ArticleMolecular and cellular biology2003
Vav1 dephosphorylation by the tyrosine phosphatase SHP-1 as a mechanism for inhibition of cellular cytotoxicity.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
142 citing papers in PubMed, 281 citations in OpenAlex.
- Recent Advances in Research on SHP Family Phosphatases: Signal Regulation Mechanisms and Disease Associations.Cell biochemistry and function · 2026Review
- A framework integrating multiscale in silico modeling and experimental data predicts CAR-NK cell cytotoxicity across target cell types.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Neutrophil CEACAMs and the Inflammatory Response toJournal of innate immunity · 2026Review
- CD47 inhibits phagocytosis through Vav dephosphorylation.The Journal of cell biology · 2025Article
- Exceptional diversity of allorecognition receptors in a nonvertebrate chordate reveals principles of innate allelic discrimination.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanoregulation of lymphocyte cytotoxicity.Nature reviews. Immunology · 2025Review
- Emerging roles of KIR2DL4 in cancer immunotherapy.Breast cancer (Tokyo, Japan) · 2025Review
- Cancer cells suppress NK cell activity by actin-driven polarization of inhibitory ligands to the immunological synapse.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Adaptive immune cells antagonize ILC2 homeostasis via SLAMF3 and SLAMF5.Science advances · 2025Article
- Inhibitory leukocyte immunoglobulin-like receptors, subfamily B (LILRBs) in human diseases: structure, roles, mechanisms, and clinical applications.Theranostics · 2025Review
- Peptide-specific natural killer cell receptors.Oxford open immunology · 2025Review
- Bulk and single-cell transcriptomics identify gene signatures of stem cell-derived NK cell donors with superior cytolytic activity.Molecular therapy. Oncology · 2024Article
- Comprehensive snapshots of natural killer cells functions, signaling, molecular mechanisms and clinical utilization.Signal transduction and targeted therapy · 2024Review
- Genetic and functional diversity of allorecognition receptors in the urochordate,bioRxiv : the preprint server for biology · 2024Article
- NKG2A genetic deletion promotes human primary NK cell anti-tumor responses better than an anti-NKG2A monoclonal antibody.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Natural killer cells in cancer immunotherapy.MedComm · 2024Review
- Positive regulation of Vav1 by Themis controls CD4 T cell pathogenicity in a mouse model of central nervous system inflammation.Cellular and molecular life sciences : CMLS · 2024Article
- Natural Killer Cell Mechanosensing in Solid Tumors.Bioengineering (Basel, Switzerland) · 2024Review
- NK cell-based tumor immunotherapy.Bioactive materials · 2024Review
- All-Atom Simulations Reveal the Intricacies of Signal Transduction upon Binding of the HLA-E Ligand to the Transmembrane Inhibitory CD94/NKG2A Receptor.Journal of chemical information and modeling · 2023Article
82 more citing papers are in PubMed but not listed here.
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 4 institutions in 2 countries.
Funding
Abstract
Here, we present data suggesting a novel mechanism for regulation of natural killer (NK) cell cytotoxicity through inhibitory receptors. Interaction of activation receptors with their ligands on target cells induces cytotoxicity by NK cells. This activation is under negative control by inhibitory receptors that recruit tyrosine phosphatase SHP-1 upon binding major histocompatibility class I on target cells. How SHP-1 blocks the activation pathway is not known. To identify SHP-1 substrates, an HLA-C-specific inhibitory receptor fused to a substrate-trapping mutant of SHP-1 was expressed in NK cells. Phosphorylated Vav1, a regulator of actin cytoskeleton, was the only protein detectably associated with the catalytic site of SHP-1 during NK cell contact with target cells expressing HLA-C. Vav1 trapping was independent of actin polymerization, suggesting that inhibition of cellular cytotoxicity occurs through an early dephosphorylation of Vav1 by SHP-1, which blocks actin-dependent activation signals. Such a mechanism explains how inhibitory receptors can block activating signals induced by different receptors.
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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.