ArticleThe Journal of physiology1999
Wortmannin, an inhibitor of phosphatidylinositol kinases, blocks the MgATP-dependent recovery of Kir6.2/SUR2A channels.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 57 citations in OpenAlex.
- CL-705G: a novel chemical Kir6.2-specific KFrontiers in pharmacology · 2023Article
- Methods to study phosphoinositide regulation of ion channels.Methods in enzymology · 2021Article
- PIPProceedings of the National Academy of Sciences of the United States of America · 2020Review
- Vitamin D actions in neurons require the PI3K pathway for both enhancing insulin signaling and rapid depolarizing effects.The Journal of steroid biochemistry and molecular biology · 2020Article
- Palmitoylation of the KProceedings of the National Academy of Sciences of the United States of America · 2020Article
- PIPeLife · 2018Article
- Running out of time: the decline of channel activity and nucleotide activation in adenosine triphosphate-sensitive K-channels.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Insulin-like growth factor-1 (IGF-1) inhibits the basolateral Cl channels in the thick ascending limb of the rat kidney.Biochimica et biophysica acta · 2012Article
- Measuring and evaluating the role of ATP-sensitive K+ channels in cardiac muscle.Journal of molecular and cellular cardiology · 2012Review
- Relief of Mg²⁺-dependent inhibition of TRPM1 by PKCα at the rod bipolar cell synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Activation of the K(ATP) channel by Mg-nucleotide interaction with SUR1.The Journal of general physiology · 2010Article
- Cardiac sarcolemmal K(ATP) channels: Latest twists in a questing tale!Journal of molecular and cellular cardiology · 2010Review
- Incomplete dissociation of glibenclamide from wild-type and mutant pancreatic K ATP channels limits their recovery from inhibition.British journal of pharmacology · 2009Article
- Long polyamines act as cofactors in PIP2 activation of inward rectifier potassium (Kir2.1) channels.The Journal of general physiology · 2005Article
- Hydrolyzable ATP and PIP(2) modulate the small-conductance K+ channel in apical membranes of rat cortical-collecting duct (CCD).The Journal of general physiology · 2002Article
- Susceptibility of ATP-sensitive K+ channels to cell stress through mediation of phosphoinositides as examined by photoirradiation.The Journal of physiology · 2000Article
- Regulation of cloned ATP-sensitive K channels by phosphorylation, MgADP, and phosphatidylinositol bisphosphate (PIP(2)): a study of channel rundown and reactivation.The Journal of general physiology · 2000Article
- On the mechanism of ADP-induced alteration of sulphonylurea sensitivity in cardiac ATP-sensitive K(+) channels.British journal of pharmacology · 2000Article
- Phospholipase C-linked receptors regulate the ATP-sensitive potassium channel by means of phosphatidylinositol 4,5-bisphosphate metabolism.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. In order to investigate the mechanism underlying MgATP-dependent recovery of ATP-sensitive potassium (KATP) channels, we expressed Kir6.2/SUR2A (inwardly rectifying K+ channel subunit/sulfonylurea receptor) or C-terminal-truncated Kir6.2 (Kir6.2DeltaC26) in COS7 cells (Green monkey kidney cells), and carried out inside-out patch clamp experiments. 2. After patch excision in ATP-free internal solution, the activity of Kir6.2/SUR2A channels could be maximally recovered by the application of 5 mM MgATP. Subsequent application of 100 microM Ca2+ induced a rapid decay of Kir6.2/SUR2A activity to 11.6 +/- 1.1 % (mean +/- s.e.m.) of the control level (Ca2+-induced run-down; n = 64). 3. MgATP (5 mM) recovered 99.4 +/- 4.2 % (n = 13) of the Ca2+-induced run-down. Protein kinase inhibitors such as W-7, H-7, H-8 and genistein did not inhibit this reaction. However, wortmannin, an inhibitor of phosphatidylinositol 3- and 4-kinases, blocked the MgATP-dependent recovery in a concentration-dependent manner; the magnitudes of recovery were 35.7 +/- 7.2 % (10 microM) and 4.3 +/- 2.5 % (100 microM) of the Ca2+-induced run-down. 4. MgUDP (10 mM) reversed the Ca2+-induced run-down of Kir6.2/SUR2A channels by 60.4 +/- 7.6 % (n = 5). Wortmannin failed to modify this reaction. 5. Kir6.2DeltaC26 channels, which opened in the absence of SUR2A, were less sensitive to Ca2+; Kir6.2DeltaC26 channels were inactivated to 44.8 +/- 4.4 % (n = 14) by 100 microM Ca2+. MgATP recovered the Ca2+-induced run-down of Kir6.2DeltaC26 by 89.8 +/- 7. 7 % (n = 9), and 100 microM wortmannin inhibited this reaction (1.8 +/- 2 %, n = 7). 6. Application of 10 microM phosphatidylinositol-4, 5-bisphosphate (PI-4,5-P2) recovered the activity of Kir6.2/SUR2A channels after Ca2+-induced run-down (104.3 +/- 6.4 %, n = 10). Even after the MgATP-dependent recovery was blocked by 100 microM wortmannin, PI-4,5-P2 reactivated the channels (102.3 +/- 8.6 %, n = 5). Similar results were obtained with Kir6.2DeltaC26. 7. These results suggest that the entity of MgATP-dependent recovery may be membrane lipid phosphorylation rather than protein phosphorylation, and that synthesis of PI-4,5-P2 or phosphatidylinositol-3,4, 5-trisphosphate may upregulate Kir6.2 channels.
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