ArticleThe EMBO journal2002
Pleiotropic defects in TCR signaling in a Vav-1-null Jurkat T-cell line.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 94 citations in OpenAlex.
- Vav2 lacks CaJournal of cell science · 2020Article
- Article
- New insights into the Vav1 activation cycle in lymphocytes.Cellular signalling · 2018Article
- A Paradoxical Tumor-Suppressor Role for the Rac1 Exchange Factor Vav1 in T Cell Acute Lymphoblastic Leukemia.Cancer cell · 2017Article
- 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
- Vav1 Regulates T-Cell Activation through a Feedback Mechanism and Crosstalk between the T-Cell Receptor and CD28.Journal of proteome research · 2015Article
- Mutation of Vav1 adaptor region reveals a new oncogenic activation.Oncotarget · 2015Article
- Clinical significance and prognostic value of Vav1 expression in Non-small cell lung cancer.American journal of cancer research · 2015Article
- Rho protein GTPases and their interactions with NFκB: crossroads of inflammation and matrix biology.Bioscience reports · 2014Review
- Article
- Coordinate control of cytoskeletal remodeling and calcium mobilization during T-cell activation.Immunological reviews · 2013Review
- The N-terminal 20-amino acid region of guanine nucleotide exchange factor Vav1 plays a distinguished role in T cell receptor-mediated calcium signaling.The Journal of biological chemistry · 2013Article
- Vav1 oncogenic mutation inhibits T cell receptor-induced calcium mobilization through inhibition of phospholipase Cγ1 activation.The Journal of biological chemistry · 2012Article
- Vav1-mediated scaffolding interactions stabilize SLP-76 microclusters and contribute to antigen-dependent T cell responses.Science signaling · 2011Article
- The distinct role of guanine nucleotide exchange factor Vav1 in Bcl-2 transcription and apoptosis inhibition in Jurkat leukemia T cells.Acta pharmacologica Sinica · 2011Article
- Tyrosine residues at the carboxyl terminus of Vav1 play an important role in regulation of its biological activity.The Journal of biological chemistry · 2010Article
- Cooperative interactions at the SLP-76 complex are critical for actin polymerization.The EMBO journal · 2010Article
- T-cell receptor early signalling complex activation in response to interferon-alpha receptor stimulation.The Biochemical journal · 2010Article
- Rho family GTPases and their regulators in lymphocytes.Nature reviews. Immunology · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The Rac/Rho-specific guanine nucleotide exchange factor, Vav-1, is a key component of the T-cell antigen receptor (TCR)-linked signaling machinery. Here we have used somatic cell gene-targeting technology to generate a Vav-1-deficient Jurkat T-cell line. The J.Vav1 cell line exhibits dramatic defects in TCR-dependent interleukin (IL)-2 promoter activation, accompanied by significant reductions in the activities of the NFAT(IL-2), NFkappaB, AP-1 and REAP transcription factors that bind to the IL-2 promoter region. In contrast, loss of Vav-1 had variable effects on early TCR-stimulated signaling events. J.Vav1 cells display a selective defect in sustained Ca(2+) signaling during TCR stimulation, and complementation of this abnormality by exogenously introduced Vav-1 is dependent on the Vav-1 calponin homology domain. While JNK activation was severely impaired, the stimulation of Ras, ERK and protein kinase C-theta activities, as well as the mobilization of lipid rafts, appeared normal in the J.Vav1 cells. Finally, evidence is presented to suggest that the alternative Vav family members, Vav-2 and Vav-3, are activated during TCR ligation, and partially compensate for the loss of Vav-1 in Jurkat T cells.
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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.