ArticleThe Journal of biological chemistry2013
Regulation of cardiac ATP-sensitive potassium channel surface expression by calcium/calmodulin-dependent protein kinase II.
Article in The Journal of biological chemistry, 2013. 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, 24 citations in OpenAlex.
- KArhiv za farmaciju · 2024Article
- The cardioprotective role of sirtuins is mediated in part by regulating KAmerican journal of physiology. Cell physiology · 2023Article
- Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022Review
- Redox-Active Drug, MnTE-2-PyPOxidative medicine and cellular longevity · 2020Article
- Research progress on the role of CaMKII in heart disease.American journal of translational research · 2020Review
- Myocardial death and dysfunction after ischemia-reperfusion injury require CaMKIIδ oxidation.Scientific reports · 2019Article
- The trafficking protein, EHD2, positively regulates cardiac sarcolemmal KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Blockade of the KMolecular psychiatry · 2018Article
- CaMKII: The molecular villain that aggravates cardiovascular disease.Experimental and therapeutic medicine · 2017Article
- Plasticity of sarcolemmal KATP channel surface expression: relevance during ischemia and ischemic preconditioning.American journal of physiology. Heart and circulatory physiology · 2016Article
- Article
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Role of CaMKII in cardiac arrhythmias.Trends in cardiovascular medicine · 2015Review
- Intracellular signalling mechanism responsible for modulation of sarcolemmal ATP-sensitive potassium channels by nitric oxide in ventricular cardiomyocytes.The Journal of physiology · 2014Article
- Sarcolemmal ATP-sensitive potassium channels modulate skeletal muscle function under low-intensity workloads.The Journal of general physiology · 2014Article
- Mechanisms of altered Ca²⁺ handling in heart failure.Circulation research · 2013Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Cardiac ATP-sensitive potassium (K(ATP)) channels are key sensors and effectors of the metabolic status of cardiomyocytes. Alteration in their expression impacts their effectiveness in maintaining cellular energy homeostasis and resistance to injury. We sought to determine how activation of calcium/calmodulin-dependent protein kinase II (CaMKII), a central regulator of calcium signaling, translates into reduced membrane expression and current capacity of cardiac K(ATP) channels. We used real-time monitoring of K(ATP) channel current density, immunohistochemistry, and biotinylation studies in isolated hearts and cardiomyocytes from wild-type and transgenic mice as well as HEK cells expressing wild-type and mutant K(ATP) channel subunits to track the dynamics of K(ATP) channel surface expression. Results showed that activation of CaMKII triggered dynamin-dependent internalization of K(ATP) channels. This process required phosphorylation of threonine at 180 and 224 and an intact (330)YSKF(333) endocytosis motif of the K(ATP) channel Kir6.2 pore-forming subunit. A molecular model of the μ2 subunit of the endocytosis adaptor protein, AP2, complexed with Kir6.2 predicted that μ2 docks by interaction with (330)YSKF(333) and Thr-180 on one and Thr-224 on the adjacent Kir6.2 subunit. Phosphorylation of Thr-180 and Thr-224 would favor interactions with the corresponding arginine- and lysine-rich loops on μ2. We concluded that calcium-dependent activation of CaMKII results in phosphorylation of Kir6.2, which promotes endocytosis of cardiac K(ATP) channel subunits. This mechanism couples the surface expression of cardiac K(ATP) channels with calcium signaling and reveals new targets to improve cardiac energy efficiency and stress resistance.
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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.