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ATP5O — FXYD1

Text-mined interactions from Literome

Fuller et al., FASEB J 2004 (Myocardial Ischemia) : Ischemia induced phosphorylation of phospholemman directly activates rat cardiac Na/K-ATPase
Silverman et al., Cardiovasc Res 2005 : Serine 68 phosphorylation of phospholemman : acute isoform-specific activation of cardiac Na/K ATPase
Zhang et al., J Appl Physiol 2006 (Ion Channel Gating...) : Phospholemman overexpression inhibits Na+-K+-ATPase in adult rat cardiac myocytes : relevance to decreased Na+ pump activity in postinfarction myocytes ... We tested the hypothesis that the previously observed reduction in Na+-K+-ATPase activity in MI rat myocytes was due to PLM overexpression
Pavlović et al., FASEB J 2007 (Ion Channel Gating) : We conclude that unphosphorylated FXYD1 inhibits Na/K ATPase , whereas S68 phosphorylated FXYD1 stimulates Na/K ATPase to a level above that seen in the absence of FXYD1
Cheung et al., Ann N Y Acad Sci 2007 : We conclude that PLM regulates cardiac contractility by modulating the activities of NCX and Na+-K+-ATPase
Beevers et al., J Biol Chem 2007 : The helix-helix packing is unusual, with Gly ( 19 ) and Gly ( 20 ) pointing to the outside of the helical bundle, facilitating potential interaction with other transmembrane proteins, thus providing a structural basis for the modulatory effect of PLM on the Na ( + ) /K ( + ) -ATPase
Bers et al., Trends Cardiovasc Med 2009 (Arrhythmias, Cardiac...) : Here, we discuss how stimulation of the Na/K-ATPase , mediated by phosphorylation of phospholemman ( a small sarcolemmal protein that associates with and modulates Na/K-ATPase ), is an additional important player in the sympathetic fight-or-flight response ... Thus, phospholemman mediated activation of the Na/K-ATPase may prevent Ca overload and triggered arrhythmias during stress
Cheung et al., Clinical and translational science 2010 (Heart Failure) : The unique role of PLM in regulation of Na ( + ) -K ( + ) -ATPase , Na(+)/Ca ( 2+ ) exchanger, and potentially L-type Ca ( 2+ ) channel in the heart, together with the changes in its expression and phosphorylation in heart failure, make PLM a rational and novel target for development of drugs in our armamentarium against heart failure
Han et al., Am J Physiol Cell Physiol 2010 : In intact cardiac myocytes, PLM associates with and inhibits Na ( + ) -K ( + ) -ATPase ( NKA ), mainly by reducing its affinity for internal Na ( + )
El-Armouche et al., FASEB J 2011 (Cardiomyopathy, Dilated...) : Phospholemman dependent regulation of the cardiac Na/K-ATPase activity is modulated by inhibitor-1 sensitive type-1 phosphatase ... Cardiac Na/K-ATPase ( NKA ) is regulated by its accessory protein phospholemman (PLM)
Moshitzky et al., J Biol Chem 2012 : The Na ( + ) /K ( + ) ATPase dependent surface expression of PLM could be facilitated by either a phosphorylation mimicking mutation at Thr-69 or a truncation of three terminal arginine residues
Cheung et al., Adv Exp Med Biol 2013 (Acute Disease...) : Coordinated regulation of cardiac Na(+)/Ca ( 2+ ) exchanger and Na ( + ) -K ( + ) -ATPase by phospholemman ( FXYD1 )