Abstract
G protein-coupled receptor kinase 2 (GRK2) phosphorylates G protein-coupled receptors resulting in uncoupling from G proteins. Receptors modulate GRK2 expression, however the mechanistic basis for this effect is largely unknown. Here we report a novel mechanism by which receptors use the extracellular signal-regulated kinase (ERK) cascade to regulate GRK2 cellular levels. ERK activation by receptor stimulation elevated endogenous GRK2 while antagonist treatment decreased cellular GRK2. Activating ERK by overexpressing constitutive active MEK-1 or Ras elevated GRK2 protein levels while blocking ERK using PD98059 or dominant negative Ras abolished this effect. These data suggest ERK is a critical regulator of GRK2 levels.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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COS Cells
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Cells, Cultured
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Cyclic AMP-Dependent Protein Kinases / biosynthesis*
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Down-Regulation
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Enzyme Inhibitors / pharmacology
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Flavonoids / pharmacology
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G-Protein-Coupled Receptor Kinase 2
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MAP Kinase Signaling System / drug effects
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Mitogen-Activated Protein Kinases / antagonists & inhibitors
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Mitogen-Activated Protein Kinases / physiology*
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Mutation
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Myocardium / enzymology*
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Proto-Oncogene Proteins p21(ras) / genetics
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Rats
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Rats, Wistar
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Receptor, Angiotensin, Type 1
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Receptors, Angiotensin / metabolism
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Up-Regulation
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beta-Adrenergic Receptor Kinases
Substances
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Enzyme Inhibitors
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Flavonoids
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Receptor, Angiotensin, Type 1
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Receptors, Angiotensin
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Cyclic AMP-Dependent Protein Kinases
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Grk2 protein, rat
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beta-Adrenergic Receptor Kinases
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G-Protein-Coupled Receptor Kinase 2
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Mitogen-Activated Protein Kinases
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Proto-Oncogene Proteins p21(ras)
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2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one