| G protein-dependent and G protein-independent signaling pathways and their impact on cardiac function. | |
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MedLine Citation:
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PMID: 21737817 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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G protein-coupled receptors signal through a variety of mechanisms that impact cardiac function, including contractility and hypertrophy. G protein-dependent and G protein-independent pathways each have the capacity to initiate numerous intracellular signaling cascades to mediate these effects. G protein-dependent signaling has been studied for decades and great strides continue to be made in defining the intricate pathways and effectors regulated by G proteins and their impact on cardiac function. G protein-independent signaling is a relatively newer concept that is being explored more frequently in the cardiovascular system. Recent studies have begun to reveal how cardiac function may be regulated via G protein-independent signaling, especially with respect to the ever-expanding cohort of β-arrestin-mediated processes. This review primarily focuses on the impact of both G protein-dependent and β-arrestin-dependent signaling pathways on cardiac function, highlighting the most recent data that illustrate the comprehensive nature of these mechanisms of G protein-coupled receptor signaling. |
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Authors:
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Douglas G Tilley |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review |
Journal Detail:
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Title: Circulation research Volume: 109 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-07-08 Completed Date: 2011-09-23 Revised Date: 2012-07-11 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: United States |
Other Details:
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Languages: eng Pagination: 217-30 Citation Subset: IM |
Affiliation:
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Department of Pharmaceutical Sciences, Jefferson School of Pharmacy, and Center for Translational Medicine, Thomas Jefferson University, 1025 Walnut Street, 402 College Building, Philadelphia, PA 19107, USA. douglas.tilley@jefferson.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Arrestins
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metabolism Heart / physiology* Humans Receptors, G-Protein-Coupled / metabolism* Signal Transduction / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL105414-01/HL/NHLBI NIH HHS; R01 HL105414-01/HL/NHLBI NIH HHS; R01 HL105414-02/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Arrestins; 0/Receptors, G-Protein-Coupled; 0/beta-arrestin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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