Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve. [electronic resource]
Producer: 20171010Description: 147-159 p. digitalISSN:- 1755-3245
- A Kinase Anchor Proteins -- deficiency
- Animals
- Calcineurin -- metabolism
- Calcium Signaling
- Calcium-Binding Proteins -- metabolism
- Cardiomyopathy, Dilated -- etiology
- Cells, Cultured
- Disease Models, Animal
- Fibrosis
- Genetic Predisposition to Disease
- Heart Failure -- etiology
- Isoproterenol
- Mice, Knockout
- Myocardial Ischemia -- complications
- Myocardial Reperfusion Injury -- complications
- Myocytes, Cardiac -- metabolism
- NFATC Transcription Factors -- genetics
- Phenotype
- RNA Interference
- Rats, Sprague-Dawley
- Ryanodine Receptor Calcium Release Channel -- metabolism
- Sarcoplasmic Reticulum -- metabolism
- Sarcoplasmic Reticulum Calcium-Transporting ATPases -- metabolism
- Time Factors
- Transfection
- Ventricular Function
- Ventricular Remodeling
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Publication Type: Journal Article
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