Extracellular signal-regulated kinases control expression of G protein-coupled receptor kinase 2 (GRK2)

详细信息    查看全文

• 作者：Theilade ; Juliane ; Lerche Hansen ; Jakob ; Haunsø ; Stig ; Sheikh ; Sø ; ren P.
• 关键词：G protein-coupled receptor ; Receptor desensitisation ; Angiotensin II ; Mitogen activated kinase ; Signal transduction
• 刊名：FEBS Letters
• 出版年：2002
• 出版时间：May 8, 2002
• 年：2002
• 卷：518
• 期：1-3
• 页码：195-199
• 全文大小：224 K

文摘

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.