ArticleThe EMBO journal2014
Dok1 and Dok2 proteins regulate natural killer cell development and function.
Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- IgG Idiotype Diversity Shapes Cytokine Profiles and Autoantibody Targets in HTLV-1 Clinical Outcomes.International journal of molecular sciences · 2025Article
- CD200R1-CD200 checkpoint inhibits phagocytosis differently from SIRPα-CD47 to suppress tumor growth.Nature communications · 2025Article
- DOK1 and DOK2 regulate CD8 T cell signaling and memory formation without affecting tumor cell killing.Scientific reports · 2024Article
- scCorrector: a robust method for integrating multi-study single-cell data.Briefings in bioinformatics · 2024Article
- The transcriptome signature analysis of the epithelial-mesenchymal transition and immune cell infiltration in colon adenocarcinoma.Scientific reports · 2023Article
- Negative intracellular regulators of T-cell receptor (TCR) signaling as potential antitumor immunotherapy targets.Journal for immunotherapy of cancer · 2023Review
- Large-scale sequencing identifies multiple genes and rare variants associated with Crohn's disease susceptibility.Nature genetics · 2022Article
- DOK2 Has Prognostic and Immunologic Significance in Adults With Acute Myeloid Leukemia: A Novel Immune-Related Therapeutic Target.Frontiers in medicine · 2022Article
- Introduction to DOK2 and its potential role in cancer.Physiological research · 2021Review
- Single-cell profiling reveals the trajectories of natural killer cell differentiation in bone marrow and a stress signature induced by acute myeloid leukemia.Cellular & molecular immunology · 2021Article
- Prognostic role of DOK family adapters in acute myeloid leukemia.Cancer gene therapy · 2019Article
- Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-ProducingMicroorganisms · 2019Article
- Genome-Wide CRISPR Screen Identifies Host Factors Required byFrontiers in cellular and infection microbiology · 2019Article
- Deconstructing deployment of the innate immune lymphocyte army for barrier homeostasis and protection.Immunological reviews · 2018Review
- Methylation-associated DOK1 and DOK2 down-regulation: Potential biomarkers for predicting adverse prognosis in acute myeloid leukemia.Journal of cellular physiology · 2018Article
- Cutting Edge: Check Your Mice-A Point Mutation in theJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Purification of zebrafish erythrocytes as a means of identifying a novel regulator of haematopoiesis.British journal of haematology · 2018Article
- Dok-1 and Dok-2 Are Required To Maintain Herpes Simplex Virus 1-Specific CD8Journal of virology · 2017Article
- c-Jun N-terminal kinase mediates mouse liver injury through a novel Sab (SH3BP5)-dependent pathway leading to inactivation of intramitochondrial Src.Hepatology (Baltimore, Md.) · 2016Article
- Circulating NKp46OncoimmunologyArticle
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Natural killer (NK) cells are involved in immune responses against tumors and microbes. NK-cell activation is regulated by intrinsic and extrinsic mechanisms that ensure NK tolerance and efficacy. Here, we show that the cytoplasmic signaling molecules Dok1 and Dok2 are tyrosine phosphorylated upon NK-cell activation. Overexpression of Dok proteins in human NK cells reduces cell activation induced by NK-cell-activating receptors. Dok1 and Dok2 gene ablation in mice induces an NK-cell maturation defect and leads to increased IFN-γ production induced by activating receptors. Taken together, these results reveal that Dok1 and Dok2 proteins are involved in an intrinsic negative feedback loop downstream of NK-cell-activating receptors in mouse and human.
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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.