Methods to Investigate β-Arrestin-Mediated Regulation of GPCR Function in Human Airway Smooth Muscle.
Publication/Presentation Date
1-1-2019
Abstract
Arrestin proteins were originally characterized as regulators of GPCR desensitization, and that function alone was sufficient to promote extreme interest in their study. It is now appreciated that arrestins also function as mediators of GPCR trafficking and G protein-independent signaling. This latter function places them as prominent players in the emerging field of qualitative signaling, which promises to launch a new area of pharmacology that defines ligands with selectivity/bias toward either G protein-dependent or -independent signaling. To meet the demands of research into arrestin function, methodology has evolved accordingly over the last three decades since the discovery of the arrestin family. Herein we describe state-of-the-art approaches for studying the role of arrestins (β-arrestin1 aka arrestin 2, β-arrestin2 aka arrestin 3) in GPCR function in a primary cell type, cultured airway smooth muscle cells.
Volume
1957
First Page
69
Last Page
82
ISSN
1940-6029
Published In/Presented At
Pera, T., & Penn, R. B. (2019). Methods to Investigate β-Arrestin-Mediated Regulation of GPCR Function in Human Airway Smooth Muscle. Methods in molecular biology (Clifton, N.J.), 1957, 69–82. https://doi.org/10.1007/978-1-4939-9158-7_4
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
30919347
Department(s)
Administration and Leadership
Document Type
Article