ArticleScience signaling2024
GPCR kinases differentially modulate biased signaling downstream of CXCR3 depending on their subcellular localization.
Article in Science signaling, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- Beyond β-Adrenergic Receptor Brake: Compartment-Selective GRK2 Programs from Heart Failure to Cardio-Oncology.Kinases and phosphatases · 2026Article
- G protein-coupled receptor kinase 3 regulates CCR7 signaling, trafficking, and T cell responses to CCL19 and CCL21.The Journal of biological chemistry · 2026Article
- β-arrestin recruitment facilitates a direct association with G proteins.Nature communications · 2026Article
- Physical interaction with Ephrin B1 promotes CXCR4 intracellular localization and oncogenic potential.Cellular and molecular life sciences : CMLS · 2026Article
- G-protein regulatory network governs receptor internalization dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Altered Intracellular Trafficking as a Mechanism for Prolonged Duration of G Protein-Coupled Receptor Activation.Journal of the American Chemical Society · 2026Article
- CXCR1 and CXCR2 display receptor bias for shared chemokine agonists.Molecular pharmacology · 2026Article
- Docosahexaenoic Acid Attenuates Visceral Pain by Suppressing Spinal CXCL10/CXCR3/ERK Signaling.Nutrients · 2026Article
- Location-biased β-arrestin conformations direct GPCR signaling.Science signaling · 2026Article
- High-affinity ELR+ CXC chemokines display balanced G protein-, GRK- and β-arrestin-associated transducer engagement at the viral G protein-coupled receptor ORF74.Frontiers in pharmacology · 2026Article
- Mechanisms of Location Bias in G Protein-Coupled Receptors.Handbook of experimental pharmacology · 2026Review
- Biased Agonists of the Type 1 Angiotensin II Receptor Promote Distinct Subcellular β-Arrestin Conformations.Biochemistry · 2025Article
- CXCR1 and CXCR2 display receptor bias for shared chemokine agonists.bioRxiv : the preprint server for biology · 2025Article
- Beyond G protein and arrestin: GRK2-biased β₂AR signaling.Trends in pharmacological sciences · 2025Article
- Critical Residues in the Gβ Subunit Mediate Selective Recruitment of the Gαq Heterotrimer to Activated G Protein-Coupled Receptors.ACS pharmacology & translational science · 2025Article
- Structural visualization of small molecule recognition by CXCR3 uncovers dual-agonism in the CXCR3-CXCR7 system.Nature communications · 2025Article
- Ligand-Induced Biased Activation of GPCRs: Recent Advances and New Directions from In Silico Approaches.Molecules (Basel, Switzerland) · 2025Review
- Quantitative approaches for studying G protein-coupled receptor signalling and pharmacology.Journal of cell science · 2025Review
- Beneath the surface: endosomal GPCR signaling.Trends in biochemical sciences · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Some G protein-coupled receptors (GPCRs) demonstrate biased signaling such that ligands of the same receptor exclusively or preferentially activate certain downstream signaling pathways over others. This phenomenon may result from ligand-specific receptor phosphorylation by GPCR kinases (GRKs). GPCR signaling can also exhibit location bias because GPCRs traffic to and signal from subcellular compartments in addition to the plasma membrane. Here, we investigated whether GRKs contributed to location bias in GPCR signaling. GRKs translocated to endosomes after stimulation of the chemokine receptor CXCR3 or other GPCRs in cultured cells. GRK2, GRK3, GRK5, and GRK6 showed distinct patterns of recruitment to the plasma membrane and to endosomes depending on the identity of the biased ligand used to activate CXCR3. Analysis of engineered forms of GRKs that localized to either the plasma membrane or endosomes demonstrated that biased CXCR3 ligands elicited different signaling profiles that depended on the subcellular location of the GRK. Each GRK exerted a distinct effect on the regulation of CXCR3 engagement of β-arrestin, internalization, and activation of the downstream effector kinase ERK. Our work highlights a role for GRKs in location-biased GPCR signaling and demonstrates the complex interactions between ligands, GRKs, and cellular location that contribute to biased signaling.
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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.