Results 21 to 30 of about 24,774 (261)
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 ...
Irene García-Higuera, Federico Mayor
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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 agonist‐induced beta‐adrenergic receptor kinase translocation in C6 glioma cells [PDF]
FEBS Letters, 1992 Exposure of C6 glioma cells to 1 μM isoproterenol leads to fast desensitization of the β‐adrenergic receptor/adenylyl cyclase system and transient receptor sequestration. It also triggers a very rapid and transient translocation to the plasma membrane or β‐adrenergic receptor kinase (βARK), a specific cytoplasmic kinase that phosphorylates only the ...
Irene García-Higuera, Federico Mayor
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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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Breast Cancer: Basic and Clinical Research, 2008 Previous data from our laboratory have indicated that there is a functional link between the beta-adrenergic receptor signaling pathway and the G-protein inwardly rectifying potassium channel (GIRK1) in breast cancer cell lines and that these pathways ...
Michael W. Hance +2 more
doaj +2 more sources
Paroxetine Attenuates Cardiac Hypertrophy Via Blocking GRK2 and ADRB1 Interaction in Hypertension
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 2021 Background ADRB1 (adrenergic receptor beta 1) responds to neuroendocrine stimulations, which have great implications in hypertension. GRK2 (G protein‐coupled receptor kinase 2) is an essential regulator for many G protein‐coupled receptors and subsequent
Xuejing Sun +9 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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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
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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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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