ReviewImmunologic research2005
The Vav family: at the crossroads of signaling pathways.
Review in Immunologic research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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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, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens.Nature genetics · 2014Pooled it
- Review
- The regulators of BCR signaling during B cell activation.Blood science (Baltimore, Md.) · 2019Review
- Review
- NK cell recognition of hematopoietic cells by SLAM-SAP families.Cellular & molecular immunology · 2019Review
- ZAP-70 in Signaling, Biology, and Disease.Annual review of immunology · 2018Review
- Association of VAV2 and VAV3 polymorphisms with cardiovascular risk factors.Scientific reports · 2017Article
- Identification of novel genes and pathways in carotid atheroma using integrated bioinformatic methods.Scientific reports · 2016Article
- VAV2, a guanine nucleotide exchange factor for Rac1, regulates glucose-stimulated insulin secretion in pancreatic beta cells.Diabetologia · 2015Article
- Negative regulation of chemokine receptor signaling and B-cell chemotaxis by p66Shc.Cell death & disease · 2014Article
- Vav Guanine nucleotide exchange factors regulate atherosclerotic lesion development in mice.Arteriosclerosis, thrombosis, and vascular biology · 2013Article
- Vav protein guanine nucleotide exchange factor regulates CD36 protein-mediated macrophage foam cell formation via calcium and dynamin-dependent processes.The Journal of biological chemistry · 2011Article
- TNF-stimulated MAP kinase activation mediated by a Rho family GTPase signaling pathway.Genes & development · 2011Article
- Article
- Vav family Rho guanine nucleotide exchange factors regulate CD36-mediated macrophage foam cell formation.The Journal of biological chemistry · 2011Article
- Inhibitory signaling blocks activating receptor clustering and induces cytoskeletal retraction in natural killer cells.The Journal of cell biology · 2011Article
- Age-related defects in the cytoskeleton signaling pathways of CD4 T cells.Ageing research reviews · 2011Review
- Article
- VAV2 and VAV3 as candidate disease genes for spontaneous glaucoma in mice and humans.PloS one · 2010Article
- Vav proteins are necessary for correct differentiation of mouse cecal and colonic enterocytes.Journal of cell science · 2009Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Vav family of Rho-guanine nucleotide exchange factors (GEFs) is thought to control a diverse array of signaling pathways emanating from antigen receptors in lymphocytes, although the exact mechanism by which Vav exerts its function is only beginning to emerge. Vav proteins are modular and contain the Dbl-homology domain, typical of all known Rho-GEFs, in addition to several other structural domains characteristic of proteins involved in signal transduction. Recently, our laboratory generated mice congenitally lacking all three Vav isoforms, providing genetic evidence that the Vav family is critical and nonredundant in T- and B-lymphocyte development and function and is essential in the formation of the adaptive immune system. These experiments also demonstrated that Vav proteins are indispensable for both T-cell receptor- and B-cell receptor-induced Ca++ fluxes. However, detailed analyses of Vav-deficient mice revealed unexpected complexity of Vav involvement in cellular activation. Notably, we observed lineage-specific Vav regulation of mitogen-activated protein kinase signaling, in which Vav was required in T-cells, but not in B-cells. Moreover, the three Vav proteins appear to function specifically in distinct signaling pathways emanating from activating receptors of natural killer cells that trigger natural cytotoxicity.
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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.