Methods to Investigate ß-Arrestin-Mediated Regulation of GPCR Function in Human Airway Smooth Muscle.
Methods Mol Biol
; 1957: 69-82, 2019.
Article
en En
| MEDLINE
| ID: mdl-30919347
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 (ß-arrestin1 aka arrestin 2, ß-arrestin2 aka arrestin 3) in GPCR function in a primary cell type, cultured airway smooth muscle cells.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Sistema Respiratorio
/
Receptores Acoplados a Proteínas G
/
Beta-Arrestinas
/
Biología Molecular
/
Músculo Liso
Tipo de estudio:
Qualitative_research
Límite:
Humans
Idioma:
En
Revista:
Methods Mol Biol
Asunto de la revista:
BIOLOGIA MOLECULAR
Año:
2019
Tipo del documento:
Article
País de afiliación:
Estados Unidos