ArticleMolecular and cellular biology2002
Effect of redox balance alterations on cellular localization of LAT and downstream T-cell receptor signaling pathways.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 96 citations in OpenAlex.
- Endogenous antigens shape the transcriptome and TCR repertoire in an autoimmune arthritis model.The Journal of clinical investigation · 2024Article
- Mechanisms of oxidative stress in interstitial cystitis/bladder pain syndrome.Nature reviews. Urology · 2024Review
- Redox Regulation of LAT Enhances T Cell-Mediated Inflammation.Antioxidants (Basel, Switzerland) · 2024Article
- The relationship of redox signaling with the risk for atherosclerosis.Frontiers in pharmacology · 2024Review
- Effect of Diet and Oxidative Stress in the Pathogenesis of Lymphoproliferative Disorders.Antioxidants (Basel, Switzerland) · 2023Review
- Redox regulation of the immune response.Cellular & molecular immunology · 2022Review
- ZAP70, too little, too much can lead to autoimmunity.Immunological reviews · 2022Review
- Immunomodulatory Effects of Green Tea Polyphenols.Molecules (Basel, Switzerland) · 2021Review
- Control of T-Cell Activation and Signaling by Amino-Acid Catabolizing Enzymes.Frontiers in cell and developmental biology · 2020Review
- Linking Immunoevasion and Metabolic Reprogramming in B-Cell-Derived Lymphomas.Frontiers in oncology · 2020Review
- Reporters of TCR signaling identify arthritogenic T cells in murine and human autoimmune arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Inhibition of T Cell Receptor Activation by Semi-Synthetic Sesquiterpene Lactone Derivatives and Molecular Modeling of Their Interaction with Glutathione and Tyrosine Kinase ZAP-70.Molecules (Basel, Switzerland) · 2019Article
- The natural sesquiterpene lactones arglabin, grosheimin, agracin, parthenolide, and estafiatin inhibit T cell receptor (TCR) activation.Phytochemistry · 2018Article
- The Immune Signaling Adaptor LAT Contributes to the Neuroanatomical Phenotype of 16p11.2 BP2-BP3 CNVs.American journal of human genetics · 2017Article
- The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.Molecular neurobiology · 2016Review
- Review
- T cells and reactive oxygen species.Journal of biomedical science · 2015Review
- Trx1/TrxR1 system regulates post-selected DP thymocytes survival by modulating ASK1-JNK/p38 MAPK activities.Immunology and cell biology · 2015Article
- TCR-triggered extracellular superoxide production is not required for T-cell activation.Cell communication and signaling : CCS · 2014Article
- IL-7- and IL-15-mediated TCR sensitization enables T cell responses to self-antigens.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The integral membrane protein linker for activation of T cells (LAT) is a central adapter protein in the T-cell receptor (TCR)-mediated signaling pathways. The cellular localization of LAT is extremely sensitive to intracellular redox balance alterations. Reduced intracellular levels of the antioxidant glutathione (GSH), a hallmark of chronic oxidative stress, resulted in the membrane displacement of LAT, abrogated TCR-mediated signaling and consequently hyporesponsiveness of T lymphocytes. The membrane displacement of LAT is accompanied by a considerable difference in the mobility of LAT upon native and nonreducing denaturing polyacrylamide gel electrophoresis analysis, a finding indicative of a conformational change. Targeted mutation of redox-sensitive cysteine residues within LAT created LAT mutants which remain membrane anchored under conditions of chronic oxidative stress. The expression of redox-insensitive LAT mutants allows for restoration of TCR-mediated signal transduction, whereas CD28-mediated signaling pathways remained impaired. These results are indicative that the membrane displacement of LAT as a result of redox balance alterations is a consequence of a conformational change interfering with the insertion of LAT into the plasma membrane. Conclusively, the data suggest a role for LAT as a crucial intermediate in the sensitivity of TCR signaling and hence T lymphocytes toward chronic oxidative stress.
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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.