ArticleMolecular and cellular biology2000
Vav family proteins couple to diverse cell surface receptors.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 147 citations in OpenAlex.
- The actin regulatory protein HS1 interacts with Arp2/3 and mediates efficient neutrophil chemotaxis.The Journal of biological chemistry · 2012Trial
- PI(3,4,5)P3-mediated Cdc42 activation regulates macrophage podosome assembly.Cellular and molecular life sciences : CMLS · 2025Article
- Vav Proteins in Development of the Brain: A Potential Relationship to the Pathogenesis of Congenital Zika Syndrome?Viruses · 2022Review
- The guanine nucleotide exchange factor Vav3 intervenes in the migration pathway of oligodendrocyte precursor cells on tenascin-C.Frontiers in cell and developmental biology · 2022Article
- The guanine nucleotide exchange factor VAV3 participates in ERBB4-mediated cancer cell migration.The Journal of biological chemistry · 2020Article
- Article
- Vav2 lacks CaJournal of cell science · 2020Article
- Differential Subcellular Distribution and Translocation of Seven 14-3-3 Isoforms in Response to EGF and During the Cell Cycle.International journal of molecular sciences · 2020Article
- Targeting Rac and Cdc42 GEFs in Metastatic Cancer.Frontiers in cell and developmental biology · 2020Review
- Article
- Hematopoietic Stem Cells as a Novel Source of Dental Tissue Cells.Scientific reports · 2018Article
- Rac3 regulates breast cancer invasion and metastasis by controlling adhesion and matrix degradation.The Journal of cell biology · 2017Article
- Interaction between Rho GTPases and 14-3-3 Proteins.International journal of molecular sciences · 2017Review
- A Novel Vav3 Homolog Identified in Lamprey, Lampetra japonica, with Roles in Lipopolysaccharide-Mediated Immune Response.International journal of molecular sciences · 2017Article
- Binding of CIB1 to the αIIb tail of αIIbβ3 is required for FAK recruitment and activation in platelets.PloS one · 2017Article
- Involvement of Tiam1, RhoG and ELMO2/ILK in Rac1-mediated phagocytosis in human trabecular meshwork cells.Experimental cell research · 2016Article
- SH2-PLA: a sensitive in-solution approach for quantification of modular domain binding by proximity ligation and real-time PCR.BMC biotechnology · 2015Article
- Mutation of Vav1 adaptor region reveals a new oncogenic activation.Oncotarget · 2015Article
- Vav3, a GEF for RhoA, Plays a Critical Role under High Glucose Conditions.Endocrinology and metabolism (Seoul, Korea) · 2014Article
- Rho protein GTPases and their interactions with NFκB: crossroads of inflammation and matrix biology.Bioscience reports · 2014Review
2 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 4 countries.
Funding
Abstract
Vav proteins are guanine nucleotide exchange factors for Rho family GTPases which activate pathways leading to actin cytoskeletal rearrangements and transcriptional alterations. Vav proteins contain several protein binding domains which can link cell surface receptors to downstream signaling proteins. Vav1 is expressed exclusively in hematopoietic cells and tyrosine phosphorylated in response to activation of multiple cell surface receptors. However, it is not known whether the recently identified isoforms Vav2 and Vav3, which are broadly expressed, can couple with similar classes of receptors, nor is it known whether all Vav isoforms possess identical functional activities. We expressed Vav1, Vav2, and Vav3 at equivalent levels to directly compare the responses of the Vav proteins to receptor activation. Although each Vav isoform was tyrosine phosphorylated upon activation of representative receptor tyrosine kinases, integrin, and lymphocyte antigen receptors, we found unique aspects of Vav protein coupling in each receptor pathway. Each Vav protein coprecipitated with activated epidermal growth factor and platelet-derived growth factor (PDGF) receptors, and multiple phosphorylated tyrosine residues on the PDGF receptor were able to mediate Vav2 tyrosine phosphorylation. Integrin-induced tyrosine phosphorylation of Vav proteins was not detected in nonhematopoietic cells unless the protein tyrosine kinase Syk was also expressed, suggesting that integrin activation of Vav proteins may be restricted to cell types that express particular tyrosine kinases. In addition, we found that Vav1, but not Vav2 or Vav3, can efficiently cooperate with T-cell receptor signaling to enhance NFAT-dependent transcription, while Vav1 and Vav3, but not Vav2, can enhance NFkappaB-dependent transcription. Thus, although each Vav isoform can respond to similar cell surface receptors, there are isoform-specific differences in their activation of downstream signaling pathways.
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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.