ArticleJournal of applied physiology (Bethesda, Md. : 1985)2006
Phospholemman overexpression inhibits Na+-K+-ATPase in adult rat cardiac myocytes: relevance to decreased Na+ pump activity in postinfarction myocytes.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- FXYD1 was identified as a hub gene in recurrent miscarriage and involved in decidualization via regulating Na/K-ATPase activity.Journal of assisted reproduction and genetics · 2025Article
- The NaFrontiers in endocrinology · 2023Review
- Epigenetic remodelling of Fxyd1 promoters in developing heart and brain tissues.Scientific reports · 2022Article
- Roles of Key Ion Channels and Transport Proteins in Age-Related Hearing Loss.International journal of molecular sciences · 2021Review
- Correcting deregulated Fxyd1 expression rescues deficits in neuronal arborization and potassium homeostasis in MeCP2 deficient male mice.Brain research · 2018Article
- Na/K-ATPase Signaling and Cardiac Pre/Postconditioning with Cardiotonic Steroids.International journal of molecular sciences · 2018Review
- Protein Phosphatase 1c Associated with the Cardiac Sodium Calcium Exchanger 1 Regulates Its Activity by Dephosphorylating Serine 68-phosphorylated Phospholemman.The Journal of biological chemistry · 2016Article
- Molecular Mechanisms and Kinetic Effects of FXYD1 and Phosphomimetic Mutants on Purified Human Na,K-ATPase.The Journal of biological chemistry · 2015Article
- Regulation of L-type calcium channel by phospholemman in cardiac myocytes.Journal of molecular and cellular cardiology · 2015Article
- Impact of phosphomimetic and non-phosphorylatable mutations of phospholemman on L-type calcium channels gating in HEK 293T cells.Journal of cellular and molecular medicine · 2015Article
- Induced overexpression of phospholemman S68E mutant improves cardiac contractility and mortality after ischemia-reperfusion.American journal of physiology. Heart and circulatory physiology · 2014Article
- Regulation of the cardiac sodium pump.Cellular and molecular life sciences : CMLS · 2013Review
- Modulation of cardiac Na+,K+-ATPase cell surface abundance by simulated ischemia-reperfusion and ouabain preconditioning.American journal of physiology. Heart and circulatory physiology · 2013Article
- Article
- Phospholemman deficiency in postinfarct hearts: enhanced contractility but increased mortality.Clinical and translational science · 2012Article
- Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: potential involvement of Na+/Ca2+ exchanger.American journal of physiology. Heart and circulatory physiology · 2012Article
- Regulation of in vivo cardiac contractility by phospholemman: role of Na+/Ca2+ exchange.American journal of physiology. Heart and circulatory physiology · 2011Article
- Amino acid substitutions in the FXYD motif enhance phospholemman-induced modulation of cardiac L-type calcium channels.American journal of physiology. Cell physiology · 2010Article
- Phospholemman: a novel cardiac stress protein.Clinical and translational science · 2010Review
- Phospholemman and beta-adrenergic stimulation in the heart.American journal of physiology. Heart and circulatory physiology · 2010Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Messenger RNA levels of phospholemman (PLM), a member of the FXYD family of small single-span membrane proteins with putative ion-transport regulatory properties, were increased in postmyocardial infarction (MI) rat myocytes. We tested the hypothesis that the previously observed reduction in Na+-K+-ATPase activity in MI rat myocytes was due to PLM overexpression. In rat hearts harvested 3 and 7 days post-MI, PLM protein expression was increased by two- and fourfold, respectively. To simulate increased PLM expression post-MI, PLM was overexpressed in normal adult rat myocytes by adenovirus-mediated gene transfer. PLM overexpression did not affect the relative level of phosphorylation on serine68 of PLM. Na+-K+-ATPase activity was measured as ouabain-sensitive Na+-K+ pump current (Ip). Compared with control myocytes overexpressing green fluorescent protein alone, Ip measured in myocytes overexpressing PLM was significantly (P < 0.0001) lower at similar membrane voltages, pipette Na+ ([Na+]pip) and extracellular K+ ([K+]o) concentrations. From -70 to +60 mV, neither [Na+]pip nor [K+]o required to attain half-maximal Ip was significantly different between control and PLM myocytes. This phenotype of decreased V(max) without appreciable changes in K(m) for Na+ and K+ in PLM-overexpressed myocytes was similar to that observed in MI rat myocytes. Inhibition of Ip by PLM overexpression was not due to decreased Na+-K+-ATPase expression because there were no changes in either protein or messenger RNA levels of either alpha1- or alpha2-isoforms of Na+-K+-ATPase. In native rat cardiac myocytes, PLM coimmunoprecipitated with alpha-subunits of Na+-K+-ATPase. Inhibition of Na+-K+-ATPase by PLM overexpression, in addition to previously reported decrease in Na+-K+-ATPase expression, may explain altered V(max) but not K(m) of Na+-K+-ATPase in postinfarction rat myocytes.
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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.