Deletion of Fstl1 (Follistatin-Like 1) From the Endocardial/Endothelial Lineage Causes Mitral Valve Disease. [electronic resource]
Producer: 20170905Description: e116-e130 p. digitalISSN:- 1524-4636
- Animals
- Bone Morphogenetic Proteins -- metabolism
- Cell Lineage
- Cell Proliferation
- Disease Models, Animal
- Disease Progression
- Endocardium -- metabolism
- Endothelial Cells -- metabolism
- Epithelial-Mesenchymal Transition
- Follistatin-Related Proteins -- deficiency
- Genetic Predisposition to Disease
- Heart Conduction System -- metabolism
- Heart Failure -- genetics
- Integrases -- genetics
- Mice, Knockout
- Mitral Valve -- metabolism
- Mitral Valve Insufficiency -- genetics
- Mitral Valve Prolapse -- genetics
- Phenotype
- Receptor, TIE-2 -- genetics
- Signal Transduction
- Time Factors
- Transcription Factors -- metabolism
- Transforming Growth Factor beta -- metabolism
- Ventricular Dysfunction, Left -- genetics
- Ventricular Function, Left
- Ventricular Remodeling
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't
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