Saito, Toshiro <br/><br/>
Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses.  [electronic resource] 

 -  Cardiovascular research  Aug 2017 
 - 1173-1185 p.  digital 
<br/><br/> Publication Type: Journal Article 
<br/><br/><label>ISSN: </label>1755-3245 
<br/><br/><label>Standard No.: </label>10.1093/cvr/cvx095  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>AMP-Activated Protein Kinases--metabolism<br/>Adaptor Proteins, Signal Transducing<br/>Animals<br/>Cardiomyopathies--genetics<br/>Carrier Proteins--metabolism<br/>Cell Cycle Proteins<br/>Electron Transport Complex IV--metabolism<br/>Energy Metabolism<br/>Eukaryotic Initiation Factors<br/>Fibroblast Growth Factor 2--metabolism<br/>Fibrosis<br/>Genetic Predisposition to Disease<br/>Heart Failure--genetics<br/>Mice, Knockout<br/>Mitochondria, Heart--metabolism<br/>Mitochondrial Proteins--deficiency<br/>Myocardial Contraction<br/>Myocytes, Cardiac--metabolism<br/>Oxidative Stress<br/>Oxygen Consumption<br/>Phenotype<br/>Phosphoproteins--metabolism<br/>Phosphorylation<br/>Ribosomal Protein S6 Kinases, 90-kDa--metabolism<br/>Stress, Physiological<br/>TOR Serine-Threonine Kinases--metabolism<br/>Unfolded Protein Response<br/>Urea--metabolism<br/>Ventricular Function, Left<br/>Ventricular Remodeling