ArticleCellular signalling2018
New insights into the Vav1 activation cycle in lymphocytes.
Article in Cellular signalling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Deep phosphotyrosine characterisation of primary murine T cells using broad spectrum optimisation of selective triggering.Proteomics · 2024Article
- Fluid shear stress enhances natural killer cell's cytotoxicity toward circulating tumor cells through NKG2D-mediated mechanosensing.APL bioengineering · 2023Article
- Facts and prospects of peptide in targeted therapy and immune regulation against triple-negative breast cancer.Frontiers in immunology · 2023Review
- Cancer-associated mutations in VAV1 trigger variegated signaling outputs and T-cell lymphomagenesis.The EMBO journal · 2021Article
- A novel role for an old target: CD45 for breast cancer immunotherapy.Oncoimmunology · 2021Article
- Identification of Genes Related to Immune Infiltration in the Tumor Microenvironment of Cutaneous Melanoma.Frontiers in oncology · 2021Article
- Downregulation of CD45 Signaling in COVID-19 Patients Is Reversed by C24D, a Novel CD45 Targeting Peptide.Frontiers in medicine · 2021Article
- Vav2 catalysis-dependent pathways contribute to skeletal muscle growth and metabolic homeostasis.Nature communications · 2020Article
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- Vav2 lacks CaJournal of cell science · 2020Article
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Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Vav1 is a hematopoietic-specific Rho GDP/GTP exchange factor and signaling adaptor. Although these activities are known to be stimulated by direct Vav1 phosphorylation, little information still exists regarding the regulatory layers that influence the overall Vav1 activation cycle. Using a collection of cell models and activation-mimetic Vav1 mutants, we show here that the dephosphorylated state of Vav1 in nonstimulated T cells requires the presence of a noncatalytic, phospholipase Cγ1-Slp76-mediated inhibitory pathway. Upon T cell stimulation, Vav1 becomes rapidly phosphorylated via the engagement of Lck and, to a much lesser extent, other Src family kinases and Zap70. In this process, Lck, Zap70 and the adaptor protein Lat contribute differently to the dynamics and amplitude of the Vav1 phosphorylated pool. Consistent with a multiphosphosite activation mechanism, the optimal stimulation of Vav1 can only be recapitulated by the combination of several activation-mimetic phosphosite mutants. The analysis of these mutants has also unveiled the presence of different Vav1 signaling competent states that are influenced by phosphosites present in the N- and C-terminal domains of the protein.
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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 Socratic graph.