ArticleAmerican journal of physiology. Cell physiology2011
Calcium-activated K+ channels increase cell proliferation independent of K+ conductance.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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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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, 36 citations in OpenAlex.
- Role of Calcium-Activated Potassium Channels in Proliferation, Migration and Invasion of Human Chronic Myeloid Leukemia K562 Cells.Membranes · 2023Article
- Mechanisms Underlying Influence of Bioelectricity in Development.Frontiers in cell and developmental biology · 2022Review
- Bioelectric Dysregulation in Cancer Initiation, Promotion, and Progression.Frontiers in oncology · 2022Review
- Cancer-Associated Intermediate Conductance CaCancers · 2019Review
- The calcium-activated potassium channel KCa3.1 is an important modulator of hepatic injury.Scientific reports · 2016Article
- Molecular Determinants of Kv1.3 Potassium Channels-induced Proliferation.The Journal of biological chemistry · 2016Article
- Activation of K(+) channel by 1-EBIO rescues the head and neck squamous cell carcinoma cells from Ca(2+) ionophore-induced cell death.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016Article
- Kv1.3 channels modulate human vascular smooth muscle cells proliferation independently of mTOR signaling pathway.Pflugers Archiv : European journal of physiology · 2015Article
- Silencing of voltage-gated potassium channel KV9.3 inhibits proliferation in human colon and lung carcinoma cells.Oncotarget · 2015Article
- Tungstate-targeting of BKαβ1 channels tunes ERK phosphorylation and cell proliferation in human vascular smooth muscle.PloS one · 2015Article
- Potassium channels in cell cycle and cell proliferation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- Evidence of K+ channel function in epithelial cell migration, proliferation, and repair.American journal of physiology. Cell physiology · 2014Review
- Intermediate conductance Ca2+-activated K+ channels modulate human placental trophoblast syncytialization.PloS one · 2014Article
- Bioelectric signaling regulates size in zebrafish fins.PLoS genetics · 2014Article
- Article
- K(+) channels and cell cycle progression in tumor cells.Frontiers in physiology · 2013Article
- Trafficking of intermediate (KCa3.1) and small (KCa2.x) conductance, Ca(2+)-activated K(+) channels: a novel target for medicinal chemistry efforts?ChemMedChem · 2012Review
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
The intermediate-conductance calcium-activated potassium channel (IK1) promotes cell proliferation of numerous cell types including endothelial cells, T lymphocytes, and several cancer cell lines. The mechanism underlying IK1-mediated cell proliferation was examined in human embryonic kidney 293 (HEK293) cells expressing recombinant human IK1 (hIK1) channels. Inhibition of hIK1 with TRAM-34 reduced cell proliferation, while expression of hIK1 in HEK293 cells increased proliferation. When HEK293 cells were transfected with a mutant (GYG/AAA) hIK1 channel, which neither conducts K(+) ions nor promotes Ca(2+) entry, proliferation was increased relative to mock-transfected cells. Furthermore, when HEK293 cells were transfected with a trafficking mutant (L18A/L25A) hIK1 channel, proliferation was also increased relative to control cells. The lack of functional activity of hIK1 mutants at the cell membrane was confirmed by a combination of whole cell patch-clamp electrophysiology and fura-2 imaging to assess store-operated Ca(2+) entry and cell surface immunoprecipitation assays. Moreover, in cells expressing hIK1, inhibition of ERK1/2 and JNK kinases, but not of p38 MAP kinase, reduced cell proliferation. We conclude that functional K(+) efflux at the plasma membrane and the consequent hyperpolarization and enhanced Ca(2+) entry are not necessary for hIK1-induced HEK293 cell proliferation. Rather, our data suggest that hIK1-induced proliferation occurs by a direct interaction with ERK1/2 and JNK signaling pathways.
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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.