ArticleAmerican journal of physiology. Cell physiology2007
The Ca(2+)-activated K(+) channel KCa3.1 compartmentalizes in the immunological synapse of human T lymphocytes.
Article in American journal of physiology. Cell physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 72 citations in OpenAlex.
- Leukocytes Transcriptome Analysis of Genes Associated with Epilepsy Duration and Age of Onset.Molecular neurobiology · 2026Article
- Potassium channels as an ionic checkpoint in tumor immunity.Frontiers in pharmacology · 2026Review
- Design and synthesis of novel small molecules targeting the Kv1.3 voltage-gated potassium ion channel.Scientific reports · 2025Article
- The RELT Family of Proteins: An Increasing Awareness of Their Importance for Cancer, the Immune System, and Development.Biomedicines · 2023Review
- Reduction of CaCells · 2023Article
- KCNN4 may weaken anti-tumor immune response via raising Tregs and diminishing resting mast cells in clear cell renal cell carcinoma.Cancer cell international · 2022Article
- Role of SNARE Proteins in the Insertion of KCa3.1 in the Plasma Membrane of a Polarized Epithelium.Frontiers in physiology · 2022Article
- Immune Synapse Residency of Orai1 Alters CaInternational journal of molecular sciences · 2021Article
- Synthesis and biological evaluation of PET tracers designed for imaging of calcium activated potassium channel 3.1 (KRSC advances · 2021Article
- C reactive protein impairs adaptive immunity in immune cells of patients with melanoma.Journal for immunotherapy of cancer · 2020Article
- Periodic Membrane Potential and CaInternational journal of molecular sciences · 2020Article
- The Endoplasmic Reticulum-Plasma Membrane Junction: A Hub for Agonist Regulation of CaCold Spring Harbor perspectives in biology · 2020Review
- Cancer-Associated Intermediate Conductance CaCancers · 2019Review
- Differential Activity of Voltage- and CaFrontiers in physiology · 2018Article
- Plasma membrane insertion of KCa2.3 (SK3) is dependent upon the SNARE proteins, syntaxin-4 and SNAP23.PloS one · 2018Article
- Cancer Immunotherapy: Whence and Whither.Molecular cancer research : MCR · 2017Review
- The functional contribution of calcium ion flux heterogeneity in T cells.Immunology and cell biology · 2015Review
- Orai/CRACM1 and KCa3.1 ion channels interact in the human lung mast cell plasma membrane.Cell communication and signaling : CCS · 2015Article
- Preferential Coupling of the NAADP Pathway to Exocytosis in T-Cells.Messenger (Los Angeles, Calif. : Print) · 2015Article
- Ion channels in innate and adaptive immunity.Annual review of immunology · 2015Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
T cell receptor engagement results in the reorganization of intracellular and membrane proteins at the T cell-antigen presenting cell interface forming the immunological synapse (IS), an event required for Ca(2+) influx. KCa3.1 channels modulate Ca(2+) signaling in activated T cells by regulating the membrane potential. Nothing is known regarding KCa3.1 membrane distribution during T cell activation. Herein, we determined whether KCa3.1 translocates to the IS in human T cells using YFP-tagged KCa3.1 channels. These channels showed electrophysiological and pharmacological properties identical to wild-type channels. IS formation was induced by either anti-CD3/CD28 antibody-coated beads for fixed microscopy experiments or Epstein-Barr virus-infected B cells for fixed and live cell microscopy. In fixed microscopy experiments, T cells were also immunolabeled for F-actin or CD3epsilon, which served as IS formation markers. The distribution of KCa3.1 was determined with confocal and fluorescence microscopy. We found that, upon T cell activation, KCa3.1 channels localize with F-actin and CD3epsilon to the IS but remain evenly distributed on the cell membrane when no stimulus is provided. Detailed imaging experiments indicated that KCa3.1 channels are recruited in the IS shortly after antigen presentation and are maintained there for at least 15-30 min. Interestingly, pretreatment of activated T cells with the specific KCa3.1 blocker TRAM-34 blocked Ca(2+) influx, but channel redistribution to the IS was not prevented. These results indicate that KCa3.1 channels are a part of the signaling complex that forms at the IS upon antigen presentation.
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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.