Hoehn, M <br/><br/>
Overexpression of protein phosphatase 2A in a murine model of chronic myocardial infarction leads to increased adverse remodeling but restores the regulation of β-catenin by glycogen synthase kinase 3β.  [electronic resource] 

 -  International journal of cardiology  Mar 2015 
 - 39-46 p.  digital 
<br/><br/> Publication Type: Journal Article 
<br/><br/><label>ISSN: </label>1874-1754 
<br/><br/><label>Standard No.: </label>10.1016/j.ijcard.2015.01.087  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Animals<br/>Atrial Remodeling--physiology<br/>Blotting, Western<br/>Cardiomyopathy, Dilated--metabolism<br/>Cardiomyopathy, Hypertrophic--metabolism<br/>Electrocardiography<br/>Gene Expression--physiology<br/>Glycogen Synthase Kinase 3--metabolism<br/>Glycogen Synthase Kinase 3 beta<br/>Male<br/>Mice<br/>Mice, Transgenic<br/>Myocardial Infarction--metabolism<br/>Protein Phosphatase 2--metabolism<br/>beta Catenin--metabolism