Cardiomyocyte-specific loss of mitochondrial p32/C1qbp causes cardiomyopathy and activates stress responses. [electronic resource]
Producer: 20180521Description: 1173-1185 p. digitalISSN:- 1755-3245
- AMP-Activated Protein Kinases -- metabolism
- Adaptor Proteins, Signal Transducing
- Animals
- Cardiomyopathies -- genetics
- Carrier Proteins -- metabolism
- Cell Cycle Proteins
- Electron Transport Complex IV -- metabolism
- Energy Metabolism
- Eukaryotic Initiation Factors
- Fibroblast Growth Factor 2 -- metabolism
- Fibrosis
- Genetic Predisposition to Disease
- Heart Failure -- genetics
- Mice, Knockout
- Mitochondria, Heart -- metabolism
- Mitochondrial Proteins -- deficiency
- Myocardial Contraction
- Myocytes, Cardiac -- metabolism
- Oxidative Stress
- Oxygen Consumption
- Phenotype
- Phosphoproteins -- metabolism
- Phosphorylation
- Ribosomal Protein S6 Kinases, 90-kDa -- metabolism
- Stress, Physiological
- TOR Serine-Threonine Kinases -- metabolism
- Unfolded Protein Response
- Urea -- metabolism
- Ventricular Function, Left
- Ventricular Remodeling
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Publication Type: Journal Article
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