In Vivo Inhibition of Elevated Myocardial b-Adrenergic Receptor Kinase Activity in Hybrid Transgenic Mice Restores Normal b-Adrenergic Signaling and Function
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Shahab A. Akhter, Andrea D. Eckhart, Howard A. Rockman, Kyle Shotwell, Robert J. -Adrenergic Signaling and Function β Hybrid Transgenic Mice Restores Normal -Adrenergic Receptor Kinase Activity in β In Vivo Inhibition of Elevated Myocardial Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1999 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: 10.1161/01.CIR.100.6.648 1999;100:648-653 Circulation. http://circ.ahajournals.org/content/100/6/648 World Wide Web at: The online version of this article, along with updated information and services, is located on the
منابع مشابه
In vivo inhibition of elevated myocardial beta-adrenergic receptor kinase activity in hybrid transgenic mice restores normal beta-adrenergic signaling and function.
BACKGROUND The clinical syndrome of heart failure (HF) is characterized by an impaired cardiac beta-adrenergic receptor (betaAR) system, which is critical in the regulation of myocardial function. Expression of the betaAR kinase (betaARK1), which phosphorylates and uncouples betaARs, is elevated in human HF; this likely contributes to the abnormal betaAR responsiveness that occurs with beta-ago...
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G protein-coupled receptor kinases (GRKs) phosphorylate activated G protein-coupled receptors, including alpha(1B)-adrenergic receptors (ARs), resulting in desensitization. In vivo analysis of GRK substrate selectivity has been limited. Therefore, we generated hybrid transgenic mice with myocardium-targeted overexpression of 1 of 3 GRKs expressed in the heart (GRK2 [commonly known as the beta-A...
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Transgenic mice were generated with cardiac-specific overexpression of the G protein-coupled receptor kinase 3 (GRK3) to explore the in vivo role of this GRK in cardiac function. GRK3 is expressed in the heart along with the β-adrenergic receptor kinase (β-ARK1) and GRK5. We have previously demonstrated that myocardial-targeted overexpression in transgenic mice of β-ARK1 (Koch, W.J., H. A. Rock...
متن کاملPhysiological induction of a beta-adrenergic receptor kinase inhibitor transgene preserves ss-adrenergic responsiveness in pressure-overload cardiac hypertrophy.
BACKGROUND Transgenic mice with constitutive myocardium-targeted expression of a peptide inhibitor of the ss-adrenergic receptor kinase (ssARKct) have increased in vivo cardiac function and enhanced ss-adrenergic receptor (ssAR) responsiveness. METHODS AND RESULTS In the present study, we created transgenic mice with myocardium-targeted ssARKct transgene expression under control of the CARP (...
متن کاملOverexpression of myocardial Gsalpha prevents full expression of catecholamine desensitization despite increased beta-adrenergic receptor kinase.
Inotropic and chronotropic responses to catecholamines in young adult transgenic mice overexpressing myocardial Gsalpha are enhanced. One might predict that over the life of the animal, this chronically enhanced beta-adrenergic receptor stimulation would result in homologous catecholamine desensitization. To test this hypothesis, old transgenic Gsalpha mice and age-matched controls were studied...
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تاریخ انتشار 1999