Comparative rates of desensitization of beta-adrenergic receptors by the beta-adrenergic receptor kinase and the cyclic AMP-dependent protein kinase. [PDF]
Proceedings of the National Academy of Sciences, 1991 Three separate processes may contribute to rapid beta-adrenergic receptor desensitization: functional uncoupling from the stimulatory guanine nucleotide-binding protein Gs, mediated by phosphorylation of the receptors by two distinct kinases, the specific beta-adrenergic receptor kinase (beta ARK) and the cyclic AMP-dependent protein kinase A (PKA), as
N S, Roth +4 more
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Mechanism of β-Adrenergic Receptor Desensitization in Cardiac Hypertrophy Is Increased β-Adrenergic Receptor Kinase [PDF]
Journal of Biological Chemistry, 1997 Pressure overload cardiac hypertrophy in the mouse was achieved following 7 days of transverse aortic constriction. This was associated with marked beta-adrenergic receptor (beta-AR) desensitization in vivo, as determined by a blunted inotropic response to dobutamine. Extracts from hypertrophied hearts had approximately 3-fold increase in cytosolic and
D J, Choi +3 more
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β-Adrenergic Receptor Kinase (GRK2) Colocalizes with β-Adrenergic Receptors during Agonist-induced Receptor Internalization [PDF]
Journal of Biological Chemistry, 1997 Rapid regulation of G protein-coupled receptors appears to involve agonist-promoted receptor phosphorylation by G protein-coupled receptor kinases (GRKs). This is followed by binding of uncoupling proteins termed arrestins and transient receptor internalization. In this report we show that the beta-adrenergic receptor kinase (betaARK-1 or GRK2) follows
A, Ruiz-Gómez, F, Mayor
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Rapid desensitization of neonatal rat liver beta-adrenergic receptors. A role for beta-adrenergic receptor kinase. [PDF]
Journal of Clinical Investigation, 1994 Exposure of beta-adrenergic receptors (BAR) to agonists often leads to a rapid loss of receptor responsiveness. The proposed mechanisms of such rapid receptor desensitization include receptor phosphorylation by either cAMP-dependent protein kinase or the specific beta-adrenergic receptor kinase (BARK), leading to functional uncoupling from adenylyl ...
I, García-Higuera, F, Mayor
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The NADPH oxidase NOX4 regulates redox and metabolic homeostasis preventing HCC progression
Hepatology, EarlyView., 2022 Loss of NOX4 in HCC tumor cells induces metabolic reprogramming in a Nrf2/MYC‐dependent manner to promote HCC progression. Abstract Background and Aims The NADPH oxidase NOX4 plays a tumor‐suppressor function in HCC. Silencing NOX4 confers higher proliferative and migratory capacity to HCC cells and increases their in vivo tumorigenic potential in ...
Irene Peñuelas‐Haro +14 more
wiley +1 more source
Inhibition of beta-adrenergic receptor kinase prevents rapid homologous desensitization of beta 2-adrenergic receptors. [PDF]
Proceedings of the National Academy of Sciences, 1989 Homologous (agonist-specific) desensitization of beta-adrenergic receptors (beta ARs) is accompanied by and appears to require phosphorylation of the receptors. We have recently described a novel protein kinase, beta AR kinase, which phosphorylates beta ARs in vitro in an agonist-dependent manner.
Lohse, MJ +3 more
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Altered expression of beta-adrenergic receptor kinase and beta 1-adrenergic receptors in the failing human heart. [PDF]
Circulation, 1993 BACKGROUND In chronic heart failure, the positive inotropic effects of beta-adrenergic receptor agonists are greatly reduced, in part as a result of two alterations of the cardiac beta-adrenergic receptors: loss of their function (receptor uncoupling) and reduction of their number (downregulation).
M, Ungerer +4 more
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Tailoring therapy for heart failure: the pharmacogenomics of adrenergic receptor signaling. [PDF]
, 2014 Heart failure is one of the leading causes of mortality in Western countries, and β-blockers are a cornerstone of its treatment. However, the response to these drugs is variable among individuals, which might be explained, at least in part, by genetic ...
Barrese, V +3 more
core +2 more sources
Frontiers in Physiology, 2021 We previously showed that the beta-3 adrenergic receptor (BAR3) is expressed in most segments of the nephron where its agonism promotes a potent antidiuretic effect.
Serena Milano +8 more
doaj +1 more source
Frontiers in Endocrinology, 2021 BackgroundInsulin resistance is a metabolic disorder that occurs in type 2 diabetes mellitus and obesity. Genetic factors such as β3-adrenoceptor polymorphism (Trp64Arg) may be involved in IR and insulin secretion.
Hai-Dan Wang +8 more
doaj +1 more source