ArticlePloS one2013
Blocking KCa3.1 channels increases tumor cell killing by a subpopulation of human natural killer lymphocytes.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- KCa3.1 channels regulate the tumor infiltration of functionally competent NK cells in head and neck cancer.Scientific reports · 2025Article
- Inhibition of KCancers · 2024Article
- Activity of Potassium Channels in CD8International journal of molecular sciences · 2024Article
- Kir6.1, a component of an ATP-sensitive potassium channel, regulates natural killer cell development.Frontiers in immunology · 2024Article
- Reduction of CaCells · 2023Article
- A bioengineered probiotic for the oral delivery of a peptide Kv1.3 channel blocker to treat rheumatoid arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Immune and ionic mechanisms mediating the effect of dexamethasone in severe COVID-19.Frontiers in immunology · 2023Article
- Horses for Courses in the Era of CARs: Advancing CAR T and CAR NK Cell Therapies.Journal of personalized medicine · 2021Review
- Midazolam's Effects on Delayed-Rectifier KInternational journal of molecular sciences · 2021Article
- Potassium Channels in Cancer.Handbook of experimental pharmacology · 2021Article
- Ion Channels Orchestrate Pancreatic Ductal Adenocarcinoma Progression and Therapy.Frontiers in pharmacology · 2020Review
- Cancer-Associated Intermediate Conductance CaCancers · 2019Review
- KCa1.1 and Kv1.3 channels regulate the interactions between fibroblast-like synoviocytes and T lymphocytes during rheumatoid arthritis.Arthritis research & therapy · 2019Article
- Immuno-Oncology: Emerging Targets and Combination Therapies.Frontiers in oncology · 2018Review
- Differences in ion channel phenotype and function between humans and animal models.Frontiers in bioscience (Landmark edition) · 2018Review
- KCa1.1 channels as therapeutic targets for rheumatoid arthritis.Expert opinion on therapeutic targets · 2017Article
- SK4 channels modulate CaMolecular oncology · 2017Article
- Functional KCa1.1 channels are crucial for regulating the proliferation, migration and differentiation of human primary skeletal myoblasts.Cell death & disease · 2016Article
- Mechanisms of the Immunological Effects of Volatile Anesthetics: A Review.Anesthesia and analgesia · 2016Review
- Molecular modeling of antibodies for the treatment of TNFα-related immunological diseases.Pharmacology research & perspectives · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Natural killer (NK) cells are large granular lymphocytes that participate in both innate and adaptive immune responses against tumors and pathogens. They are also involved in other conditions, including organ rejection, graft-versus-host disease, recurrent spontaneous abortions, and autoimmune diseases such as multiple sclerosis. We demonstrate that human NK cells express the potassium channels Kv1.3 and KCa3.1. Expression of these channels does not vary with expression levels of maturation markers but varies between adherent and non-adherent NK cell subpopulations. Upon activation by mitogens or tumor cells, adherent NK (A-NK) cells preferentially up-regulate KCa3.1 and non-adherent (NA-NK) cells preferentially up-regulate Kv1.3. Consistent with this different phenotype, A-NK and NA-NK do not display the same sensitivity to the selective KCa3.1 blockers TRAM-34 and NS6180 and to the selective Kv1.3 blockers ShK-186 and PAP-1 in functional assays. Kv1.3 block inhibits the proliferation and degranulation of NA-NK cells with minimal effects on A-NK cells. In contrast, blocking KCa3.1 increases the degranulation and cytotoxicity of A-NK cells, but not of NA-NK cells. TRAM-34, however, does not affect their ability to form conjugates with target tumor cells, to migrate, or to express chemokine receptors. TRAM-34 and NS6180 also increase the proliferation of both A-NK and NA-NK cells. This results in a TRAM-34-induced increased ability of A-NK cells to reduce in vivo tumor growth. Taken together, our results suggest that targeting KCa3.1 on NK cells with selective blockers may be beneficial in cancer immunotherapy.
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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.