ArticleBiophysical journal2014
Identification of a cholesterol-binding pocket in inward rectifier K(+) (Kir) channels.
Article in Biophysical journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Structural and functional studies of inward rectifier Kir7.1 and its regulation by the Melanocortin-4 receptor.Nature communications · 2026Article
- Endocannabinoid regulation of inward rectifier potassium (Kir) channels.Frontiers in pharmacology · 2024Article
- From Crosstalk to Synergism: The Combined Effect of Cholesterol and PI(4,5)PAdvances in experimental medicine and biology · 2023Review
- Cryo-electron microscopy unveils unique structural features of the human Kir2.1 channel.Science advances · 2022Article
- Cholesterol-induced suppression of Kir2 channels is mediated by decoupling at the inter-subunit interfaces.iScience · 2022Article
- A Cholesterol Dimer Stabilizes the Inactivated State of an Inward-Rectifier Potassium Channel.Angewandte Chemie (International ed. in English) · 2022Article
- The epithelial potassium channel Kir7.1 is stimulated by progesterone.The Journal of general physiology · 2021Article
- Interfacial Binding Sites for Cholesterol on Kir, Kv, KBiophysical journal · 2020Article
- Defining how multiple lipid species interact with inward rectifier potassium (Kir2) channels.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Comparative docking analysis of cholesterol analogs to ion channels to discriminate between stereospecific binding vs. stereospecific response.Channels (Austin, Tex.) · 2019Article
- Emerging Diversity in Lipid-Protein Interactions.Chemical reviews · 2019Review
- Characterization of Lipid-Protein Interactions and Lipid-Mediated Modulation of Membrane Protein Function through Molecular Simulation.Chemical reviews · 2019Review
- An Inward-Rectifier Potassium Channel Coordinates the Properties of Biologically Derived Membranes.Biophysical journal · 2019Article
- Molecular Dynamics Simulations of Kir2.2 Interactions with an Ensemble of Cholesterol Molecules.Biophysical journal · 2018Article
- Inward Rectifier Potassium Channels (Kir2.x) and Caveolin-3 Domain-Specific Interaction: Implications for Purkinje Cell-Dependent Ventricular Arrhythmias.Circulation. Arrhythmia and electrophysiology · 2018Article
- Protein crowding and lipid complexity influence the nanoscale dynamic organization of ion channels in cell membranes.Scientific reports · 2017Article
- Dual activation of neuronal G protein-gated inwardly rectifying potassium (GIRK) channels by cholesterol and alcohol.Scientific reports · 2017Article
- Lipid interaction sites on channels, transporters and receptors: Recent insights from molecular dynamics simulations.Biochimica et biophysica acta · 2016Review
- Sphingolipid Organization in the Plasma Membrane and the Mechanisms That Influence It.Frontiers in cell and developmental biology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Cholesterol is the major sterol component of all mammalian plasma membranes. Recent studies have shown that cholesterol inhibits both bacterial (KirBac1.1 and KirBac3.1) and eukaryotic (Kir2.1) inward rectifier K(+) (Kir) channels. Lipid-sterol interactions are not enantioselective, and the enantiomer of cholesterol (ent-cholesterol) does not inhibit Kir channel activity, suggesting that inhibition results from direct enantiospecific binding to the channel, and not indirect effects of changes to the bilayer. Furthermore, conservation of the effect of cholesterol among prokaryotic and eukaryotic Kir channels suggests an evolutionary conserved cholesterol-binding pocket, which we aimed to identify. Computational experiments were performed by docking cholesterol to the atomic structures of Kir2.2 (PDB: 3SPI) and KirBac1.1 (PDB: 2WLL) using Autodock 4.2. Poses were assessed to ensure biologically relevant orientation and then clustered according to location and orientation. The stability of cholesterol in each of these poses was then confirmed by molecular dynamics simulations. Finally, mutation of key residues (S95H and I171L) in this putative binding pocket found within the transmembrane domain of Kir2.1 channels were shown to lead to a loss of inhibition by cholesterol. Together, these data provide support for this location as a biologically relevant pocket.
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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.