ArticleThe Journal of biological chemistry
A novel luminescence-based β-arrestin recruitment assay for unmodified receptors.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Next-generation chemogenetic inhibition using a brain-permeant non-prescription agent.Signal transduction and targeted therapy · 2026Article
- Light-Based Molecular Tools to Precisely Monitor and Operate β-Adrenoceptors.Medicinal research reviews · 2026Review
- Biased Allosteric Modulation in GPCR Drug Discovery.Handbook of experimental pharmacology · 2026Review
- FDA Drug Repurposing Uncovers Modulators of Dopamine DJournal of medicinal chemistry · 2025Article
- Integrated Transcriptomic and Metabolomic Analyses Reveal the Adaptive Mechanisms of a Low-Salinity Selected Population of Pacific White Shrimp (Litopenaeus vannamei).Marine biotechnology (New York, N.Y.) · 2025Article
- The role of protease-activated receptors (PARs) in the functioning of platelets and platelet-derived microparticles (PMPs).Frontiers in molecular biosciences · 2025Review
- G Protein-Coupled Receptor 17 Inhibits Glucagon-like Peptide-1 Secretion via a Gi/o-Dependent Mechanism in Enteroendocrine Cells.Biomolecules · 2024Article
- G protein-coupled receptor 17 inhibits glucagon-like peptide-1 secretion via a Gi/o-dependent mechanism in enteroendocrine cells.bioRxiv : the preprint server for biology · 2024Article
- Protein-Based Tools for Studying Neuromodulation.ACS chemical biology · 2024Review
- High expression of GPR160 in prostate cancer is unrelated to CARTp-mediated signaling pathways.Acta pharmaceutica Sinica. B · 2024Article
- Accessible and Generalizable in Vitro Luminescence Assay for Detecting GPCR Activation.ACS measurement science au · 2023Article
- In-Cell Arrestin-Receptor Interaction Assays.Current protocols · 2023Article
- Liver-expressed antimicrobial peptide 2 elevation contributes to age-associated cognitive decline.JCI insight · 2023Article
- Investigating G-protein coupled receptor signalling with light-emitting biosensors.Frontiers in physiology · 2023Review
- Structural basis of GPCR coupling to distinct signal transducers: implications for biased signaling.Trends in biochemical sciences · 2022Review
- GPCR systems pharmacology: a different perspective on the development of biased therapeutics.American journal of physiology. Cell physiology · 2022Review
- Encoding mu-opioid receptor biased agonism with interaction fingerprints.Journal of computer-aided molecular design · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
G protein-coupled receptors (GPCRs) signal through activation of G proteins and subsequent modulation of downstream effectors. More recently, signaling mediated by β-arrestin has also been implicated in important physiological functions. This has led to great interest in the identification of biased ligands that favor either G protein or β-arrestin-signaling pathways. However, nearly all screening techniques for measuring β-arrestin recruitment have required C-terminal receptor modifications that can in principle alter protein interactions and thus signaling. Here, we have developed a novel luminescence-based assay to measure β-arrestin recruitment to the membrane or early endosomes by unmodified receptors. Our strategy uses NanoLuc, an engineered luciferase from Oplophorus gracilirostris (deep-sea shrimp) that is smaller and brighter than other well-established luciferases. Recently, several publications have explored functional NanoLuc split sites for use in complementation assays. We have identified a unique split site within NanoLuc and fused the corresponding N-terminal fragment to either a plasma membrane or early endosome tether and the C-terminal fragment to β-arrestins, which form the basis for the MeNArC and EeNArC assays, respectively. Upon receptor activation, β-arrestin is recruited to the membrane and subsequently internalized in an agonist concentration-dependent manner. This recruitment promotes complementation of the two NanoLuc fragments, thereby reconstituting functional NanoLuc, allowing for quantification of β-arrestin recruitment with a single luminescence signal. Our assay avoids potential artifacts related to C-terminal receptor modification and has promise as a new generic assay for measuring β-arrestin recruitment to diverse GPCR types in heterologous or native cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.