ArticleThe Journal of experimental medicine2000
The Src homology 2 domain of Vav is required for its compartmentation to the plasma membrane and activation of c-Jun NH(2)-terminal kinase 1.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 74 citations in OpenAlex.
- Molecular Expression Differences in Specific Blood Mononuclear Cell-Types Identify Patients With AL Amyloidosis.Journal of cellular and molecular medicine · 2025Article
- Functional roles of Syk in macrophage-mediated inflammatory responses.Mediators of inflammation · 2014Review
- A mechanistic model of early FcεRI signaling: lipid rafts and the question of protection from dephosphorylation.PloS one · 2012Article
- The role of Syk kinase in ultraviolet-mediated skin damage.The British journal of dermatology · 2011Article
- Vav1-mediated scaffolding interactions stabilize SLP-76 microclusters and contribute to antigen-dependent T cell responses.Science signaling · 2011Article
- Function of the nucleotide exchange activity of vav1 in T cell development and activation.Science signaling · 2009Article
- Adapters in the organization of mast cell signaling.Immunological reviews · 2009Review
- 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.The Journal of biological chemistry · 2006Article
- Spatial compartmentalization of tumor necrosis factor (TNF) receptor 1-dependent signaling pathways in human airway smooth muscle cells. Lipid rafts are essential for TNF-alpha-mediated activation of RhoA but dispensable for the activation of the NF-kappaB and MAPK pathways.The Journal of biological chemistry · 2006Article
- Cholesterol deficiency in a mouse model of Smith-Lemli-Opitz syndrome reveals increased mast cell responsiveness.The Journal of experimental medicine · 2006Article
- Negative regulation of immunoglobulin E-dependent allergic responses by Lyn kinase.The Journal of experimental medicine · 2004Article
- WIP regulates signaling via the high affinity receptor for immunoglobulin E in mast cells.The Journal of experimental medicine · 2004Article
- Activation of Syk protein tyrosine kinase in response to osmotic stress requires interaction with p21-activated protein kinase Pak2/gamma-PAK.Molecular and cellular biology · 2004Article
- Preferential signaling and induction of allergy-promoting lymphokines upon weak stimulation of the high affinity IgE receptor on mast cells.The Journal of experimental medicine · 2003Article
- Vav1 is a component of transcriptionally active complexes.The Journal of experimental medicine · 2002Article
- Metabolic labelling of membrane microdomains/rafts in Jurkat cells indicates the presence of glycerophospholipids implicated in signal transduction by the CD3 T-cell receptor.The Biochemical journal · 2002Article
- Vav regulates activation of Rac but not Cdc42 during FcgammaR-mediated phagocytosis.Molecular biology of the cell · 2002Article
- Vav3 modulates B cell receptor responses by regulating phosphoinositide 3-kinase activation.The Journal of experimental medicine · 2002Article
- Structure-function analysis of Lyn kinase association with lipid rafts and initiation of early signaling events after Fcepsilon receptor I aggregation.Molecular and cellular biology · 2001Article
- Vav proteins, adaptors and cell signaling.Oncogene · 2001Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Vav is a hematopoietic cell-specific guanine nucleotide exchange factor (GEF) whose activation is mediated by receptor engagement. The relationship of Vav localization to its function is presently unclear. We found that Vav redistributes to the plasma membrane in response to Fcin receptor I (FcinRI) engagement. The redistribution of Vav was mediated by its Src homology 2 (SH2) domain and required Syk activity. The FcinRI and Vav were found to colocalize and were recruited to glycosphingolipid-enriched microdomains (GEMs). The scaffold protein, linker for activation of T cells (LAT), and Rac1 (a target of Vav activity) were constitutively present in GEMs. Expression of an SH2 domain-containing COOH-terminal fragment of Vav inhibited Vav phosphorylation and movement to the GEMs but had no effect on the tyrosine phosphorylation of the adaptor protein, SLP-76 (SH2 domain-containing leukocyte protein of 76 kD), and LAT. However, assembly of the multiprotein complex containing these proteins was inhibited. In addition, FcinRI-dependent activation of c-Jun NH(2)-terminal kinase 1 (JNK1) was also inhibited. Thus, Vav localization to the plasma membrane is mediated by its SH2 domain and may serve to regulate downstream effectors like JNK1.
Indexed as
Identifiers
What OpenQuestion holds
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.