ArticleMolecular and cellular biology2000
Vav2 activates Rac1, Cdc42, and RhoA downstream from growth factor receptors but not beta1 integrins.
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 104 papers.
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Who cites it
104 citing papers in PubMed, 200 citations in OpenAlex.
- CDC42-related genes are upregulated in helper T cells from obese asthmatic children.The Journal of allergy and clinical immunology · 2018Trial
- Monocyte Migration Emerges from a Divergent Chemokine Signaling Network.bioRxiv : the preprint server for biology · 2026Article
- Rho/PAK signaling: a key driver of anthracycline and taxane resistance in breast cancer.Medical oncology (Northwood, London, England) · 2026Review
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- Optogenetic storage and release of protein and mRNA in live cells and animals.Nature communications · 2025Article
- Activity-dependent regulation of Cdc42 by Ephexin5 drives synapse growth and stabilization.Science advances · 2025Article
- Leveraging AAV1-Rac1T17N to prevent experimental proliferative vitreoretinopathy.Journal of translational medicine · 2025Article
- PI(3,4,5)P3-mediated Cdc42 activation regulates macrophage podosome assembly.Cellular and molecular life sciences : CMLS · 2025Article
- Cell migration signaling through the EGFR-VAV2-Rac1 pathway is sustained in endosomes.Journal of cell science · 2025Article
- Effects of HTLV-1 on leukocyte trafficking and migration in ACs compared to healthy individuals.BMC research notes · 2024Article
- AFAP1L1 promotes gastric cancer progression by interacting with VAV2 to facilitate CDC42-mediated activation of ITGA5 signaling pathway.Journal of translational medicine · 2023Article
- Phosphorylation of guanosine monophosphate reductase triggers a GTP-dependent switch from pro- to anti-oncogenic function of EPHA4.Cell chemical biology · 2022Article
- TC10 regulates breast cancer invasion and metastasis by controlling membrane type-1 matrix metalloproteinase at invadopodia.Communications biology · 2021Article
- The RhoA dependent anti-metastatic function of RKIP in breast cancer.Scientific reports · 2021Article
- RAC1 induces nuclear alterations through the LINC complex to enhance melanoma invasiveness.Molecular biology of the cell · 2020Article
- Rho GTPases in the Amygdala-A Switch for Fears?Cells · 2020Review
- Collective Migrations ofGenetics · 2020Review
- Ubiquitination of the scaffold protein IQGAP1 diminishes its interaction with and activation of the Rho GTPase CDC42.The Journal of biological chemistry · 2020Article
- The focal adhesion scaffold protein Hic-5 regulates vimentin organization in fibroblasts.Molecular biology of the cell · 2019Article
- High-Throughput, Time-Resolved Mechanical Phenotyping of Prostate Cancer Cells.Scientific reports · 2019Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Rho family of GTPases plays a major role in the organization of the actin cytoskeleton. These G proteins are activated by guanine nucleotide exchange factors that stimulate the exchange of bound GDP for GTP. In their GTP-bound state, these G proteins interact with downstream effectors. Vav2 is an exchange factor for Rho family GTPases. It is a ubiquitously expressed homologue of Vav1, and like Vav1, it has previously been shown to be activated by tyrosine phosphorylation. Because Vav1 becomes tyrosine phosphorylated and activated following integrin engagement in hematopoietic cells, we investigated the tyrosine phosphorylation of Vav2 in response to integrin-mediated adhesion in fibroblasts and epithelial cells. However, no tyrosine phosphorylation of Vav2 was detected in response to integrin engagement. In contrast, treating cells with either epidermal growth factor or platelet-derived growth factor stimulated tyrosine phosphorylation of Vav2. We have examined the effects of overexpressing either wild-type or amino-terminally truncated (constitutively active) forms of Vav2 as fusion proteins with green fluorescent protein. Overexpression of either wild-type or constitutively active Vav2 resulted in prominent membrane ruffles and enhanced stress fibers. These cells revealed elevated rates of cell migration that were inhibited by expression of dominant negative forms of Rac1 and Cdc42. Using a binding assay to measure the activity of Rac1, Cdc42, and RhoA, we found that overexpression of Vav2 resulted in increased activity of each of these G proteins. Expression of a carboxy-terminal fragment of Vav2 decreased the elevation of Rac1 activity induced by epidermal growth factor, consistent with Vav2 mediating activation of Rac1 downstream from growth factor receptors.
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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.