ArticleBiochimica et biophysica acta2012
Rituximab inhibits Kv1.3 channels in human B lymphoma cells via activation of FcγRIIB receptors.
Article in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Severe Hypokalemic Paralysis Following Rituximab Infusion in a Patient With Microscopic Polyangitis.Cureus · 2025Article
- Case report: One case of refractory membranous nephropathy with hypokalemia after rituximab infusion was switched to obinutuzumab without recurrence of hypokalemia.Frontiers in pharmacology · 2024Article
- Hypokalemia after rituximab administration in nephrotic syndrome: two case reports.BMC nephrology · 2023Article
- High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6.American journal of physiology. Renal physiology · 2019Article
- Inhibition of TRPC6 reduces non-small cell lung cancer cell proliferation and invasion.Oncotarget · 2017Article
- Acute ethanol induces apoptosis by stimulating TRPC6 via elevation of superoxide in oxygenated podocytes.Biochimica et biophysica acta · 2015Article
- Lovastatin inhibits human B lymphoma cell proliferation by reducing intracellular ROS and TRPC6 expression.Biochimica et biophysica acta · 2014Article
- Ion channels and apoptosis in cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- High glucose induces podocyte apoptosis by stimulating TRPC6 via elevation of reactive oxygen species.Biochimica et biophysica acta · 2013Article
- Article
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Authors and funding
11 authors.
Funding
Abstract
Kv1.3 channels play an important role in modulating lymphocyte proliferation and apoptosis. We hypothesized that Kv1.3 channels in B lymphocytes might be regulated by rituximab, an antibody to CD20, a drug for treatments of B-cell lymphomas and autoimmune diseases. Using both whole-cell and cell-attached patch-clamp techniques, we found that rituximab inhibited Kv1.3 channels in Daudi human B lymphoma cells by promoting the channel inactivation at a concentration which was much greater than that required for activation of CD20. The effect of rituximab on Kv1.3 channels was abolished after selective blockade of FcγRIIB receptors with anti-FcγRIIB antibody. Western blot experiments showed that Daudi B cells expressed both Kv1.3 channel and the low affinity Fc receptor, FcγRIIB, which could be activated by the Fc region of rituximab. In contrast, normal lymphocytes expressed less Kv1.3 channels with faster inactivation. Confocal microscopy and flow cytometry data showed that rituximab induced apoptosis of Daudi B cells and that the effect was attenuated by blockade of FcγRIIB receptors and partially mimicked by inhibition of Kv1.3 channels. These results suggest that in addition to previously described complement-dependent cytotoxicity, rituximab also induces apoptosis of malignant B lymphocyte by stimulating FcγRIIB receptors and inhibiting Kv1.3 channels.
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