ArticleOncology letters2018
A role for GPI-CD59 in promoting T-cell signal transduction via LAT.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Differential Transcriptome Analysis of Intrauterine UPD6pat Fetuses With Distinct Phenotypes.Molecular genetics & genomic medicine · 2026Article
- Protein lipidation in the tumor microenvironment: enzymology, signaling pathways, and therapeutics.Molecular cancer · 2025Review
- Deciphering CD59: Unveiling Its Role in Immune Microenvironment and Prognostic Significance.Cancers · 2024Article
- Multiple CD59 Polymorphisms in Chinese Patients withJournal of immunology research · 2023Article
- Novel LAT Pathogenic Variants in a POI Family and Its Role in the Ovary.Frontiers in genetics · 2021Article
- High Expression of PIGC Predicts Unfavorable Survival in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2021Article
- Amplification of Stem Genes: New Potential Metastatic Makers in Patients with an Early Form of Breast Cancer.Journal of Korean medical science · 2019Article
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cluster of differentiation 59 (CD59) is a glycosylphosphatidylinositol-anchored protein. Cross-linking of CD59 with specific monoclonal antibodies can cause a series of intracellular signal transduction events. However, the underlying molecular mechanisms are poorly understood. Linker for activation of T-cells (LAT) is a crucial adaptor protein in T-cell signaling, and its phosphorylation and palmitoylation are essential for its localization and function. In a previous study by the present authors, it was demonstrated that CD59 may be responsible for LAT palmitoylation, thereby regulating T-cell signal transduction. The present study detected the co-localization of LAT and CD59 in lipid rafts by transfecting Jurkat cells with lentivirus vectors carrying the LAT-enhanced green fluorescent protein fusion protein. In addition, LAT and CD59 were shown to have a synergistic effect on the proliferation of Jurkat cells. The results also indicated that CD59 may transfer the palmitate group from phosphatidylinositol to LAT to form LAT palmitate, which then localizes to lipid rafts to regulate T-cell activation. The results of the present study provided novel insights into the role of CD59 in T-cell signal transduction.
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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.