ArticleMolecular and cellular biology1994
Activation of Ras in vitro and in intact fibroblasts by the Vav guanine nucleotide exchange protein.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 78 citations in OpenAlex.
- Analysis of Ras-effector interaction competition in large intestine and colorectal cancer context.Small GTPases · 2021Article
- Bach1 is critical for the transformation of mouse embryonic fibroblasts by Ras(V12) and maintains ERK signaling.Oncogene · 2013Article
- Article
- The product of the cph oncogene is a truncated, nucleotide-binding protein that enhances cellular survival to stress.Oncogene · 1999Article
- Vav regulates peptide-specific apoptosis in thymocytes.The Journal of experimental medicine · 1998Article
- Dissociation of intracellular signaling pathways in response to partial agonist ligands of the T cell receptor.The Journal of experimental medicine · 1998Article
- Cloning and characterization of Ras-GRF2, a novel guanine nucleotide exchange factor for Ras.Molecular and cellular biology · 1997Article
- Lck regulates Vav activation of members of the Rho family of GTPases.Molecular and cellular biology · 1997Article
- Vav in natural killer cells is tyrosine phosphorylated upon cross-linking of Fc gamma RIIIA and is constitutively associated with a serine/threonine kinase.The Biochemical journal · 1996Article
- p95vav associates with the nuclear protein Ku-70.Molecular and cellular biology · 1996Article
- A functional T-cell receptor signaling pathway is required for p95vav activity.Molecular and cellular biology · 1995Article
- Tyrosine phosphorylation of the proto-oncogene product Vav and its association with the adapter Grb2/Ash in a human leukemia cell line UT-7.Japanese journal of cancer research : Gann · 1995Article
- Association of the vav proto-oncogene product with poly(rC)-specific RNA-binding proteins.Molecular and cellular biology · 1995Article
- Tyrosine phosphorylation of p95Vav in myeloid cells is regulated by GM-CSF, IL-3 and steel factor and is constitutively increased by p210BCR/ABL.The EMBO journal · 1995Article
- The vav proto-oncogene is required early in embryogenesis but not for hematopoietic development in vitro.The EMBO journal · 1995Article
- Signal transduction by Ras-like GTPases: a potential target for anticancer drugs.Gene expression · 1995Review
- Binding of Vav to Grb2 through dimerization of Src homology 3 domains.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- Consensus sequences for ATP-binding sites in protein kinases do not apply to diacylglycerol kinases.The Biochemical journal · 1994Article
- Dbl and Vav mediate transformation via mitogen-activated protein kinase pathways that are distinct from those activated by oncogenic Ras.Molecular and cellular biology · 1994Article
- Tyrosine phosphorylation and activation of Bruton tyrosine kinase upon Fc epsilon RI cross-linking.Molecular and cellular biology · 1994Article
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9 authors at 1 institution in 1 country.
Funding
Abstract
We recently identified Vav, the product of the vav proto-oncogene, as a guanine nucleotide exchange factor (GEF) for Ras. Vav is enzymatically activated by lymphocyte antigen receptor-coupled protein tyrosine kinases or independently by diglycerides. To further evaluate the physiological role of Vav, we assessed its GDP-GTP exchange activity against several Ras-related proteins in vitro and determined whether Vav activation in transfected NIH 3T3 fibroblasts correlates with the activity status of Ras and mitogen-activated protein (MAP) kinases. In vitro translated purified Vav activated by phorbol myristate acetate (PMA) or phosphorylation with recombinant p56lck displayed GEF activity against Ras but not against recombinant RacI, RacII, Ral, or RhoA proteins. Expression of vav or proto-vav in stably transfected NIH 3T3 cells led to a approximately 10-fold increase in basal or PMA-stimulated Ras exchange activity, respectively, in total-cell lysates and Vav immunoprecipitates. Elevated GEF activity was paralleled in each case by a significant increase in the proportion of active, GTP-bound Ras. PMA had a minimal effect on the low Ras. GTP level in untransfected control fibroblasts but increased it from 20 to 37% in proto-vav-transfected cells. vav-transfected cells displayed a constitutively elevated Ras. GTP level (35%), which was not increased further by PMA treatment. MAP kinases, known downstream intermediates in Ras-dependent signaling pathways, similarly exhibited increased basal or PMA-stimulated activity in Vav-expressing cells by comparison with normal NIH 3T3 cells. These results demonstrate a physiologic interaction between Vav and its target, Ras, leading to MAP kinase activation.
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