ArticleGene therapy2003
Effects of two Gbetagamma-binding proteins--N-terminally truncated phosducin and beta-adrenergic receptor kinase C terminus (betaARKct)--in heart failure.
Article in Gene therapy, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Medium-chain fatty acids modulate myocardial function via a cardiac odorant receptor.Basic research in cardiology · 2017Article
- Cardioprotective effects of lixisenatide in rat myocardial ischemia-reperfusion injury studies.Journal of translational medicine · 2013Article
- Targeting GRK2 by gene therapy for heart failure: benefits above β-blockade.Gene therapy · 2012Review
- Taking the heart failure battle inside the cell: small molecule targeting of Gβγ subunits.Journal of molecular and cellular cardiology · 2011Review
- G protein coupled receptor kinases as therapeutic targets in cardiovascular disease.Circulation research · 2011Review
- The physiological roles of phosducin: from retinal function to stress-dependent hypertension.Cellular and molecular life sciences : CMLS · 2011Review
- The inotropic peptide βARKct improves βAR responsiveness in normal and failing cardiomyocytes through G(βγ)-mediated L-type calcium current disinhibition.Circulation research · 2011Article
- Rational design of a selective covalent modifier of G protein βγ subunits.Molecular pharmacology · 2011Article
- Small molecule disruption of G beta gamma signaling inhibits the progression of heart failure.Circulation research · 2010Article
- GRK mythology: G-protein receptor kinases in cardiovascular disease.Journal of molecular medicine (Berlin, Germany) · 2009Review
- Novel pharmacotherapies to abrogate postinfarction ventricular remodeling.Nature reviews. Cardiology · 2009Review
- A new type of ERK1/2 autophosphorylation causes cardiac hypertrophy.Nature medicine · 2009Article
- G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure.Circulation research · 2008Article
- G protein betagamma subunits as targets for small molecule therapeutic development.Combinatorial chemistry & high throughput screening · 2008Review
- Beta-adrenergic receptor signaling in cardiac function and heart failure.McGill journal of medicine : MJM : an international forum for the advancement of medical sciences by students · 2007Article
- Beta-adrenoceptor blocker treatment and the cardiac beta-adrenoceptor-G-protein(s)-adenylyl cyclase system in chronic heart failure.Naunyn-Schmiedeberg's archives of pharmacology · 2007Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial overexpression of the C-terminus of beta-adrenergic receptor kinase (betaARKct) has been shown to result in a positive inotropic effect or an improvement of survival in heart failure. However, it is not clear whether this beneficial effect is mainly because of dominant-negative inhibition of betaARK1, and a consecutive resensitization of beta-adrenergic receptors (betaAR), or rather due to inhibition of other Gbetagamma-mediated effects. In this study, we tested whether overexpression of N-terminally truncated phosducin (nt-del-phosducin), another Gbetagamma-binding protein that does not resensitize betaARs owing to simultaneous inhibition of GDP release from Galpha subunits, shows the same effects as betaARKct. Adenoviral gene transfer was used to express nt-del-phosducin and betaARKct in isolated ventricular cardiomyocytes and in myocardium of rabbits, which suffered from heart failure because of rapid ventricular pacing. BetaAR-stimulated cAMP formation was increased by betaARKct, but not by nt-del-phosducin, whereas both proteins inhibited Gbetagamma-mediated effects. Both transgenes also increased contractility of normal and failing isolated cardiomyocytes and improved contractility in rabbits with heart failure after gene transfer in vivo. In conclusion, overexpression of nt-del-phosducin enhances the contractility of cardiomyocytes to the same extent as betaARKct, suggesting that the effects of betaARKct might be owing to inhibition of Gbetagamma rather than to betaAR resensitization.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.