ArticleThe Journal of cell biology2001
Vav2 is required for cell spreading.
Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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
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Who cites it
49 citing papers in PubMed, 99 citations in OpenAlex.
- Structure-based drug repurposing and in vitro evaluation of VAV2-associated candidates for suppression of macrophage foam-cell formation in atherosclerosis.Molecular diversity · 2026Article
- Cell migration signaling through the EGFR-VAV2-Rac1 pathway is sustained in endosomes.Journal of cell science · 2025Article
- Role of RhoG as a regulator of cellular functions: integrating insights on immune cell activation, migration, and functions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Platelets-related signature based diagnostic model in rheumatoid arthritis using WGCNA and machine learning.Frontiers in immunology · 2023Article
- Vav2 is a novel APP-interacting protein that regulates APP protein level.Scientific reports · 2022Article
- Vav Proteins in Development of the Brain: A Potential Relationship to the Pathogenesis of Congenital Zika Syndrome?Viruses · 2022Review
- Whole-genome screen identifies diverse pathways that negatively regulate ciliogenesis.Molecular biology of the cell · 2021Article
- Phosphorylated cortactin recruits Vav2 guanine nucleotide exchange factor to activate Rac3 and promote invadopodial function in invasive breast cancer cells.Molecular biology of the cell · 2017Article
- Synaptopodin Is a Coincidence Detector of Tyrosine versus Serine/Threonine Phosphorylation for the Modulation of Rho Protein Crosstalk in Podocytes.Journal of the American Society of Nephrology : JASN · 2017Article
- Modeling, signaling and cytoskeleton dynamics: integrated modeling-experimental frameworks in cell migration.Wiley interdisciplinary reviews. Systems biology and medicine · 2017Review
- Blood Brothers: Hemodynamics and Cell-Matrix Interactions in Endothelial Function.Antioxidants & redox signaling · 2016Review
- Vimentin regulates lung cancer cell adhesion through a VAV2-Rac1 pathway to control focal adhesion kinase activity.Oncogene · 2015Article
- An Elmo-Dock complex locally controls Rho GTPases and actin remodeling during cadherin-mediated adhesion.The Journal of cell biology · 2014Article
- Simultaneous and independent tuning of RhoA and Rac1 activity with orthogonally inducible promoters.Integrative biology : quantitative biosciences from nano to macro · 2014Article
- PTP-PEST targets a novel tyrosine site in p120 catenin to control epithelial cell motility and Rho GTPase activity.Journal of cell science · 2014Article
- The on-off relationship of Rho and Rac during integrin-mediated adhesion and cell migration.Small GTPases · 2014Review
- The actin-bundling protein L-plastin supports T-cell motility and activation.Immunological reviews · 2013Review
- Thy-1-mediated cell-cell contact induces astrocyte migration through the engagement of αVβ3 integrin and syndecan-4.Biochimica et biophysica acta · 2013Article
- Paxillin kinase linker (PKL) regulates Vav2 signaling during cell spreading and migration.Molecular biology of the cell · 2013Article
- Potassium-chloride cotransporter 3 interacts with Vav2 to synchronize the cell volume decrease response with cell protrusion dynamics.PloS one · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Vav2 is a widely expressed Rho family guanine nucleotide exchange factor highly homologous to Vav1 and Vav3. Activated versions of Vav2 are transforming, but the normal function of Vav2 and how it is regulated are not known. We investigated the pathways that regulate Vav2 exchange activity in vivo and characterized its function. Overexpression of Vav2 activates Rac as assessed by both direct measurement of Rac-GTP and cell morphology. Vav2 also catalyzes exchange for RhoA, but does not cause morphologic changes indicative of RhoA activation. Vav2 nucleotide exchange is Src-dependent in vivo, since the coexpression of Vav2 and dominant negative Src, or treatment with the Src inhibitor PP2, blocks both Vav2-dependent Rac activation and lamellipodia formation. A mutation in the pleckstrin homology (PH) domain eliminates exchange activity and this construct does not induce lamellipodia, indicating the PH domain is necessary to catalyze nucleotide exchange. To further investigate the function of Vav2, we mutated the dbl homology (DH) domain and asked whether this mutant would function as a dominant negative to block Rac-dependent events. Studies using this mutant indicate that Vav2 is not necessary for platelet-derived growth factor- or epidermal growth factor-dependent activation of Rac. The Vav2 DH mutant did act as a dominant negative to inhibit spreading of NIH3T3 cells on fibronectin, specifically by blocking lamellipodia formation. These findings indicate that in fibroblasts Vav2 is necessary for integrin, but not growth factor-dependent activation of Rac leading to lamellipodia.
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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.