ArticleiScience2023
Sequence-directed concentration of G protein-coupled receptors in COPII vesicles.
Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 10 citations in OpenAlex.
- Remaking an exit: dynamic regulation of ER exit sites by post-translational modifications.Trends in cell biology · 2026Review
- The UFSP2-C1orf27 complex positions nascent GPCRs to the ufmylation system for ER export control.iScience · 2026Article
- ADGRF4 and ADGRL4 as novel prognostic biomarkers and potential therapeutic implications in stomach adenocarcinoma.BMC gastroenterology · 2026Article
- Interaction with COPII Member SAR1 Is Critical for the Delivery ofPlants (Basel, Switzerland) · 2026Article
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- The ufmylation cascade controls COPII recruitment, anterograde transport, and sorting of nascent GPCRs at ER.Science advances · 2024Article
- Segregation of nascent GPCRs in the ER-to-Golgi transport by CCHCR1 via direct interaction.Journal of cell science · 2024Article
- ER exit in physiology and disease.Frontiers in molecular biosciences · 2024Review
- Control of CCR5 Cell-Surface Targeting by the PRAF2 Gatekeeper.International journal of molecular sciences · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
G protein-coupled receptors (GPCRs) constitute the largest superfamily of plasma membrane signaling proteins. However, virtually nothing is known about their recruitment to COPII vesicles for forward delivery after synthesis in the endoplasmic reticulum (ER). Here, we demonstrate that some GPCRs are highly concentrated at ER exit sites (ERES) before COPII budding. Angiotensin II type 2 receptor (AT2R) and CXCR4 concentration are directed by a di-acidic motif and a 9-residue domain, respectively, and these motifs also control receptor ER-Golgi traffic. We further show that AT2R interacts with Sar1 GTPase and that distinct GPCRs have different ER-Golgi transport rates via COPII which is independent of their concentration at ERES. Collectively, these data demonstrate that GPCRs can be actively captured by COPII via specific motifs and direct interaction with COPII components that in turn affects their export dynamics, and provide important insights into COPII targeting and forward trafficking of nascent GPCRs.
Indexed as
Identifiers
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.