ArticleProceedings of the National Academy of Sciences of the United States of America2000
T-cell receptor antagonists induce Vav phosphorylation by selective activation of Fyn kinase.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 65 citations in OpenAlex.
- In search of the Aplysia immunome: an in silico study.BMC genomics · 2022Article
- Molecular insights into pathogenesis and targeted therapy of peripheral T cell lymphoma.Experimental hematology & oncology · 2020Review
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- How a Proposed Hypothesis during My PhD Training Shaped My Career.Critical reviews in immunology · 2020Article
- p115 RhoGEF activates the Rac1 GTPase signaling cascade in MCP1 chemokine-induced vascular smooth muscle cell migration and proliferation.The Journal of biological chemistry · 2017Article
- FYN expression potentiates FLT3-ITD induced STAT5 signaling in acute myeloid leukemia.Oncotarget · 2016Article
- AKAP9 regulates activation-induced retention of T lymphocytes at sites of inflammation.Nature communications · 2015Article
- IQGAP1: insights into the function of a molecular puppeteer.Molecular immunology · 2015Review
- Article
- IQGAP1: a regulator of intracellular spacetime relativity.Journal of immunology (Baltimore, Md. : 1950) · 2012Review
- T cell recognition of weak ligands: roles of signaling, receptor number, and affinity.Immunologic research · 2011Review
- Tyrosine residues at the carboxyl terminus of Vav1 play an important role in regulation of its biological activity.The Journal of biological chemistry · 2010Article
- Unaltered negative selection and Treg development of self-reactive thymocytes in TCR transgenic Fyn-deficient mice.European journal of immunology · 2010Article
- Suboptimal engagement of the T-cell receptor by a variety of peptide-MHC ligands triggers T-cell anergy.Immunology · 2010Review
- Normal development and activation but altered cytokine production of Fyn-deficient CD4+ T cells.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- MTOC translocation modulates IS formation and controls sustained T cell signaling.The Journal of cell biology · 2008Article
- Activation, coactivation, and costimulation of resting human natural killer cells.Immunological reviews · 2006Review
- Growth arrest-inducing genes are activated in Dbl-transformed mouse fibroblasts.Gene expression · 2006Article
- Activation of naïve CD4 T cells by anti-CD3 reveals an important role for Fyn in Lck-mediated signaling.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- T cell receptor antagonism interferes with MHC clustering and integrin patterning during immunological synapse formation.The Journal of cell biology · 2004Article
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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
T cell receptor (TCR) antagonists inhibit antigen-induced T cell activation and by themselves fail to induce phenotypic changes associated with T cell activation. However, we have recently shown that TCR antagonists are inducers of antigen-presenting cell (APC)-T cell conjugates. The signaling pathway associated with this cytoskeleton-dependent event appears to involve tyrosine phosphorylation and activation of Vav. In this study, we investigated the role played by the protein tyrosine kinases Fyn, Lck, and ZAP-70 in antagonist-induced signaling pathway. Antagonist stimulation increased tyrosine phosphorylation and kinase activity of Fyn severalfold, whereas little or no increase in Lck and ZAP-70 activity was observed. Second, TCR stimulation of Lck(-), Fyn(hi) Jurkat cells induced strong tyrosine phosphorylation of Vav. In contrast, minimal increase in tyrosine phosphorylation of Vav was observed in Lck(hi), Fyn(lo) Jurkat cells. Finally, study of T cells from a Fyn-deficient TCR transgenic mouse also showed that Fyn was required for tyrosine phosphorylation and activation of Vav induced by both antagonist and agonist peptides. The deficiency in Vav phosphorylation in Fyn-deficient T cells was associated with a defect in the formation of APC-T cell conjugates when T cells were stimulated with either agonist or antagonist peptide. We conclude from these results that Vav is a selective substrate for Fyn, especially under conditions of low-affinity TCR-mediated signaling, and that this signaling pathway involving Fyn, Vav, and Rac-1 is required for the cytoskeletal reorganization that leads to T cell-APC conjugates and the formation of the immunologic synapse.
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