ArticleThe Journal of biological chemistry2006
Vav1 acidic region tyrosine 174 is required for the formation of T cell receptor-induced microclusters and is essential in T cell development and activation.
Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- NKG2D gene polymorphisms are associated with disease control of chronic myeloid leukemia by dasatinib.International journal of hematology · 2017Trial
- Trial
- Article
- A Natural Variant of the T Cell Receptor-Signaling Molecule Vav1 Reduces Both Effector T Cell Functions and Susceptibility to Neuroinflammation.PLoS genetics · 2016Article
- Distinct structural and catalytic roles for Zap70 in formation of the immunological synapse in CTL.eLife · 2014Article
- "Cell biology meets physiology: functional organization of vertebrate plasma membranes"--the immunological synapse.Current topics in membranes · 2013Article
- Mechanism and function of Vav1 localisation in TCR signalling.Journal of cell science · 2012Article
- Programmed cell death 1 forms negative costimulatory microclusters that directly inhibit T cell receptor signaling by recruiting phosphatase SHP2.The Journal of experimental medicine · 2012Article
- Vav1 oncogenic mutation inhibits T cell receptor-induced calcium mobilization through inhibition of phospholipase Cγ1 activation.The Journal of biological chemistry · 2012Article
- Vav1-mediated scaffolding interactions stabilize SLP-76 microclusters and contribute to antigen-dependent T cell responses.Science signaling · 2011Article
- Systems biology in immunology: a computational modeling perspective.Annual review of immunology · 2011Review
- Itk: the rheostat of the T cell response.Journal of signal transduction · 2011Article
- Mediation of T-cell activation by actin meshworks.Cold Spring Harbor perspectives in biology · 2010Review
- Tyrosine residues at the carboxyl terminus of Vav1 play an important role in regulation of its biological activity.The Journal of biological chemistry · 2010Article
- Balanced Vav2 GEF activity regulates neurite outgrowth and branching in vitro and in vivo.Molecular and cellular neurosciences · 2010Article
- Article
- Synergistic signals for natural cytotoxicity are required to overcome inhibition by c-Cbl ubiquitin ligase.Immunity · 2010Article
- Structural and energetic mechanisms of cooperative autoinhibition and activation of Vav1.Cell · 2010Article
- Vav and Rac activation in B cell antigen receptor endocytosis involves Vav recruitment to the adapter protein LAB.The Journal of biological chemistry · 2009Article
- B cell antigen receptor endocytosis and antigen presentation to T cells require Vav and dynamin.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Vav proteins are multidomain signaling molecules critical for mediating signals downstream of several surface receptors, including the antigen receptors of T and B lymphocytes. The catalytic guanine nucleotide exchange factor (GEF) activity of the Vav Dbl homology (DH) domain is thought to be controlled by an intramolecular autoinhibitory mechanism involving an N-terminal extension and phosphorylation of tyrosine residues in the acidic region (AC). Here, we report that the sequences surrounding the Vav1 AC: Tyr(142), Tyr(160), and Tyr(174) are evolutionarily conserved, conform to consensus SH2 domain binding motifs, and bind several proteins implicated in TCR signaling, including Lck, PI3K p85alpha, and PLCgamma1, through direct interactions with their SH2 domains. In addition, the AC tyrosines regulate tyrosine phosphorylation of Vav1. We also show that Tyr(174) is required for the maintenance of TCR-signaling microclusters and for normal T cell development and activation. In this regard, our data demonstrate that while Vav1 Tyr(174) is essential for maintaining the inhibitory constraint of the DH domain in both developing and mature T cells, constitutively activated Vav GEF disrupts TCR-signaling microclusters and leads to defective T cell development and proliferation.
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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.