ArticleProceedings of the National Academy of Sciences of the United States of America1999
The Rho-family GTP exchange factor Vav is a critical transducer of T cell receptor signals to the calcium, ERK, and NF-kappaB pathways.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 238 citations in OpenAlex.
- TCR-pMHC recognition mediates target phagocytosis by T cells.Mechanobiology in medicine · 2026Article
- Targeting liver metastases in uveal melanoma: ATX-LPA mediated immunosuppression and novel therapeutic approaches.Frontiers in immunology · 2026Article
- Mutations in Ras homolog family member A in patients with peripheral T-cell lymphoma and implications for personalized medicine.Cancer biology & medicine · 2024Review
- Vav proteins do not influence dengue virus replication but are associated with induction of phospho-ERK, IL-6, and viperin mRNA following DENV infectionMicrobiology spectrum · 2024Article
- Review
- Mapping the SLP76 interactome in T cells lacking each of the GRB2-family adaptors reveals molecular plasticity of the TCR signaling pathway.Frontiers in immunology · 2023Article
- Vav1 Promotes B-Cell Lymphoma Development.Cells · 2022Article
- Biomechanics of T Cell Dysfunctions in Chronic Diseases.Frontiers in immunology · 2021Review
- ERK Activation in CAR T Cells Is Amplified by CD28-Mediated Increase in CD3ζ Phosphorylation.iScience · 2020Article
- Roscovitine enhances all-Oncotarget · 2020Article
- Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway.Genetics and molecular biology · 2020Article
- Article
- Review
- Vav1 mutations identified in human cancers give rise to different oncogenic phenotypes.Oncogenesis · 2018Article
- A Natural Variant of the Signaling Molecule Vav1 Enhances Susceptibility to Myasthenia Gravis and Influences the T Cell Receptor Repertoire.Frontiers in immunology · 2018Article
- An Effective Model of the Retinoic Acid Induced HL-60 Differentiation Program.Scientific reports · 2017Article
- A Novel Vav3 Homolog Identified in Lamprey, Lampetra japonica, with Roles in Lipopolysaccharide-Mediated Immune Response.International journal of molecular sciences · 2017Article
- Activating mutations and translocations in the guanine exchange factor VAV1 in peripheral T-cell lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Effect of Rho-kinase Inhibitor, Y27632, on Porcine Corneal Endothelial Cell Culture, Inflammation and Immune Regulation.Ocular immunology and inflammation · 2016Article
- A Natural Variant of the T Cell Receptor-Signaling Molecule Vav1 Reduces Both Effector T Cell Functions and Susceptibility to Neuroinflammation.PLoS genetics · 2016Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vav is a GTP/GDP exchange factor (GEF) for members of the Rho-family of GTPases that is rapidly tyrosine-phosphorylated after engagement of the T cell receptor (TCR), suggesting that it may transduce signals from the receptor. T cells from mice made Vav-deficient by gene targeting (Vav-/-) fail to proliferate in response to TCR stimulation because they fail to secrete IL-2. We now show that this is due at least in part to the failure to initiate IL-2 gene transcription. Furthermore, we analyze TCR-proximal signaling pathways in Vav-/- T cells and show that despite normal activation of the Lck and ZAP-70 tyrosine kinases, the mutant cells have specific defects in TCR-induced intracellular calcium fluxes, in the activation of extracellular signal-regulated mitogen-activated protein kinases and in the activation of the NF-kappaB transcription factor. Finally, we show that the greatly reduced TCR-induced calcium flux of Vav-deficient T cells is an important cause of their proliferative defect, because restoration of the calcium flux with a calcium ionophore reverses the phenotype.
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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.