ArticlePloS one2020
Bypassing ubiquitination enables LAT recycling to the cell surface and enhanced signaling in T cells.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 25 citations in OpenAlex.
- RNA-seq analysis of small intestine transcriptional changes induced by starvation stress in piglets.Animal biotechnology · 2024Article
- Redox Regulation of LAT Enhances T Cell-Mediated Inflammation.Antioxidants (Basel, Switzerland) · 2024Article
- Exploring the biomarkers and potential therapeutic drugs for sepsis via integrated bioinformatic analysis.BMC infectious diseases · 2024Article
- Nanoscale, antigen encounter-dependent, IL-12 delivery by CAR T cells plus PD-L1 blockade for cancer treatment.Journal of translational medicine · 2023Article
- Contextual reprogramming of CAR-T cells for treatment of HER2Journal of translational medicine · 2021Article
- Article
- Screening of Key Genes of Sepsis and Septic Shock Using Bioinformatics Analysis.Journal of inflammation research · 2021Article
- Microclusters as T Cell Signaling Hubs: Structure, Kinetics, and Regulation.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
LAT molecules defective in ubiquitination have an increased half-life and induce enhanced signaling when expressed in T cells. In this study, we have examined the role of ubiquitination in regulating LAT endocytosis, recycling, and degradation in resting and stimulated T cells. By tracking and comparing plasma membrane-labeled wild type and ubiquitination-resistant 2KR LAT, we find that ubiquitination promotes the degradation of surface LAT in T cells. Activation of T cells increases LAT ubiquitination and promotes trafficking of internalized LAT to lysosomes for degradation. Ubiquitination of LAT does not change internalization rates from the cell surface, but prevents efficient recycling of LAT to the surface of T cells. Our study demonstrates that surface LAT levels are tightly controlled by ubiquitination. LAT in unstimulated cells lacks ubiquitin allowing for increased LAT stability and efficient T cell activation upon TCR triggering; ubiquitination leads to efficient removal of LAT after activation.
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Registered trials
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