ArticleEMBO reports2020
Keys to the Kingdom: GPCR phosphorylation patterns direct β-arrestin.
Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 7 citations in OpenAlex.
- Action of the Terminal Complement Pathway on Cell Membranes.The Journal of membrane biology · 2025Review
- Systematic assessment of chemokine ligand bias at the human chemokine receptor CXCR2 indicates G protein bias over β-arrestin recruitment and receptor internalization.Cell communication and signaling : CCS · 2024Article
- Allosteric Regulation of G-Protein-Coupled Receptors: From Diversity of Molecular Mechanisms to Multiple Allosteric Sites and Their Ligands.International journal of molecular sciences · 2023Review
- Middle-Down Mass Spectrometry Reveals Activity-Modifying Phosphorylation Barcode in a Class C G Protein-Coupled Receptor.Journal of the American Chemical Society · 2022Article
- Review
- Keys to the Kingdom: GPCR phosphorylation patterns direct β-arrestin.EMBO reports · 2020Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The β-arrestin proteins are key regulators of G protein-coupled receptors, serving at least three distinct functions: inhibiting receptor signaling through G proteins, directing receptor trafficking from the cell surface after activation, and transmitting receptor-initiated signals directly. How the two β-arrestin proteins perform these many functions for hundreds of receptor types throughout the body, and specifically how β-arrestin-mediated signaling can be tuned to cellular conditions, remains an open question. Function-based evidence and recent structure-based evidence have suggested that patterns of receptor phosphorylation ("barcodes") may be a critical determinant of β-arrestin action. In this issue of EMBO Reports, Baidya and colleagues (Baidya et al, 2020a) report that specific receptor phosphorylation site clusters ("codes") determine whether β-arrestin 1 acts to promote or inhibit receptor activation of Erk mitogen-activated protein kinases. They provide direct evidence for a functional barcode system by transferring inhibitory and stimulatory codes between receptors, suggesting future work to understand just how code site location in a receptor and its phosphorylation status can lead to very different functions of bound β-arrestin proteins.
Indexed as
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What Socratic 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 Socratic graph.