Abstract |
The G protein-coupled receptor kinases (GRKs) participate with arrestins in the regulation and signal propagation of multiple G protein-coupled receptors (GPCR) of key physiological and pharmacological relevance in the cardiovascular system. The complex mechanisms of regulation of GRK expression, degradation and function are being unveiled gradually. The levels of these kinases are known to change in pathological situations such as heart failure, hypertrophy and hypertension, and in animal models of these diseases. A better understanding of the mechanisms underlying these changes and of how these alterations participate in the triggering or progression of cardiovascular disease may contribute to the design of novel diagnostic and therapeutic strategies.
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Authors | Petronila Penela, Cristina Murga, Catalina Ribas, Antonio S Tutor, Sandra Peregrín, Federico Mayor Jr |
Journal | Cardiovascular research
(Cardiovasc Res)
Vol. 69
Issue 1
Pg. 46-56
(Jan 2006)
ISSN: 0008-6363 [Print] England |
PMID | 16288730
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Isoenzymes
- Receptors, G-Protein-Coupled
- beta-Adrenergic Receptor Kinases
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Topics |
- Animals
- Cardiovascular Diseases
(enzymology, metabolism)
- Isoenzymes
(metabolism)
- Myocardium
(enzymology)
- Receptors, G-Protein-Coupled
(metabolism)
- Signal Transduction
(physiology)
- beta-Adrenergic Receptor Kinases
(metabolism)
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