ArticleThe Journal of biological chemistry2016
Molecular Determinants of Kv1.3 Potassium Channels-induced Proliferation.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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Who cites it
32 citing papers in PubMed.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Identification of Novel Kv1.3 Channel-Interacting Proteins Using Proximity Labelling in T-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2025Article
- Inside-Out IPFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Vascular Smooth Muscle Cell Migration and P70S6K: Key Players in Intimal Hyperplasia Development.Journal of the American Heart Association · 2025Article
- Article
- BioID-based intact cell interactome of the Kv1.3 potassium channel identifies a Kv1.3-STAT3-p53 cellular signaling pathway.Science advances · 2024Article
- Proximity Labeling Proteomics Reveals Kv1.3 Potassium Channel Immune Interactors in Microglia.Molecular & cellular proteomics : MCP · 2024Article
- A sex-dependent role of Kv1.3 channels from macrophages in metabolic syndrome.Frontiers in physiology · 2024Article
- Cycling matters: Sex hormone regulation of vascular potassium channels.Channels (Austin, Tex.) · 2023Review
- The Phosphorylation of Kv1.3: A Modulatory Mechanism for a Multifunctional Ion Channel.Cancers · 2023Review
- The Role οf Ion Channels in the Development and Progression of Prostate Cancer.Molecular diagnosis & therapy · 2023Review
- A Meta-Analysis Study to Infer Voltage-Gated KAntioxidants (Basel, Switzerland) · 2023Article
- Non-conducting functions of potassium channels in cancer and neurological disease.Current topics in membranes · 2023Review
- Article
- Genetic Knockout of TRPM2 Increases Neuronal Excitability of Hippocampal Neurons by Inhibiting Kv7 Channel in Epilepsy.Molecular neurobiology · 2022Article
- Homeostatic regulation of extracellular signal-regulated kinase 1/2 activity and axonal KFrontiers in cellular neuroscience · 2022Article
- Article
- Kv1.3 voltage-gated potassium channels link cellular respiration to proliferation through a non-conducting mechanism.Cell death & disease · 2021Article
- Review on Biological Characteristics of Kv1.3 and Its Role in Liver Diseases.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in voltage-dependent potassium channels (Kv channels) associate to proliferation in many cell types, including transfected HEK293 cells. In this system Kv1.5 overexpression decreases proliferation, whereas Kv1.3 expression increases it independently of K(+) fluxes. To identify Kv1.3 domains involved in a proliferation-associated signaling mechanism(s), we constructed chimeric Kv1.3-Kv1.5 channels and point-mutant Kv1.3 channels, which were expressed as GFP- or cherry-fusion proteins. We studied their trafficking and functional expression, combining immunocytochemical and electrophysiological methods, and their impact on cell proliferation. We found that the C terminus is necessary for Kv1.3-induced proliferation. We distinguished two residues (Tyr-447 and Ser-459) whose mutation to alanine abolished proliferation. The insertion into Kv1.5 of a sequence comprising these two residues increased proliferation rate. Moreover, Kv1.3 voltage-dependent transitions from closed to open conformation induced MEK-ERK1/2-dependent Tyr-447 phosphorylation. We conclude that the mechanisms for Kv1.3-induced proliferation involve the accessibility of key docking sites at the C terminus. For one of these sites (Tyr-447) we demonstrated the contribution of MEK/ERK-dependent phosphorylation, which is regulated by voltage-induced conformational changes.
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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.