QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

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

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ma, L. Articles by Pei, G. Search for Related Content PubMed PubMed Citation Articles by Ma, L. Articles by Pei, G. Social Bookmarking                         What's this?

-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

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				A. Lymperopoulos, G. Rengo, C. Zincarelli, J. Kim, S. Soltys, and W. J. Koch An adrenal {beta}-arrestin 1-mediated signaling pathway underlies angiotensin II-induced aldosterone production in vitro and in vivo PNAS, April 7, 2009; 106(14): 5825 - 5830. [Abstract] [Full Text] [PDF]

				K. Gong, Z. Li, M. Xu, J. Du, Z. Lv, and Y. Zhang A Novel Protein Kinase A-independent, {beta}-Arrestin-1-dependent Signaling Pathway for p38 Mitogen-activated Protein Kinase Activation by {beta}2-Adrenergic Receptors J. Biol. Chem., October 24, 2008; 283(43): 29028 - 29036. [Abstract] [Full Text] [PDF]

				M.-H. Lee, H. M. El-Shewy, D. K. Luttrell, and L. M. Luttrell Role of -Arrestin-mediated Desensitization and Signaling in the Control of Angiotensin AT1a Receptor-stimulated Transcription J. Biol. Chem., January 25, 2008; 283(4): 2088 - 2097. [Abstract] [Full Text] [PDF]

				H. Zheng, H. H. Loh, and P.-Y. Law -Arrestin-Dependent {micro}-Opioid Receptor-Activated Extracellular Signal-Regulated Kinases (ERKs) Translocate to Nucleus in Contrast to G Protein-Dependent ERK Activation Mol. Pharmacol., January 1, 2008; 73(1): 178 - 190. [Abstract] [Full Text] [PDF]