ArticleMolecular and cellular biology1991
Loss of the amino-terminal helix-loop-helix domain of the vav proto-oncogene activates its transforming potential.
Article in Molecular and cellular biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 165 citations in OpenAlex.
- Review
- Potential multi-modal effects of provirus integration on HIV-1 persistence: lessons from other viruses.Trends in immunology · 2022Review
- Filgotinib suppresses HIV-1-driven gene transcription by inhibiting HIV-1 splicing and T cell activation.The Journal of clinical investigation · 2020Article
- Single-cell transcriptional landscapes reveal HIV-1-driven aberrant host gene transcription as a potential therapeutic target.Science translational medicine · 2020Article
- Vav1 mutations identified in human cancers give rise to different oncogenic phenotypes.Oncogenesis · 2018Article
- Activating mutations and translocations in the guanine exchange factor VAV1 in peripheral T-cell lymphomas.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Vav1: A Dr. Jekyll and Mr. Hyde protein--good for the hematopoietic system, bad for cancer.Oncotarget · 2015Review
- Cross-species epigenetics identifies a critical role for VAV1 in SHH subgroup medulloblastoma maintenance.Oncogene · 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
- Article
- Vav family exchange factors: an integrated regulatory and functional view.Small GTPases · 2014Review
- Vav1 oncogenic mutation inhibits T cell receptor-induced calcium mobilization through inhibition of phospholipase Cγ1 activation.The Journal of biological chemistry · 2012Article
- Human Vav1 expression in hematopoietic and cancer cell lines is regulated by c-Myb and by CpG methylation.PloS one · 2012Article
- Vav1 in hematologic neoplasms, a mini review.American journal of blood research · 2012Article
- Article
- Autoinhibition of GEF activity in Intersectin 1 is mediated by the short SH3-DH domain linker.Protein science : a publication of the Protein Society · 2010Article
- Tyrosine residues at the carboxyl terminus of Vav1 play an important role in regulation of its biological activity.The Journal of biological chemistry · 2010Article
- Structural and energetic mechanisms of cooperative autoinhibition and activation of Vav1.Cell · 2010Article
- Internal dynamics control activation and activity of the autoinhibited Vav DH domain.Nature structural & molecular biology · 2008Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
vav, a novel human oncogene, was originally generated in vitro by replacement of its normal 5' coding sequences with sequences from pSV2neo DNA, cotransfected as a selectable marker (S. Katzav, D. Martin-Zanca, and M. Barbacid, EMBO J. 8:2283-2290, 1989). The vav proto-oncogene is normally expressed in cells of hematopoietic origin. To determine whether the 5' rearrangement of vav or its ectopic expression in NIH 3T3 cells contributes to its transforming potential, we isolated murine and human proto-vav cDNA clones as well as human genomic clones corresponding to the 5' end of the gene. Normal proto-vav was poorly transforming in NIH 3T3 cells, whereas truncation of its 5' end greatly enhanced its transforming activity. The relative failure of full-length proto-vav cDNA clones to transform NIH 3T3 cells indicates that the transforming activity of vav is not simply due to ectopic expression. Analysis of the predicted amino terminus of the vav proto-oncogene shows that it contains a helix-loop-helix domain and a leucine zipper motif similar to that of myc family proteins, though it lacks a basic region that is usually found adjacent to helix-loop-helix domains. Loss of the helix-loop-helix domain of proto-vav, either by truncation or by rearrangement with pSV2neo sequences, activates its oncogenic potential.
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