ArticleMolecular and cellular biology1993
Phosphatidylinositol (PI) 3-kinase and PI 4-kinase binding to the CD4-p56lck complex: the p56lck SH3 domain binds to PI 3-kinase but not PI 4-kinase.
Article in Molecular and cellular biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 142 citations in OpenAlex.
- How the Discovery of the CD4/CD8-p56Frontiers in cell and developmental biology · 2021Review
- Hypomorphic mutation in TTC7A causes combined immunodeficiency with mild structural intestinal defects.Blood · 2015Article
- The Fyn-ADAP Axis: Cytotoxicity Versus Cytokine Production in Killer Cells.Frontiers in immunology · 2015Review
- Type II PtdIns 4-kinase β associates with CD4-p56lck complex and is involved in CD4 receptor signaling.Molecular and cellular biochemistry · 2014Article
- Fyn kinase regulates type II PtdIns 4-kinases in RBL 2H3 cells.Molecular and cellular biochemistry · 2014Article
- Article
- LCK, survivin and PI-3K in the molecular biomarker profiling of oral lichen planus and oral squamous cell carcinoma.Bioinformation · 2009Article
- PIP3 pathway in regulatory T cells and autoimmunity.Immunologic research · 2007Review
- Article
- Specific interactions among transmembrane 4 superfamily (TM4SF) proteins and phosphoinositide 4-kinase.The Biochemical journal · 2000Article
- Src-like adaptor protein (SLAP) is a negative regulator of T cell receptor signaling.The Journal of experimental medicine · 2000Article
- Lipids and retroviruses.Lipids · 2000Review
- ErbB3 (HER3) interaction with the p85 regulatory subunit of phosphoinositide 3-kinase.The Biochemical journal · 1998Article
- The protein tyrosine kinase p56lck is required for triggering NF-kappaB activation upon interaction of human immunodeficiency virus type 1 envelope glycoprotein gp120 with cell surface CD4.Journal of virology · 1998Article
- Genetic evidence of a role for Lck in T-cell receptor function independent or downstream of ZAP-70/Syk protein tyrosine kinases.Molecular and cellular biology · 1998Article
- Src-induced activation of inducible T cell kinase (ITK) requires phosphatidylinositol 3-kinase activity and the Pleckstrin homology domain of inducible T cell kinase.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- T helper cell activation and human retroviral pathogenesis.Microbiological reviews · 1996Review
- The kinase, SH3, and SH2 domains of Lck play critical roles in T-cell activation after ZAP-70 membrane localization.Molecular and cellular biology · 1996Article
- 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
- CD28: a signalling perspective.The Biochemical journal · 1996Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
CD4 serves as a receptor for major histocompatibility complex class II antigens and as a receptor for the human immunodeficiency virus type 1 (HIV-1) viral coat protein gp120. It is coupled to the protein-tyrosine kinase p56lck, an interaction necessary for an optimal response of certain T cells to antigen. In addition to the protein-tyrosine kinase domain, p56lck possesses Src homology 2 and 3 (SH2 and SH3) domains as well as a unique N-terminal region. The mechanism by which p56lck generates intracellular signals is unclear, although it has the potential to interact with various downstream molecules. One such downstream target is the lipid kinase phosphatidylinositol 3-kinase (PI 3-kinase), which has been found to bind to activated pp60src and receptor-tyrosine kinases. In this study, we verified that PI 3-kinase associates with the CD4:p56lck complex as judged by the presence of PI 3-phosphate generated from anti-CD4 immunoprecipitates and detected by high-pressure liquid chromatographic analysis. However, surprisingly, CD4-p56lck was also found to associate with another lipid kinase, phosphatidylinositol 4-kinase (PI 4-kinase). The level of associated PI 4-kinase was generally higher than PI 3-kinase activity. HIV-1 gp120 and antibody-mediated cross-linking induced a 5- to 10-fold increase in the level of CD4-associated PI 4- and PI 3-kinases. The use of glutathione S-transferase fusion proteins carrying Lck-SH2, Lck-SH3, and Lck-SH2/SH3 domains showed PI 3-kinase binding to the SH3 domain of p56lck, an interaction facilitated by the presence of an adjacent SH2 domain. PI 4-kinase bound to neither the SH2 nor the SH3 domain of p56lck. CD4-p56lck contributes PI 3- and PI 4-kinase to the activation process of T cells and may play a role in HIV-1-induced immune defects.
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