|1.||Kranias, Evangelia G: 30 articles (01/2015 - 01/2002)|
|2.||Kranias, E G: 10 articles (12/2005 - 04/2000)|
|3.||Haghighi, Kobra: 9 articles (01/2013 - 03/2003)|
|4.||Mattiazzi, Alicia: 7 articles (01/2014 - 01/2002)|
|5.||Hajjar, Roger J: 6 articles (01/2015 - 02/2002)|
|6.||Waggoner, Jason R: 6 articles (03/2012 - 03/2004)|
|7.||Fan, Guo-Chang: 5 articles (03/2012 - 03/2003)|
|8.||Hoshijima, Masahiko: 5 articles (01/2011 - 08/2002)|
|9.||Asahi, Michio: 5 articles (10/2010 - 02/2003)|
|10.||Dorn, Gerald W: 5 articles (05/2008 - 03/2003)|
01/01/2013 - "Furthermore, long-term expression of active inhibitor-1 via recombinant adeno-associated virus type 9 gene transfer in rats with pressure-overload induced heart failure improved function and prevented remodeling, associated with increased phosphorylation of phospholamban at Ser16 and Thr17. "
08/01/1997 - "A number of studies have suggested a decrease in SERCA2a relative to phospholamban in heart failure. "
02/01/2015 - "Herein we focus on hereditary mutants of phospholamban that are associated with heart failure, such as Arg(9)-Cys, Arg(9)-Leu, Arg(9)-His, and Arg(14)-deletion. "
01/01/2015 - "A mutation in the coding region of the phospholamban (PLN) gene (R14del) is identified in families with hereditary heart failure. "
02/01/2012 - "Phosphorylated phospholamban (P-PLB), the form that does not inhibit SERCA, was also reduced by chronic heart failure. "
01/01/2014 - "High resolution systematic digital histological quantification of cardiac fibrosis and adipose tissue in phospholamban p.Arg14del mutation associated cardiomyopathy."
01/01/2012 - "LV-interstitial fibrosis was quantified and protein levels of phospholamban (PLB), Serca2a and glucose transporters (GLUT1 and GLUT4) were determined by immunohistochemistry. "
09/01/2013 - "Neither myocardial fibrosis nor hypertrophy were detected in db/db, whereas titin N2B expression was increased and phosphorylation of phospholamban was reduced both being prevented by HR reduction in db/db-Iva. "
08/01/2003 - "At an elevated final blood pressure similar to that of the DS/T- rats, DS/T+ rats exhibited (1) a decrease in left ventricular (LV) mass associated with decreases in both cardiomyocyte size and interstitial fibrosis; (2) improvement of both systolic and diastolic LV function; and (3) an increase in caffeine contraction after constant Ca(2+)-loading with 8-bromo-cAMP into the sarcoplasmic reticulum (SR) associated with an increase in Ser16-phosphorylated phospholamban, as compared with the DS/T- rats. "
04/01/2006 - "IVRT was not related with gene expression of desmin, collagen I, phospholamban, the Na+-Ca2+ exchanger, the ryanodine receptor or interstitial fibrosis but correlated inversely with SERCA2a (r = -0.48; p = 0.02). "
|3.||Hypertension (High Blood Pressure)
10/01/1996 - "This comparative study investigates the relationship between sarcoplasmic reticulum (SR) calcium(Ca2+)-ATPase transport activity and phospholamban (PLB) phosphorylation in whole cardiac homogenates of spontaneously hypertensive rats (SHR) and their parent, normotensive Wistar Kyoto (WKY) strain during early postnatal development at days 1, 3, 6, 12 and at day 40 to ascertain any difference in SR Ca2+ handling before the onset of hypertension. "
11/01/2007 - "Calcineurin abundance increases in pressure-overload hypertrophy and may reduce agonist-mediated phospholamban (PLB) phosphorylation to underlie blunted beta-adrenergic receptor (beta-AR) responsiveness in hypertension. "
11/30/2001 - "Using Dahl salt-sensitive rats with hypertension, changes of myocardial contraction, intracellular Ca2+ transients, SR Ca2+ uptake, protein levels of SR Ca2+ ATPase (SERCA2), phospholamban, and calsequestrin (CSQ), and mRNA levels of SERCA2 and CSQ were serially determined and compared between the established stage of LV hypertrophy (LVH) and the subsequent stage of overt LV dysfunction (CHF). "
07/01/2011 - "BNP gene delivery also improved fractional shortening and ejection fraction in angiotensin II-mediated hypertension as well as decreased myocardial fibrosis and LV collagen III mRNA levels but had no effect on angiogenesis or Ca(2+)-ATPase expression and phospholamban phosphorylation. "
|4.||Cardiac Arrhythmias (Arrythmia)
05/24/2011 - "ES causes Ca(2+)/calmodulin-dependent protein kinase II activation and phospholamban dephosphorylation, which can explain the vicious cycle of arrhythmia promotion and mechanical dysfunction that characterizes ES."
08/07/2007 - "Treatment of transgenic animals with the Gi/o inhibitor pertussis toxin normalized the phospholamban phosphorylation by protein kinase A, reversed the action potential prolongation, and significantly reduced the frequency of cardiac arrhythmias in Ras transgenic animals. "
03/01/2005 - "Abnormalities in the ryanodine receptor-calcium release channel complex (RyR)2, FK-506 binding protein (FKBP 12.6), cardiac sarcoplasmic reticulum calcium ATPase (SERCA2a) and phospholamban (PLB) are involved in the initiation of cardiac arrhythmias, and can be identified as targets for therapeutic interventions."
|5.||Myocardial Ischemia (Ischemic Heart Diseases)
02/01/2004 - "It has therefore been proposed that normalization of sarcoplasmic reticulum Ca(2+) cycling through inhibition or ablation of the Ca(2+) ATP-ase inhibitor phospholamban (PLN), which shows promise as a treatment for heart failure, could be beneficial in ischemic heart disease. "
01/01/1989 - "Acute myocardial ischemia maintained for 30 and 60 min with subsequent reperfusion did not induced alterations in the cyclic AMP-mediated phosphorylation capacity of phospholamban and troponin I. Inotropic stimulation of the normal heart with 0.1/uM isoprenaline for 2 min resulted in a simultaneous P-incorporation into phospholamban and troponin I to 44.4 +/- 7.5 pmoles P/mg protein and 42.4 +/- 2.9 pmoles P/mg protein, respectively, assayed by a standardized back-phosphorylation procedure. "
|2.||Adenosine Triphosphatases (ATPase)
|3.||Messenger RNA (mRNA)
|4.||Calcium-Transporting ATPases (Ca2+ ATPase)
|5.||Protein Isoforms (Isoforms)
|6.||Peptidyl-Dipeptidase A (Angiotensin Converting Enzyme)
|7.||Cyclic AMP-Dependent Protein Kinases (cAMP-Dependent Protein Kinase)
|8.||Adenosine Triphosphate (ATP)