ReviewThe Journal of physiology2006
MaxiK channel partners: physiological impact.
Review in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 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
127 citing papers in PubMed.
- Pharmacological Relevance of β-, γ-, and LINGO Auxiliary Subunits in BK Channel Modulation.ChemMedChem · 2026Review
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Tuning the gate and the gear: The LRRC26 (γ1) subunit modulates intrinsic gating and voltage-sensor coupling of the BK channel.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Tuning the gate and the gear: The LRRC26 (bioRxiv : the preprint server for biology · 2025Article
- KCurrent neuropharmacology · 2023Review
- Specificities of Protein Homology Modeling for Allosteric Drug Design.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Revisiting the Large-Conductance Calcium-Activated Potassium (BKCa) Channels in the Pulmonary Circulation.Biomolecules · 2021Review
- Why do platelets express KPlatelets · 2021Review
- Upregulated LRRC55 promotes BK channel activation and aggravates cell injury in podocytes.The Journal of experimental medicine · 2021Article
- BKCa channels regulate the immunomodulatory properties of WJ-MSCs by affecting the exosome protein profiles during the inflammatory response.Stem cell research & therapy · 2020Article
- Review
- Mechanism of Manganese Dysregulation of Dopamine Neuronal Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Intercalated cell BKα subunit is required for flow-induced K+ secretion.JCI insight · 2020Article
- BKCells · 2019Article
- BKCa participates in E2 inducing endometrial adenocarcinoma by activating MEK/ERK pathway.BMC cancer · 2018Article
- Calcium- and voltage-gated BK channels in vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2018Review
- Activation of human smooth muscle BK channels by hydrochlorothiazide requires cell integrity and the presence of BK βActa pharmacologica Sinica · 2018Article
- Membrane depolarization activates BK channels through ROCK-mediated β1 subunit surface trafficking to limit vasoconstriction.Science signaling · 2017Article
- Molecular Mechanisms Underlying Renin-Angiotensin-Aldosterone System Mediated Regulation of BK Channels.Frontiers in physiology · 2017Review
- Alcohol modulation of BK channel gating depends on β subunit composition.The Journal of general physiology · 2016Article
67 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
6 authors.
Funding
Abstract
The basic functional unit of the large-conductance, voltage- and Ca2+-activated K+ (MaxiK, BK, BKCa) channel is a tetramer of the pore-forming alpha-subunit (MaxiKalpha) encoded by a single gene, Slo, holding multiple alternative exons. Depending on the tissue, MaxiKalpha can associate with modulatory beta-subunits (beta1-beta4) increasing its functional diversity. As MaxiK senses and regulates membrane voltage and intracellular Ca2+, it links cell excitability with cell signalling and metabolism. Thus, MaxiK is a key regulator of vital body functions, like blood flow, uresis, immunity and neurotransmission. Epilepsy with paroxysmal dyskinesia syndrome has been recognized as a MaxiKalpha-related disorder caused by a gain-of-function C-terminus mutation. This channel region is also emerging as a key recognition module containing sequences for MaxiKalpha interaction with its surrounding signalling partners, and its targeting to cell-specific microdomains. The growing list of interacting proteins highlights the possibility that associations with the C-terminus of MaxiKalpha are dynamic and depending on each cellular environment. We speculate that the molecular multiplicity of the C-terminus (and intracellular loops) dictated by alternative exons may modulate or create additional interacting sites in a tissue-specific manner. A challenge is the dissection of MaxiK macromolecular signalling complexes in different tissues and their temporal association/dissociation according to the stimulus.
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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.