β-Arrestins 1 and 2 are critical regulators of inflammation

28Citations
Citations of this article
46Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

β-Arrestins 1 and 2 couple to seven trans-membrane receptors and regulate G protein-dependent signaling, receptor endocytosis and ubiquitylation. Recent studies have uncovered several unanticipated functions of β-arrestins, suggesting that the role of β-arrestins in cell signaling is much broader than originally thought. It is now recognized that β-arrestins can transduce receptor signaling independent of G proteins. The expression of β-arrestins is differentially regulated in immune cells and tissues in response to specific inflammatory stimuli, and β-arrestins are critical regulators of the inflammatory response. This review will focus on β-arrestins in immune cells and the impact of altered expression on the pathogenesis of specific inflammatory diseases. Understanding the role of β-arrestins in inflammation may lead to new strategies to treat inflammatory diseases, such as sepsis, rheumatoid arthritis, asthma, multiple sclerosis, inflammatory bowel disease and atherosclerosis. © The Author(s) 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.

Cite

CITATION STYLE

APA

Fan, H. (2014). β-Arrestins 1 and 2 are critical regulators of inflammation. Innate Immunity. SAGE Publications Ltd. https://doi.org/10.1177/1753425913501098

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free