GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
PMID:7761854
| Citation |
Koch, WJ, Rockman, HA, Samama, P, Hamilton, RA, Bond, RA, Milano, CA and Lefkowitz, RJ (1995) Cardiac function in mice overexpressing the beta-adrenergic receptor kinase or a beta ARK inhibitor. Science 268:1350-3 |
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| Abstract |
Transgenic mice were created with cardiac-specific overexpression of the beta-adrenergic receptor kinase-1 (beta ARK1) or a beta ARK inhibitor. Animals overexpressing beta ARK1 demonstrated attenuation of isoproterenol-stimulated left ventricular contractility in vivo, dampening of myocardial adenylyl cyclase activity, and reduced functional coupling of beta-adrenergic receptors. Conversely, mice expressing the beta ARK inhibitor displayed enhanced cardiac contractility in vivo with or without isoproterenol. These animals demonstrate the important role of beta ARK in modulating in vivo myocardial function. Because increased amounts of beta ARK1 and diminished cardiac beta-adrenergic responsiveness characterize heart failure, these animals may provide experimental models to study the role of beta ARK in heart disease. |
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| Keywords |
Adenylate Cyclase/metabolism; Animals; Blood Pressure; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors; Cyclic AMP-Dependent Protein Kinases/genetics; Cyclic AMP-Dependent Protein Kinases/metabolism; GTP-Binding Proteins/metabolism; Heart/physiology; Isoproterenol/pharmacology; Mice; Mice, Transgenic; Myocardial Contraction/drug effects; Myocardium/enzymology; Phenotype; Receptors, Adrenergic, beta/metabolism; Sarcolemma/enzymology; Ventricular Pressure; beta-Adrenergic Receptor Kinases |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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