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Extracellular signal‐regulated kinases control expression of G protein‐coupled receptor kinase 2 (GRK2)
Author(s) -
Theilade Juliane,
Lerche Hansen Jakob,
Haunsø Stig,
Sheikh Søren P
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)02701-1
Subject(s) - beta adrenergic receptor kinase , g protein coupled receptor kinase , mapk/erk pathway , microbiology and biotechnology , kinase , receptor , signal transduction , chemistry , protein kinase a , extracellular , biology , g protein coupled receptor , biochemistry
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.