ArticleAmerican journal of physiology. Cell physiology2009
Inhibition of the KCa3.1 channels by AMP-activated protein kinase in human airway epithelial cells.
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 30 papers.
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Who cites it
30 citing papers in PubMed, 73 citations in OpenAlex.
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- SubSol-HIe is an AMPK-dependent hypoxia-responsive subnucleus of the nucleus tractus solitarius that coordinates the hypoxic ventilatory response and protects against apnoea in mice.Pflugers Archiv : European journal of physiology · 2024Article
- Regulation of the intestinal NaAmerican journal of physiology. Cell physiology · 2024Article
- Long-term adjuvant administration of temozolomide impacts serum ions concentration in high-grade glioma.Chinese neurosurgical journal · 2022Article
- Comparison of KHandbook of experimental pharmacology · 2021Article
- AMPK and the Need to Breathe and Feed: What's the Matter with Oxygen?International journal of molecular sciences · 2020Review
- Identification of Clotrimazole Derivatives as Specific Inhibitors of Arenavirus Fusion.Journal of virology · 2019Article
- AMP-Activated Protein Kinase (AMPK)-Dependent Regulation of Renal Transport.International journal of molecular sciences · 2018Review
- Structure, Gating and Basic Functions of the Ca2+-activated K Channel of Intermediate Conductance.Current neuropharmacology · 2018Review
- The emerging role of AMPK in the regulation of breathing and oxygen supply.The Biochemical journal · 2016Review
- Investigating CFTR and KCa3.1 Protein/Protein Interactions.PloS one · 2016Article
- Complementary roles of KCa3.1 channels and β1-integrin during alveolar epithelial repair.Respiratory research · 2015Article
- Junctional abnormalities in human airway epithelial cells expressing F508del CFTR.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- The Blockage of KCa3.1 Channel Inhibited Proliferation, Migration and Promoted Apoptosis of Human Hepatocellular Carcinoma Cells.Journal of Cancer · 2015Article
- Article
- Minireview: hey U(PS): metabolic and proteolytic homeostasis linked via AMPK and the ubiquitin proteasome system.Molecular endocrinology (Baltimore, Md.) · 2014Review
- Aromatic-aromatic interactions between residues in KCa3.1 pore helix and S5 transmembrane segment control the channel gating process.The Journal of general physiology · 2014Article
- AMPK: a cellular metabolic and redox sensor. A minireview.Frontiers in bioscience (Landmark edition) · 2014Review
- Regulation of ion channels and transporters by AMP-activated kinase (AMPK).Channels (Austin, Tex.) · 2014Review
- Functional KCa3.1 channels regulate steroid insensitivity in bronchial smooth muscle cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The vectorial transport of ions and water across epithelial cells depends to a large extent on the coordination of the apical and basolateral ion fluxes with energy supply. In this work we provide the first evidence for a regulation by the 5'-AMP-activated protein kinase (AMPK) of the calcium-activated potassium channel KCa3.1 expressed at the basolateral membrane of a large variety of epithelial cells. Inside-out patch-clamp experiments performed on human embryonic kidney (HEK) cells stably transfected with KCa3.1 first revealed a decrease in KCa3.1 activity following the internal addition of AMP at a fixed ATP concentration. This effect was dose dependent with half inhibition at 140 muM AMP in 1 mM ATP. Evidence for an interaction between the COOH-terminal region of KCa3.1 and the gamma1-subunit of AMPK was next obtained by two-hybrid screening and pull-down experiments. Our two-hybrid analysis confirmed in addition that the amino acids extending from Asp(380) to Ala(400) in COOH-terminal were essential for the interaction AMPK-gamma1/KCa3.1. Inside-out experiments on cells coexpressing KCa3.1 with the dominant negative AMPK-gamma1-R299G mutant showed a reduced sensitivity of KCa3.1 to AMP, arguing for a functional link between KCa3.1 and the gamma1-subunit of AMPK. More importantly, coimmunoprecipitation experiments carried out on bronchial epithelial NuLi cells provided direct evidence for the formation of a KCa3.1/AMPK-gamma1 complex at endogenous AMPK and KCa3.1 expression levels. Finally, treating NuLi monolayers with the membrane permeant AMPK activator 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) caused a significant decrease of the KCa3.1-mediated short-circuit currents, an effect reversible by coincubation with the AMPK inhibitor Compound C. These observations argue for a regulation of KCa3.1 by AMPK in a functional epithelium through protein/protein interactions involving the gamma1-subunit of AMPK.
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