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First published online January 10, 2007
doi: 10.1242/10.1242/jcs.03338

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-arrestin signaling and regulation of transcription

¹ Pharmacology Research Center, Shanghai Medical College and Institutes of Brain Science, Fudan University, 138 Yi Xue Yuan Road, Shanghai 200032, China
² Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Science, Chinese Academy of Sciences, 320 Yue Yang Road, Shanghai 200031, China

Authors for correspondence (e-mail: lanma{at}fudan.edu.cn; gpei{at}sibs.ac.cn)

Accepted 13 November 2006

-arrestin 1 and -arrestin 2 are well-known negative regulators of G-protein-coupled receptor (GPCR) signaling. Upon GPCR activation, -arrestins translocate to the cell membrane and bind to the agonist-occupied receptors. This uncouples these receptors from G proteins and promotes their internalization, thus causing desensitization. However, accumulating evidence indicates that -arrestins also function as scaffold proteins that interact with several cytoplasmic proteins and link GPCRs to intracellular signaling pathways such as MAPK cascades. Recent work has also revealed that, in response to activation of certain GPCRs, -arrestins translocate from the cytoplasm to the nucleus and associate with transcription cofactors such as p300 and cAMP-response element-binding protein (CREB) at the promoters of target genes to promote transcription. They also interact with regulators of transcription factors, such as IB and MDM2, in the cytoplasm and regulate transcription indirectly. This -arrestin-mediated regulation of transcription appears to play important roles in cell growth, apoptosis and modulation of immune functions.

Key words: -arrestins, G-protein-coupled receptors, Transcription, Signal transduction

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