ArticleMolecular and cellular biology1994
Dbl and Vav mediate transformation via mitogen-activated protein kinase pathways that are distinct from those activated by oncogenic Ras.
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 41 papers.
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Who cites it
41 citing papers in PubMed, 135 citations in OpenAlex.
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- Functional and biological heterogeneity of KRASScience signaling · 2022Article
- The Crossroads between RAS and RHO Signaling Pathways in Cellular Transformation, Motility and Contraction.Genes · 2021Review
- Gain-of-FunctionCancer discovery · 2020Article
- Activation of Rho Family GTPases by Small Molecules.ACS chemical biology · 2018Article
- Vav1 promotes lung cancer growth by instigating tumor-microenvironment cross-talk via growth factor secretion.Oncotarget · 2014Article
- Tyrosine phosphorylation of Dbl regulates GTPase signaling.The Journal of biological chemistry · 2014Article
- The heme oxygenase-1 protein is overexpressed in human renal cancer cells following activation of the Ras-Raf-ERK pathway and mediates anti-apoptotic signal.The Journal of biological chemistry · 2011Article
- Article
- Transformation by a nucleotide-activated P2Y receptor is mediated by activation of Galphai, Galphaq and Rho-dependent signaling pathways.Journal of molecular signaling · 2010Article
- Identification of CRMP4 as a convergent regulator of axon outgrowth inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- The Sprouty-related protein, Spred, inhibits cell motility, metastasis, and Rho-mediated actin reorganization.Oncogene · 2004Article
- Article
- RhoGEF specificity mutants implicate RhoA as a target for Dbs transforming activity.Molecular and cellular biology · 2002Article
- Opposing roles of the extracellular signal-regulated kinase and p38 mitogen-activated protein kinase cascades in Ras-mediated downregulation of tropomyosin.Molecular and cellular biology · 2002Article
- Direct interaction of insulin-like growth factor-1 receptor with leukemia-associated RhoGEF.The Journal of cell biology · 2001Article
- Autoinhibition mechanism of proto-Dbl.Molecular and cellular biology · 2001Article
- Ezrin function is required for ROCK-mediated fibroblast transformation by the Net and Dbl oncogenes.The EMBO journal · 2000Article
- G2A is an oncogenic G protein-coupled receptor.Oncogene · 2000Article
- A rac homolog is required for induction of hyphal growth in the dimorphic yeast Yarrowia lipolytica.Journal of bacteriology · 2000Article
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Vav and Dbl are members of a novel class of oncogene proteins that share significant sequence identity in a approximately 250-amino-acid domain, designated the Dbl homology domain. Although Dbl functions as a guanine nucleotide exchange factor (GEF) and activator of Rho family proteins, recent evidence has demonstrated that Vav functions as a GEF for Ras proteins. Thus, transformation by Vav and Dbl may be a consequence of constitutive activation of Ras and Rho proteins, respectively. To address this possibility, we have compared the transforming activities of Vav and Dbl with that of the Ras GEF, GRF/CDC25. As expected, GRF-transformed cells exhibited the same reduction in actin stress fibers and focal adhesions as Ras-transformed cells. In contrast, Vav- and Dbl-transformed cells showed the same well-developed stress fibers and focal adhesions observed in normal or RhoA(63L)-transformed NIH 3T3 cells. Furthermore, neither Vav- or Dbl-transformed cells exhibited the elevated levels of Ras-GTP (60%) observed with GRF-transformed cells. Finally, GRF, but not Vav or Dbl, induced transcriptional activation from Ras-responsive DNA elements (ets/AP-1, fos promoter, and kappa B). However, like Ras- and GRF-transformed cells, both Vav- and Dbl-transformed cells exhibited constitutively activated mitogen-activated protein kinases (MAPKs) (primarily p42MAPK/ERK2). Since kinase-deficient forms of p42MAPK/ERK2 and p44MAPK/ERK1 inhibited Dbl transformation, MAPK activation may be an important component of its transforming activity. Taken together, our observations indicate that Vav and Dbl transformation is not a consequence of Ras activation and instead may involve the constitutive activation of MAPKs.
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