ArticlePflugers Archiv : European journal of physiology2007
An intermediate-conductance Ca(2+)-activated K (+) channel mediates B lymphoma cell cycle progression induced by serum.
Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
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- 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
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Altered expression and functional role of ion channels in leukemia: bench to bedside.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Review
- Let's Talk About BiTEs and Other Drugs in the Real-Life Setting for B-Cell Acute Lymphoblastic Leukemia.Frontiers in immunology · 2019Review
- SK4 channels modulate CaMolecular oncology · 2017Article
- KCa3.1 as an Effective Target for Inhibition of Growth and Progression of Intrahepatic Cholangiocarcinoma.Journal of Cancer · 2017Article
- Functional cooperation between KCa3.1 and TRPC1 channels in human breast cancer: Role in cell proliferation and patient prognosis.Oncotarget · 2016Article
- Article
- Lovastatin inhibits human B lymphoma cell proliferation by reducing intracellular ROS and TRPC6 expression.Biochimica et biophysica acta · 2014Article
- Transmembrane voltage potential is an essential cellular parameter for the detection and control of tumor development in a Xenopus model.Disease models & mechanisms · 2013Article
- K(+) channels and cell cycle progression in tumor cells.Frontiers in physiology · 2013Article
- Multiple cholinergic signaling pathways in pituitary gonadotrophs.Endocrinology · 2013Article
- Rituximab inhibits Kv1.3 channels in human B lymphoma cells via activation of FcγRIIB receptors.Biochimica et biophysica acta · 2012Article
- Calcium-activated K+ channels increase cell proliferation independent of K+ conductance.American journal of physiology. Cell physiology · 2011Article
- The intermediate conductance Ca2+-activated K+ channel inhibitor TRAM-34 stimulates proliferation of breast cancer cells via activation of oestrogen receptors.British journal of pharmacology · 2010Article
- A PI3-kinase-mediated negative feedback regulates neuronal excitability.PLoS genetics · 2008Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
We have previously reported that Kv1.3 channel is expressed in Daudi cells. However, the present study demonstrates that Daudi cell cycle progression is not affected by margatoxin, a Kv1.3 channel blocker, but can be suppressed by tetraethylammonium (TEA) and 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (TRAM-34), a selective blocker of intermediate-conductance Ca(2+)-activated K(+) (IK) channels. Our patch-clamp data indicate that Daudi cells express an IK channel because it has a unit conductance of about 30 pS, is voltage-independent, and can be activated by submicromolar Ca(2+) and blocked by TRAM-34. Fetal bovine serum (FBS) elevated intracellular Ca(2+) concentration ([Ca(2+)](i)) and activated this IK channel. Conversely, Rituximab, a human-mouse chimeric monoclonal antibody of CD20, significantly decreased [Ca(2+)](i) and inhibited the channel. Furthermore, both FBS-induced IK channel expression and cell cycle progression were attenuated by the treatment with LY-294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. These data together suggest that a growth factor(s) in FBS triggers cell cycle progression by elevating both IK channel activity via CD20 and IK channel expression on the cell surface via PI3K. Thus, elevated IK channel activity and expression may account, in part, for Daudi cell malignant growth and proliferation.
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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.