ArticleProceedings of the National Academy of Sciences of the United States of America2006
A voltage-driven switch for ion-independent signaling by ether-à-go-go K+ channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 140 citations in OpenAlex.
- Potassium channel ether à go-go1 is aberrantly expressed in human liposarcoma and promotes tumorigenesis.BioMed research international · 2014Trial
- Forward genetics reveals a conserved CNBHD-CNBHD interface that restrains EAG channel activation to regulate sleep.PLoS genetics · 2026Article
- Potassium channels in cancer: from hallmarks to therapeutic targeting.Journal of physiology and biochemistry · 2026Review
- Gating modulation and potentiation of amiodarone blockage of the Kv10.1 potassium channel bu KB130015, an amiodarone derived molecule.Channels (Austin, Tex.) · 2025Article
- Endogenous ether lipids differentially promote tumor aggressiveness by regulating the SK3 channel.Journal of lipid research · 2024Article
- The hEag1 KInternational journal of molecular sciences · 2022Article
- The Kv10.1 Channel: A Promising Target in Cancer.International journal of molecular sciences · 2022Review
- Bioelectric Dysregulation in Cancer Initiation, Promotion, and Progression.Frontiers in oncology · 2022Review
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Potassium and Chloride Ion Channels in Cancer: A Novel Paradigm for Cancer Therapeutics.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Dronedarone blockage of the tumor-related Kv10.1 channel: a comparison with amiodarone.Pflugers Archiv : European journal of physiology · 2020Article
- Bioelectric Control of Metastasis in Solid Tumors.Bioelectricity · 2019Article
- Review
- Remodeling neuronal ER-PM junctions is a conserved nonconducting function of Kv2 plasma membrane ion channels.Molecular biology of the cell · 2018Article
- Correction to: Inhibition of the KPflugers Archiv : European journal of physiology · 2018Article
- Cardiac fibroblasts : Active players in (atrial) electrophysiology?Herzschrittmachertherapie & Elektrophysiologie · 2018Review
- Inhibition of the KPflugers Archiv : European journal of physiology · 2018Article
- Eag1 Voltage-Dependent Potassium Channels: Structure, Electrophysiological Characteristics, and Function in Cancer.The Journal of membrane biology · 2017Review
- Impact of intracellular ion channels on cancer development and progression.European biophysics journal : EBJ · 2016Review
- hERG1/Kv11.1 activation stimulates transcription of p21waf/cip in breast cancer cells via a calcineurin-dependent mechanism.Oncotarget · 2016Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Voltage-gated channels maintain cellular resting potentials and generate neuronal action potentials by regulating ion flux. Here, we show that Ether-à-go-go (EAG) K+ channels also regulate intracellular signaling pathways by a mechanism that is independent of ion flux and depends on the position of the voltage sensor. Regulation of intracellular signaling was initially inferred from changes in proliferation. Specifically, transfection of NIH 3T3 fibroblasts or C2C12 myoblasts with either wild-type or nonconducting (F456A) eag resulted in dramatic increases in cell density and BrdUrd incorporation over vector- and Shaker-transfected controls. The effect of EAG was independent of serum and unaffected by changes in extracellular calcium. Inhibitors of p38 mitogen-activated protein (MAP) kinases, but not p44/42 MAP kinases (extracellular signal-regulated kinases), blocked the proliferation induced by nonconducting EAG in serum-free media, and EAG increased p38 MAP kinase activity. Importantly, mutations that increased the proportion of channels in the open state inhibited EAG-induced proliferation, and this effect could not be explained by changes in the surface expression of EAG. These results indicate that channel conformation is a switch for the signaling activity of EAG and suggest an alternative mechanism for linking channel activity to the activity of intracellular messengers, a role that previously has been ascribed only to channels that regulate calcium influx.
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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.