ArticleMethods in molecular biology (Clifton, N.J.)2019
Methods to Investigate β-Arrestin-Mediated Regulation of GPCR Function in Human Airway Smooth Muscle.
Article in Methods in molecular biology (Clifton, N.J.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Cooperativity between β-agonists and c-Abl inhibitors in regulating airway smooth muscle relaxation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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.
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