ArticleThe EMBO journal1994
Association of p56lck with the cytoplasmic domain of CD4 modulates HIV-1 expression.
Article in The EMBO journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 66 citations in OpenAlex.
- Nef Obtained from Individuals with HIV-1 Vary in Their Ability to Antagonize SERINC3- and SERINC5-Mediated HIV-1 Restriction.Viruses · 2021Article
- How the Discovery of the CD4/CD8-p56Frontiers in cell and developmental biology · 2021Review
- Dendritic cell immunoreceptor is a new target for anti-AIDS drug development: identification of DCIR/HIV-1 inhibitors.PloS one · 2013Article
- HIV: cell binding and entry.Cold Spring Harbor perspectives in medicine · 2012Review
- The role of unintegrated DNA in HIV infection.Retrovirology · 2011Review
- Expression of Nef from unintegrated HIV-1 DNA downregulates cell surface CXCR4 and CCR5 on T-lymphocytes.Retrovirology · 2010Article
- The Src kinase Lck facilitates assembly of HIV-1 at the plasma membrane.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Differential control of CXCR4 and CD4 downregulation by HIV-1 Gag.Virology journal · 2008Article
- Application of proteomics technology for analyzing the interactions between host cells and intracellular infectious agents.Proteomics · 2008Review
- HIV-1 infection is facilitated in T cells by decreasing p56lck protein tyrosine kinase activity.Clinical and experimental immunology · 2003Article
- Segregation of CD4 and CXCR4 into distinct lipid microdomains in T lymphocytes suggests a mechanism for membrane destabilization by human immunodeficiency virus.Journal of virology · 2002Article
- Recombinant human IL-16 inhibits HIV-1 replication and protects against activation-induced cell death (AICD).Clinical and experimental immunology · 1998Article
- Delayed human immunodeficiency virus type 1-induced apoptosis in cells expressing truncated forms of CD4.Journal of virology · 1998Article
- Upregulation of human immunodeficiency virus (HIV) replication by CD4 cross-linking in peripheral blood mononuclear cells of HIV-infected adults.Journal of virology · 1997Article
- Binding of human immunodeficiency virus type 1 to CD4 induces association of Lck and Raf-1 and activates Raf-1 by a Ras-independent pathway.Molecular and cellular biology · 1996Article
- Repression of human immunodeficiency virus type 1 long terminal repeat-driven gene expression by binding of the virus to its primary cellular receptor, the CD4 molecule.Journal of virology · 1996Article
- HIV-induced apoptosis requires the CD4 receptor cytoplasmic tail and is accelerated by interaction of CD4 with p56lck.The Journal of experimental medicine · 1996Article
- The cytoplasmic tail of CD4 is required for inhibition of human immunodeficiency virus type 1 replication by antibodies that bind to the immunoglobulin CDR3-like region in domain 1 of CD4.Journal of virology · 1995Article
- The human immunodeficiency virus type 1 (HIV-1) CD4 receptor and its central role in promotion of HIV-1 infection.Microbiological reviews · 1995Review
- Homologous interference resulting from the presence of defective particles of human immunodeficiency virus type 1.Journal of virology · 1995Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the role played by the cytoplasmic domain of the CD4 glycoprotein in the process of HIV infection, we have transfected two CD4-negative human T cell lines with cDNAs encoding the full-length CD4 and a truncated form of the molecule, lacking most of the cytoplasmic domain. Levels of viral replication were significantly higher in cells carrying the truncated version of CD4, in comparison with cells expressing the full-length CD4, as measured by the percentage of cells expressing viral p24 protein and the number of infectious particles released into culture supernatants. The extent of viral entry and reverse transcription was similar in each case, as monitored by an enzymatic test and quantitative PCR. Quantitative differences at RNA and protein levels were responsible for changes in viral production. To further characterize the mechanisms responsible for decreased rates of HIV replication in CD4-expressing cells we have treated the different cell lines, very early after HIV infection, with azidothymidine and soluble CD4, two antiviral agents that inhibit replication of HIV at different stages in the virus replicative cycle. Results from these experiments indicate that a cellular signal is mediated by the CD4 molecule, which negatively regulates the expression of viral DNA already present in such cells. This signal would be initiated following oligomerization of the CD4 molecule by the virus itself. Results from experiments with a CD4 construct containing mutations of the cysteine residues which are responsible for association of CD4 with p56lck demonstrate that p56lck is implicated in the transduction of the signal negatively regulating HIV replication.
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