ArticleAmerican journal of physiology. Cell physiology2009
The role of cell cholesterol and the cytoskeleton in the interaction between IK1 and maxi-K channels.
Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- The orientation of cholesterol's hydroxy group affects its membrane dynamics and intracellular transport.iScience · 2026Article
- Review
- Methyl-Beta-Cyclodextrin Restores KJournal of Alzheimer's disease reports · 2021Article
- Cholesterol Stimulates the Transient Receptor Potential Melastatin 4 Channel in mpkCCDFrontiers in pharmacology · 2021Article
- Effects of host cell sterol composition upon internalization ofThe Journal of biological chemistry · 2018Article
- The effect of sterol structure upon clathrin-mediated and clathrin-independent endocytosis.Journal of cell science · 2017Article
- Review
- Mechanism and synergism in epithelial fluid and electrolyte secretion.Pflugers Archiv : European journal of physiology · 2014Review
- Ca²⁺-dependent K⁺ channels in exocrine salivary glands.Cell calcium · 2014Review
- Expression of PTRF in PC-3 Cells modulates cholesterol dynamics and the actin cytoskeleton impacting secretion pathways.Molecular & cellular proteomics : MCP · 2012Article
- Apical Ca2+-activated potassium channels in mouse parotid acinar cells.The Journal of general physiology · 2012Article
- Cholesterol regulates micro-opioid receptor-induced beta-arrestin 2 translocation to membrane lipid rafts.Molecular pharmacology · 2011Article
- Cholesterol tuning of BK ethanol response is enantioselective, and is a function of accompanying lipids.PloS one · 2011Article
- Dietary cholesterol modulates the excitability of rabbit hippocampal CA1 pyramidal neurons.Neuroscience letters · 2010Article
- Cholesterol and ion channels.Sub-cellular biochemistry · 2010Review
- Mechanistic details of BK channel inhibition by the intermediate conductance, Ca2+-activated K channel.Channels (Austin, Tex.)Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Recently, we demonstrated a novel interaction between large-conductance (maxi-K or K(Ca)1.1) and intermediate-conductance (IK1 or K(Ca)3.1) Ca(2+)-activated K channels: activation of IK1 channels causes the inhibition of maxi-K activity (Thompson J and Begenisich T. J Gen Physiol 127: 159-169, 2006). Here we show that the interaction between these two channels can be regulated by the membrane cholesterol level in parotid acinar cells. Depletion of cholesterol using methyl-beta-cyclodextrin weakened, while cholesterol enrichment increased, the ability of IK1 activation to inhibit maxi-K channels. Cholesterol's stereoisomer, epicholesterol, was unable to substitute for cholesterol in the interaction between the two K channels, suggesting a specific cholesterol-protein interaction. This suggestion was strengthened by the results of experiments in which cholesterol was replaced by coprostanol and epicoprostanol. These two sterols have nearly identical effects on membrane physical properties and cholesterol-rich microdomain stability, but had very different effects on the IK1/maxi-K interaction. In addition, the IK1/maxi-K interaction was unaltered in cells lacking caveolin, the protein essential for formation and stability of caveolae. Finally, disruption of the actin cytoskeleton restored the IK1-induced maxi-K inhibition that was lost with cell cholesterol depletion, demonstrating the importance of an intact cytoskeleton for the cholesterol-dependent regulation of the IK1/maxi-K interaction.
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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.