ArticleFrontiers in immunology2017
Kv1.3 Channel Blockade Modulates the Effector Function of B Cells in Granulomatosis with Polyangiitis.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Animal Venoms Targeting Cellular Mechanisms: Advances and Implications for Drug Discovery and Disease Therapy.Toxins · 2026Review
- Kv1.3 blockade by ShK186 modulates CD4+ effector memory T-cell activity of patients with granulomatosis with polyangiitis.Rheumatology (Oxford, England) · 2024Article
- Structure of the voltage-gated potassium channel KChannels (Austin, Tex.) · 2023Review
- Combination treatment with telitacicept, cyclophosphamide and glucocorticoids for severe Granulomatous polyangiitis: a case report and literature review.Frontiers in immunology · 2023Review
- Pharmacological blockade of KV1.3 channel as a promising treatment in autoimmune diseases.Journal of translational autoimmunity · 2022Review
- B Lineage Cells in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021Review
- Suppressing Kv1.3 Ion Channel Activity with a Novel Small Molecule Inhibitor Ameliorates Inflammation in a Humanised Mouse Model of Ulcerative Colitis.Journal of Crohn's & colitis · 2021Article
- Modulation of Adaptive Immunity and Viral Infections by Ion Channels.Frontiers in physiology · 2021Review
- A Recurrent Motif: Diversity and Evolution of ShKT Domain Containing Proteins in the Vampire SnailToxins · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B cells are central to the pathogenesis of granulomatosis with polyangiitis (GPA), exhibiting both (auto)antibody-dependent and -independent properties. Class-switched memory B cells in particular are a major source of pathogenic autoantibodies. These cells are characterized by high expression levels of Kv1.3 potassium channels, which may offer therapeutic potential for Kv1.3 blockade. In this study, we investigated the effect of the highly potent Kv1.3 blocker ShK-186 on B cell properties in GPA
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Registered trials
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