Recombinant Mouse Cardiac phospholamban (Pln), partial

1. Oxidative stress upregulates pVHL expression to induce PLN degradation in failing hearts. PMID:29068413
2. A single-dose injection of PLN-targeting locked nucleic acid antisense oligonucleotide improved contractility in pressure overload-induced cardiac dysfunction. PMID:27811197
3. PLN overexpression is associated with severe muscle atrophy and weakness. PMID:28278204
4. 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. PMID:26966065
5. the commercially available overexpressing phospholamban mouse phenotypically resembles human Centronuclear myopathy and could be used as a model to test potential mechanisms and therapeutic strategies. PMID:26035394
6. Cardioprotective effects of H2S are mediated through acGMP/PKG/phospholamban pathway. PMID:25870184
7. PLN pentamers reduce phosphorylation of monomers at baseline and delay monomer phosphorylation upon PKA stimulation leading to increased interaction of PLN monomers with SERCA2a. PMID:25562800
8. combined deletion of Phd2 and Phd3 dramatically decreased expression of phospholamban (PLN), resulted in sustained activation of calcium/calmodulin-activated kinase II (CaMKII), and sensitized mice to chronic beta-adrenergic stress-induced myocardial injury PMID:26075818
9. the N termini of SLN and PLB influence their respective unique functions PMID:25882845
10. CaMKII-dependent increase in PLN phosphorylation during reperfusion opposes rather than contributes to ischemia/reperfusion damage. PMID:24949568
11. TNAP plays a role in governing the phosphorylation status of phospholamban in the sarcoplasmic reticulum. PMID:25015959
12. SLN and PLN are co-expressed in most fibers, which suggests that super-inhibition of SERCAs may be physiologically important in the regulation of intracellular Ca2+ in human skeletal muscle. PMID:24358354
13. Epac1 KO exhibited decreased cardiac contractility with reduced phospholamban (PLN) phosphorylation at serine-16, the major PKA-mediated phosphorylation site. PMID:24892712
14. Phospholamban knockout breaks cell-wide propagating spontaneous Ca2+ waves in isolated ventricular myocytes & protects RyR2-mutant mice from stress-induced ventricular tachycardia. PMID:23856523
15. Data indicate that phospholamban (PLB) is not involved in heat generation and that sarcolipin (SLN) alone is responsible for muscle thermogenesis. PMID:23341466
16. PLN is a critical target for CaMKII effects on FFR, while CaMKII effects on frequency-dependent acceleration of relaxation partially require PLN-alternative targets. PMID:22796260
17. Dynamic regulation of the SERCA pump by phospholamban and/or sarcolipin maintains cardiac contractility in normal conditions and during pathophysiological states. PMID:20833651
18. Data indicate that cardiomyocytes from PLN-KO/CaMKII-TG mice showed poor viability, improved by inhibiting SR Ca(2+) release and mitochondrial Ca(2+) loading. PMID:19959778
19. although both phospholamban phosphorylation sites are involved in the mechanical recovery after myocardial ischemia, Thr17 appears to play a major role. PMID:12763747
20. PLB phosphorylation by CaMKII plays an important role in limiting the decline in Ca transients (and contraction) during acidosis PMID:14734049
21. Enhanced contractile heart function is enriched in PLN-knockout mutant hearts PMID:14982994
22. increased PLN expression in slow-twitch skeletal muscle is associated with impaired contractile function and muscle remodeling PMID:15059971
23. Results show that caffeine-induced CaMKII activation and phospholamban phosphorylation play a role in the relaxation of gastric fundus smooth muscles. PMID:15659716
24. The expression of SLN and PLB mRNA and protein relative to SERCA1 or SERCA2 was assessed in ventricle, atrium, and skeltal msucle of mouse, rat, rabbit and pig. PMID:15801907
25. the nonreversible superinhibitory function of mutant PLN-R14Del may lead to inherited dilated cardiomyopathy and premature death in both humans and mice PMID:16432188
26. A 60% reduction of PLN transcript & protein occurred with persistent ss2AR activation, due to receptor overexpression in airway smooth muscle cells. This decreased the maximal airway contraction & the sensitivity to the agonist methacholine. PMID:16849635
27. There is a trend for increased Iso-induced apoptosis in AC3-I mice lacking PLN. Findings show CaMKII is proapoptotic in vivo and regulation of SR Ca(2+) content by PLN contributes to the antiapoptotic mechanism of CaMKII inhibition PMID:16861697
28. The observed trafficking of PLB to the plasma membrane suggests an important role for PLB during muscle differentiation, which is distinct from its previously recognized role in the regulation of the Ca(2+)-ATPase. PMID:17287364
29. cGMP dependent phosphorylation analysis showed that some proteins were phosphorylated by cGMP to a lesser extent in PLB-KO compared with WT myocytes, suggesting impaired cGMP-kinase function in PLB-KO cardiac myocytes. PMID:17595525
30. Aerobic interval training enhances cardiomyocyte contractility and Ca2+ cycling by phosphorylation of CaMKII and thr-17 of Pln. PMID:17689560
31. These findings suggest that PLB is an important modulator of gastric antrum smooth muscle contractility by modulation of SR Ca(2+) release and CaM kinase II activity. PMID:18045856
32. proteomics surveys of cardiac ventricle isolated from a mouse model of cardiomyopathy overexpressing a phospholamban mutant, was performed. PMID:18056057
33. Down-regulation of PLN led to enhanced cell shortening and relaxation and to a decrease in the time constant of calcium decay, signs of improved contractility and calcium handling. PMID:18064719
34. Suggest that in isolated mouse ventricular cardiac myocytes, the combined chronic CaMKII inhibition and PLN ablation slowed Ca(2+) release at physiological frequencies. PMID:18359893
35. Examine roles of NCX1 and Atp1a1 in phospholamban regulation of cardiomyocyte contractility. PMID:18708446
36. These data demonstrate that alphaKAP exhibits a novel interaction with SERCA2a and may serve to spatially position CaMKII isoforms at the SR and to uniquely modulate the phosphorylation of PLN. PMID:19671701
37. Data show that Akt interacts with and phosphorylates phospholamban at Thr(17) while silencing Akt signaling through the knock-out of phosphatidylinositol-dependent kinase-1 results in reduced phosphorylation of PLN. PMID:19696029

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UNIGENE: Mm.34145

KEGG: mmu:18821

STRING: 10090.ENSMUSP00000045709