ArticleNature communications2018
Lack of beta-arrestin signaling in the absence of active G proteins.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers.
What it found
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Who cites it
201 citing papers in PubMed, 367 citations in OpenAlex.
- G protein signaling capabilities at the bradykinin 2 receptor.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- β-arrestin recruitment facilitates a direct association with G proteins.Nature communications · 2026Article
- G-protein regulatory network governs receptor internalization dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- β-Arrestin1/2 are essential for embryonic lymphatic vessel development.JCI insight · 2026Article
- RGS proteins: Potential regulators of mouse melanopsin's signaling phototransduction cascade across ipRGC subtypes.Biophysical journal · 2026Article
- GPCR kinases shape ACKR4 functions via differential C-terminal phosphorylation.Nature communications · 2026Article
- The atypical adhesion GPCR ADGRA1 controls hippocampal inhibitory circuit function.Cell reports · 2026Article
- Cytoplasmic tail diversity determines the effector bias of the adhesion GPCR ADGRL2.Cell chemical biology · 2026Article
- Allostery between Distant Structural Regions Dictates Selectivity in GPCR:G Protein Coupling.Biochemistry · 2026Article
- Arrestin-3 sca-olds multiple MAP3Ks driving stress-induced JNK3 activation and cell death.bioRxiv : the preprint server for biology · 2026Article
- GPCR systems coordinate cellular resilience against aging-associated stress.Frontiers in molecular biosciences · 2026Review
- Patchouli alcohol triggers autophagic cell death in non-small cell lung cancer cells through targeting GNAI1 to dissociate the GNAI1/ARRB1 complex.International journal of biological sciences · 2026Article
- Article
- Membrane-domain compartmentalization of active GPCRs by β-arrestins through PtdIns(4,5)PNature chemical biology · 2025Article
- The adhesion GPCR ADGRL2 engages Gα13 to enable epidermal differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Discovery of novel and selective GPR17 antagonists as pharmacological tools for developing new therapeutic strategies in diabetes and obesity.European journal of medicinal chemistry · 2025Article
- Gαq-Stimulated Gene Expression Is Insensitive to Bromo Extra Terminal Domain Inhibitors in HEK 293 Cells.International journal of molecular sciences · 2025Article
- Arrestins as Possible Drug Targets.Biomolecules & therapeutics · 2025Review
- Amylin receptor subunit interactions are modulated by agonists and determine signaling.Science signaling · 2025Article
- Cytoplasmic tail composition modulates the G protein and arrestin-3 signaling bias of the adhesion GPCR LPHN2.bioRxiv : the preprint server for biology · 2025Article
141 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein-independent, arrestin-dependent signaling is a paradigm that broadens the signaling scope of G protein-coupled receptors (GPCRs) beyond G proteins for numerous biological processes. However, arrestin signaling in the collective absence of functional G proteins has never been demonstrated. Here we achieve a state of "zero functional G" at the cellular level using HEK293 cells depleted by CRISPR/Cas9 technology of the Gs/q/12 families of Gα proteins, along with pertussis toxin-mediated inactivation of Gi/o. Together with HEK293 cells lacking β-arrestins ("zero arrestin"), we systematically dissect G protein- from arrestin-driven signaling outcomes for a broad set of GPCRs. We use biochemical, biophysical, label-free whole-cell biosensing and ERK phosphorylation to identify four salient features for all receptors at "zero functional G": arrestin recruitment and internalization, but-unexpectedly-complete failure to activate ERK and whole-cell responses. These findings change our understanding of how GPCRs function and in particular of how they activate ERK1/2.
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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.