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2 lethal PLN mutations, R9C and R25C, which lead to dilated cardiomyopathy, were studied by biomolecular NMR. R25C enhances phospholmaban dynamics and shifts the conformational equilibrium toward the R state. R9C drives the amphipathic cytoplasmic domain toward the membrane-associate state, enriching the T state.
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Structure-Function Relationship of the SERCA Pump and Its Regulation by Phospholamban and Sarcolipin.
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The co-transfection of VHL and PLN in HEK293 cells decreased PLN expression under oxidative stress, whereas knockdown of VHL increased PLN expression both under normal and oxidative stress conditions.
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Hearts from patients with a p. Arg14del PLN mutation have a pattern of Right Ventricle Fibrofatty Replacement and Left Ventricular Fibrosis with fatty changes mostly in the posterolateral wall, independently of clinical presentation.
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LMOD1, SYNPO2, PDLIM7, PLN, and SYNM down-regulation reflect the altered phenotype of smooth muscle cells in vascular disease and could be early sensitive markers of SMC dedifferentiation.
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microRNAs (miRNAs) 1 and 21 bind PLN strongly and relieve PLN inhibition of SERCA to a greater extent than a similar length random sequence RNA mixture.
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Data suggest phospholamban (PLN) gene is a rare cause of cardiomyopathy in African patients.
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Phospholamban and sarcolipin are membrane proteins that differentially regulate SERCA function. (Review)
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PLN may be a key molecular player in rigid substrate-induced cellular hypertrophy in eosinophilic esophagitis.
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These data suggest that PLN is, at least partially, oligo-ubiquitinated at Lys(3) and degraded through Ser(16)-phosphorylation-mediated poly-ubiquitination during heart failure.
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hereditary mutants of phospholamban are associated with heart failure [review]
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PLN pentamers reduce phosphorylation of monomers at baseline and delay monomer phosphorylation upon PKA stimulation leading to increased interaction of PLN monomers with SERCA2a.
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Phospholamban R14del mutation carriers are at high risk for malignant ventricular arrhythmias and end-stage heart failure, with left ventricular ejection fraction <45% and sustained or nonsustained ventricular tachycardia as independent risk factors.
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Although SLN and PLB binding to SERCA have different functional outcomes on the coupling efficiency of SERCA, both proteins decrease the apparent Ca(2+) affinity of the pump, suggesting that SLN and PLB inhibit SERCA by using a similar mechanism.
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Phospholamban, and its interacting partners, regulates excitation contraction coupling and myocardial contraction. [Review]
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PLN mutations rarely cause cardiomyopathy
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analysis of how the conformational dynamics of protein kinase A induced by a lethal mutant of phospholamban hinder phosphorylation
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Aim of the present study is to determine the exact pattern of fibrosis and fatty replacement in PLN p.Arg14del mutation positive patients.
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Engineered upregulation of PLB expression in hESC/iPSC-vCMs restores a positive inotropic response to beta-adrenergic stimulation.
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a previously unrecognized mechanism for ESM cell contraction that depends on TGF-beta1, its receptors, and PLN.
