ReviewPflugers Archiv : European journal of physiology2014
MaxiK channel and cell signalling.
Review in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 91 citations in OpenAlex.
- BK Channels Orchestrate Cardiac Homeostasis Through Mitochondrial Uncoupling Proteins.bioRxiv : the preprint server for biology · 2026Article
- The progression of triple-negative breast cancer is linked to a gradual decrease of the BK channel in the plasma membrane and an increase in intracellular structures.Pflugers Archiv : European journal of physiology · 2026Article
- Lysosomal Ion Channels and Transporters: Recent Findings, Therapeutic Potential, and Technical Approaches.Bioelectricity · 2025Review
- Transcriptional Up-Regulation of FBXW7 by KInternational journal of molecular sciences · 2024Article
- The BKPhysiological reports · 2024Article
- Article
- Exploring the Impact of BKInternational journal of molecular sciences · 2024Review
- Kir6.1, a component of an ATP-sensitive potassium channel, regulates natural killer cell development.Frontiers in immunology · 2024Article
- Design, synthesis, and biological evaluation of a novel series of 1,2,4-oxadiazole inhibitors of SLACK potassium channels: Identification of in vitro tool VU0935685.Bioorganic & medicinal chemistry · 2023Article
- Slo1 deficiency impaired skeletal muscle regeneration and slow-twitch fibre formation.Journal of cachexia, sarcopenia and muscle · 2023Article
- [Peripheral bloodNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- KCurrent neuropharmacology · 2023Review
- Sex differences in pituitary corticotroph excitability.Frontiers in physiology · 2023Article
- Specificities of Protein Homology Modeling for Allosteric Drug Design.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Deletion of large-conductance calcium-activated potassium channels promotes vascular remodelling through the CTRP7-mediated PI3K/Akt signaling pathway.Acta biochimica et biophysica Sinica · 2022Article
- Contributions of SGK3 to transporter-related diseases.Frontiers in cell and developmental biology · 2022Review
- KCurrent topics in membranes · 2022Review
- KScientific reports · 2021Article
- Article
- Bibliometric analysis of chloride channel research (2004-2019).Channels (Austin, Tex.) · 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
6 authors at 1 institution in 1 country.
Funding
Abstract
The large-conductance Ca2+- and voltage-activated K+ (MaxiK, BK, BKCa, Slo1, KCa1.1) channel role in cell signalling is becoming apparent as we learn how the channel interacts with a multiplicity of proteins not only at the plasma membrane but also in intracellular organelles including the endoplasmic reticulum, nucleus, and mitochondria. In this review, we focus on the interactions of MaxiK channels with seven-transmembrane G protein-coupled receptors and discuss information suggesting that, the channel big C-terminus may act as the nucleus of signalling molecules including kinases relevant for cell death and survival. Increasing evidence indicates that the channel is able to associate with a variety of receptors including β-adrenergic receptors, G protein-coupled estrogen receptors, acetylcholine receptors, thromboxane A2 receptors, and angiotensin II receptors, which highlights the varied functions that the channel has (or may have) not only in regulating contraction/relaxation of muscle cells or neurotransmission in the brain but also in cell metabolism, proliferation, migration, and gene expression. In line with this view, MaxiK channels have been implicated in obesity and in brain, prostate, and mammary cancers. A better understanding on the molecular mechanisms underlying or triggered by MaxiK channel abnormalities like overexpression in certain cancers may lead to new therapeutics to prevent devastating diseases.
Indexed as
Identifiers
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.