ArticleMethods in enzymology2017
Approaches to Assess Biased Signaling at the CB1R Receptor.
Article in Methods in enzymology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- Structural basis of THC analog activity at the Cannabinoid 1 receptor.Nature communications · 2025Article
- Structural basis of ΔResearch square · 2024Article
- Anxiety and cognitive-related effects of ΔPsychopharmacology · 2022Article
- The endocannabinoid system in cardiovascular function: novel insights and clinical implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2018Review
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Authors and funding
3 authors.
Funding
Abstract
G protein-coupled receptors, such as the cannabinoid type 1 receptor (CB1R), have been shown to interact with multiple binding partners to transmit signals. In both transfected cell systems and in endogenously expressing cell lines, CB1R signaling has been described as multifaceted. The question remains as to how this highly widely expressed receptor signals in a given cell at a given time in vivo. The concept of functional selectivity, or biased agonism, describes the ability of an agonist to engage the receptor in a manner that preferentially engages certain signaling interactions (e.g., G proteins) over others (e.g., β-arrestins), presumably by stabilizing certain receptor conformations. There is growing interest in using such properties of ligands to direct signaling downstream of CB1R toward desirable therapeutic outcomes and to avoid adverse side effects. While it is not currently clear what pathways should be engaged and which should be avoided, the development of biased agonist tool compounds will aid in answering these questions. In this chapter, we discuss the approaches and caveats to assessing biased agonism at the CB1R.
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