ArticleImmunology2020
Actin polymerization regulates recruitment of Nck to CD3ε upon T-cell receptor triggering.
Article in Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- The Y105 phosphosite between the SH3.1 and SH3.2 domains of Nck1 regulates its binding to CD3ϵ.iScience · 2026Article
- Nck1 regulates the in vitro development of human regulatory T cells through AKT pathway.Clinical and experimental immunology · 2025Article
- Human T-cell receptor triggering requires inactivation of Lim kinase-1 by Slingshot-1 phosphatase.Communications biology · 2024Article
- Lack of Nck1 protein and Nck-CD3 interaction caused the increment of lipid content in Jurkat T cells.BMC molecular and cell biology · 2022Article
- Wiskott-Aldrich Syndrome Protein: Roles in Signal Transduction in T Cells.Frontiers in cell and developmental biology · 2021Review
- Identification and Validation of Prognostic Factors of Lipid Metabolism in Obstructive Sleep Apnea.Frontiers in genetics · 2021Article
- The Clinical Aspect of Adaptor Molecules in T Cell Signaling: Lessons Learnt From Inborn Errors of Immunity.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following T-cell antigen receptor (TCR) engagement, rearrangement of the actin cytoskeleton supports intracellular signal transduction and T-cell activation. The non-catalytic region of the tyrosine kinase (Nck) molecule is an adapter protein implicated in TCR-induced actin polymerization. Further, Nck is recruited to the CD3ε subunit of the TCR upon TCR triggering. Here we examine the role of actin polymerization in the recruitment of Nck to the TCR. To this end, Nck binding to CD3ε was quantified in Jurkat cells using the proximity ligation assay. We show that inhibition of actin polymerization using cytochalasin D delayed the recruitment of Nck1 to the TCR upon TCR triggering. Interestingly, CD3ε phosphorylation was also delayed. These findings suggest that actin polymerization promotes the recruitment of Nck to the TCR, enhancing downstream signaling, such as phosphorylation of CD3ε.
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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.