ArticleScience signaling2011
Vav1-mediated scaffolding interactions stabilize SLP-76 microclusters and contribute to antigen-dependent T cell responses.
Article in Science signaling, 2011. 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.
- LFA-1 and kindlin-3 enable the collaborative transport of SLP-76 microclusters by myosin and dynein motors.Journal of cell science · 2021Article
- The Multiple Roles of the Cytosolic Adapter Proteins ADAP, SKAP1 and SKAP2 for TCR/CD3 -Mediated Signaling Events.Frontiers in immunology · 2021Review
- Vav2 lacks CaJournal of cell science · 2020Article
- Review
- ADAP is an upstream regulator that precedes SLP-76 at sites of TCR engagement and stabilizes signaling microclusters.Journal of cell science · 2018Article
- Timed Regulation of 3BP2 Induction Is Critical for Sustaining CD8Cell reports · 2018Article
- A Natural Variant of the T Cell Receptor-Signaling Molecule Vav1 Reduces Both Effector T Cell Functions and Susceptibility to Neuroinflammation.PLoS genetics · 2016Article
- The linker for activation of T cells (LAT) signaling hub: from signaling complexes to microclusters.The Journal of biological chemistry · 2015Review
- Vav1 Regulates T-Cell Activation through a Feedback Mechanism and Crosstalk between the T-Cell Receptor and CD28.Journal of proteome research · 2015Article
- Vav family exchange factors: an integrated regulatory and functional view.Small GTPases · 2014Review
- The N terminus of SKAP55 enables T cell adhesion to TCR and integrin ligands via distinct mechanisms.The Journal of cell biology · 2013Article
- Regulation of T-cell receptor signaling by the actin cytoskeleton and poroelastic cytoplasm.Immunological reviews · 2013Review
- Multipoint binding of the SLP-76 SH2 domain to ADAP is critical for oligomerization of SLP-76 signaling complexes in stimulated T cells.Molecular and cellular biology · 2013Article
- Multimolecular analysis of stable immunological synapses reveals sustained recruitment and sequential assembly of signaling clusters.Molecular & cellular proteomics : MCP · 2013Article
- CD25 and CD69 induction by α4β1 outside-in signalling requires TCR early signalling complex proteins.The Biochemical journal · 2013Article
- Activation of extracellular signal-regulated kinase but not of p38 mitogen-activated protein kinase pathways in lymphocytes requires allosteric activation of SOS.Molecular and cellular biology · 2013Article
- The N-terminal 20-amino acid region of guanine nucleotide exchange factor Vav1 plays a distinguished role in T cell receptor-mediated calcium signaling.The Journal of biological chemistry · 2013Article
- "Cell biology meets physiology: functional organization of vertebrate plasma membranes"--the immunological synapse.Current topics in membranes · 2013Article
- Signaling for synergistic activation of natural killer cells.Immune network · 2012Article
- Mechanism and function of Vav1 localisation in TCR signalling.Journal of cell science · 2012Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The guanine nucleotide exchange factor (GEF) Vav1 synergizes with the adaptor protein SLP-76 (Src homology 2 domain--containing leukocyte phosphoprotein of 76 kD) to support T cell development and activation. In response to ligation of the T cell receptor (TCR), SLP-76 is assembled into microclusters that provide an essential platform for the signaling events that drive T cell activation. We found that Vav1 selectively entered SLP-76 microclusters, rather than TCR microclusters, influencing their stability and function. The carboxyl terminus of Vav1, which consists of Src homology domains, was both necessary and sufficient for the entry of Vav1 into SLP-76 microclusters; however, this fragment of Vav1 was insufficient to stabilize the microclusters, and it potently suppressed T cell activation. This indicated that the amino terminus of Vav1, which has the GEF domain, also contributed to the integrity of SLP-76 microclusters and thereby to T cell activation. These microcluster-stabilizing functions were independent of the GEF activity in the amino terminus of Vav1 and were unaffected if the GEF function of Vav1 was either inactivated or constitutively activated by mutation. In contrast, Vav1 deletion mutants lacking either the calponin homology domain or the catalytic core of the GEF exhibited mild scaffolding defects, but they differentially affected TCR-dependent calcium ion (Ca²+) responses. We conclude that multiple GEF-independent scaffolding functions distributed throughout the amino terminus of Vav1 contribute to the activation of T cells by acting synergistically to increase the stability and function of SLP-76 microclusters.
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