ReviewJournal of molecular and cellular cardiology2005
ATP-sensitive K+ channel channel/enzyme multimer: metabolic gating in the heart.
Review in Journal of molecular and cellular cardiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed.
- KScientific reports · 2022Article
- IAPP toxicity activates HIF1α/PFKFB3 signaling delaying β-cell loss at the expense of β-cell function.Nature communications · 2019Article
- Article
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Molecular determinants of ATP-sensitive potassium channel MgATPase activity: diabetes risk variants and diazoxide sensitivity.Bioscience reports · 2015Article
- Antiobesity strategy targets energy economy safeguards.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
- ABCC9 is a novel Brugada and early repolarization syndrome susceptibility gene.International journal of cardiology · 2014Article
- The unusual stoichiometry of ADP activation of the KATP channel.Frontiers in physiology · 2014Article
- Kir6.2 limits Ca(2+) overload and mitochondrial oscillations of ventricular myocytes in response to metabolic stress.American journal of physiology. Heart and circulatory physiology · 2013Article
- Role of genetic polymorphisms of ion channels in the pathophysiology of coronary microvascular dysfunction and ischemic heart disease.Basic research in cardiology · 2013Observational
- Reinterpreting the action of ATP analogs on K(ATP) channels.The Journal of biological chemistry · 2013Article
- Regulation of the ATP-sensitive potassium channel subunit, Kir6.2, by a Ca2+-dependent protein kinase C.The Journal of biological chemistry · 2012Article
- Compartmentation of membrane processes and nucleotide dynamics in diffusion-restricted cardiac cell microenvironment.Journal of molecular and cellular cardiology · 2012Review
- ATP-sensitive potassium (KATP) channel activation decreases intraocular pressure in the anterior chamber of the eye.Investigative ophthalmology & visual science · 2011Article
- Advances in cardiac ATP-sensitive K+ channelopathies from molecules to populations.Circulation. Arrhythmia and electrophysiology · 2011Article
- Cardiac ATP-sensitive K+ channel associates with the glycolytic enzyme complex.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- K(ATP) channel-dependent metaboproteome decoded: systems approaches to heart failure prediction, diagnosis, and therapy.Cardiovascular research · 2011Review
- K(ATP) channels process nucleotide signals in muscle thermogenic response.Critical reviews in biochemistry and molecular biology · 2010Article
- Human K(ATP) channelopathies: diseases of metabolic homeostasis.Pflugers Archiv : European journal of physiology · 2010Review
- A novel mitochondrial K(ATP) channel assay.Circulation research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Cardiac ATP-sensitive K(+) (K(ATP)) channels, gated by cellular metabolism, are formed by association of the inwardly rectifying potassium channel Kir6.2, the potassium conducting subunit, and SUR2A, the ATP-binding cassette protein that serves as the regulatory subunit. Kir6.2 is the principal site of ATP-induced channel inhibition, while SUR2A regulates K(+) flux through adenine nucleotide binding and catalysis. The ATPase-driven conformations within the regulatory SUR2A subunit of the K(ATP) channel complex have determinate linkage with the states of the channel's pore. The probability and life-time of ATPase-induced SUR2A intermediates, rather than competitive nucleotide binding alone, defines nucleotide-dependent K(ATP) channel gating. Cooperative interaction, instead of independent contribution of individual nucleotide binding domains within the SUR2A subunit, serves a decisive role in defining K(ATP) channel behavior. Integration of K(ATP) channels with the cellular energetic network renders these channel/enzyme heteromultimers high-fidelity metabolic sensors. This vital function is facilitated through phosphotransfer enzyme-mediated transmission of controllable energetic signals. By virtue of coupling with cellular energetic networks and the ability to decode metabolic signals, K(ATP) channels set membrane excitability to match demand for homeostatic maintenance. This new paradigm in the operation of an ion channel multimer is essential in providing the basis for K(ATP) channel function in the cardiac cell, and for understanding genetic defects associated with life-threatening diseases that result from the inability of the channel complex to optimally fulfill its physiological role.
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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.