membrane for Virus Assembly.Frontiers in microbiology · 2012Article
- Cellular kinases incorporated into HIV-1 particles: passive or active passengers?Retrovirology · 2011Review
- Retroviral matrix and lipids, the intimate interaction.Retrovirology · 2011Review
- Polymeric immunoglobulin receptor-mediated invasion of Streptococcus pneumoniae into host cells requires a coordinate signaling of SRC family of protein-tyrosine kinases, ERK, and c-Jun N-terminal kinase.The Journal of biological chemistry · 2010Article
- Combinatorial signals from CD28 differentially regulate human immunodeficiency virus transcription in T cells.The Journal of biological chemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
HIV type 1 (HIV-1) assembly and egress are driven by the viral protein Gag and occur at the plasma membrane in T cells. Recent evidence indicates that secretory vesicles and machinery are essential components of virus packaging in both T cells and macrophages. However, the pathways and cellular mediators of Gag targeting to the plasma membrane are not well characterized. Lck, a lymphoid specific Src kinase critical for T cell activation, is found in the plasma membrane as well as various intracellular compartments and it has been suggested to influence HIV-1 replication. To investigate Lck as a potential regulator of Gag targeting, we assessed HIV-1 replication and Gag-induced virus-like particle release in the presence and absence of Lck. Release of HIV-1 and virus-like particles was reduced in the absence of Lck. This decrease in replication was not due to altered HIV-1 infection, transcription or protein translation. However, in T cells lacking Lck, HIV-1 accumulated intracellularly. In addition, expressing Lck in HeLa cells promoted HIV-1 Gag plasma membrane localization. Palmitoylation of the Lck unique domain, which is essential for directing Lck to the plasma membrane, was critical for its effect on HIV-1 replication. Furthermore, HIV-1 Gag directly interacted with the Lck unique domain in the context of infected cells. These results indicate that Lck plays a key role in targeting HIV-1 Gag to the plasma membrane in T cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.