ReviewPflugers Archiv : European journal of physiology2016
Kv10.1 K(+) channel: from physiology to cancer.
Review in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 76 citations in OpenAlex.
- The molecular basis of KCNH1-related epileptic encephalopathy and the challenge of developing targeted therapeutics.Brain : a journal of neurology · 2026Review
- A nomogram model integrating transcriptomics and clinical features for predicting the risk of cervical intraepithelial lesion progression.Frontiers in oncology · 2026Article
- Scorpion Venom as a Source of Cancer Drugs: A Comprehensive Proteomic Analysis and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Proteomic Analysis of Invasive Breast Cancer Cells Treated with CBD Reveals Proteins Associated with the Reversal of Their Epithelial-Mesenchymal Transition Induced by IL-1β.International journal of molecular sciences · 2025Article
- Review
- Inhibition of the oncogenic channel Kv10.1 by the antipsychotic drug penfluridol.Frontiers in pharmacology · 2025Article
- Review of electrophysiological models to study membrane potential changes in breast cancer cell transformation and tumor progression.Frontiers in physiology · 2025Review
- Electrical excitability of cancer cells-CELEX model updated.Cancer metastasis reviews · 2024Review
- 14-3-3 proteins regulate cullin 7-mediated Eag1 degradation.Cell & bioscience · 2023Article
- Flavonoids as Modulators of Potassium Channels.International journal of molecular sciences · 2023Review
- The hEag1 KInternational journal of molecular sciences · 2022Article
- Potassium Channel KCNH1 Activating Variants Cause Altered Functional and Morphological Ciliogenesis.Molecular neurobiology · 2022Article
- Novel Therapeutic Approaches of Ion Channels and Transporters in Cancer.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Targeting Ion Channels for Cancer Treatment: Current Progress and Future Challenges.Reviews of physiology, biochemistry and pharmacology · 2022Review
- Potassium Channels as a Target for Cancer Therapy: Current Perspectives.OncoTargets and therapy · 2022Review
- Influence of Kv11.1 (hERG1) KPflugers Archiv : European journal of physiology · 2021Article
- Ion Channels in Lung Cancer.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Effects of the Tumor Environment on Ion Channels: Implication for Breast Cancer Progression.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Focus on Triple-Negative Breast Cancer: Potassium Channel Expression and Clinical Correlates.Frontiers in pharmacology · 2020Review
- Dronedarone blockage of the tumor-related Kv10.1 channel: a comparison with amiodarone.Pflugers Archiv : European journal of physiology · 2020Article
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 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
K(+) ions play a major role in many cellular processes. The deregulation of K(+) signaling is associated with a variety of diseases including cancer. Ether-à-go-go-1 (Eag1, Kv10.1, KCNH1) is a member of the voltage-activated potassium channel family and was the first K(+) channel to be associated with oncogenesis and tumor development. Interestingly, in healthy tissue, Kv10.1 is only detected in the central nervous system, where it is involved in the regulation of excitability under repeated stimulation. Kv10.1 is in contrast robustly expressed in over 70 % human tumors, where its expression seems to be controlled by key regulators of proliferation and survival such as p53 and E2F1, often altered in cancer. Otherwise, Kv10.1 is involved in cell proliferation, survival, angiogenesis, migration, and invasion. This review aims to provide a comprehensive overview of the current status of research on the role of Kv10.1 channel in physiopathology. Focus is placed on biophysical and pharmacological properties of Kv10.1 channel, as well as its cycling, trafficking, and its role in the neuron and cancer. The possible mechanisms by which Kv10.1 channel affects tumor cell migration and survival in breast cancer and its regulation by extracellular proteins are discussed.
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What OpenQuestion holds
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.