Evidence map›Paper›PMID 32978390›Full record

ArticleNature communications2020

The atypical chemokine receptor 3 interacts with Connexin 43 inhibiting astrocytic gap junctional intercellular communication.

Amos Fumagalli, Joyce Heuninck, Anne Pizzoccaro, Enora Moutin, Joyce Koenen, Martial Séveno, Thierry Durroux, Marie-Pierre Junier, Géraldine Schlecht-Louf, Francoise Bachelerie and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Atypical GPCR Activation Resolved by Nanobody Engineering.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Atypical chemokine receptors in the immune system.Nature reviews. Immunology · 2024
    Review
  13. Article
  14. Article
  15. Conformational dynamics underlying atypical chemokine receptor 3 activation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
  17. Activation of the CXCR4 Receptor by Chemokine CXCL12 Increases the Excitability of Neurons in the Rat Central Amygdala.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 3 countries.

Amos FumagalliInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.
Joyce HeuninckInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.
Anne PizzoccaroInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.
Enora MoutinInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.ORCID http://orcid.org/0000-0001-8250-703X
Joyce KoenenUniversité Paris-Saclay, Inserm, Inflammation, Microbiome and Immunosurveillance, 92140, Clamart, France.ORCID http://orcid.org/0000-0002-7913-1518
Martial SévenoBiocampus Montpellier, Université de Montpellier, CNRS, INSERM, Montpellier, France.ORCID http://orcid.org/0000-0002-5000-8735
Thierry DurrouxInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.
Marie-Pierre JunierCNRS UMR8246, Inserm U1130, Neuroscience Paris Seine-IBPS, Sorbonne Universités, Paris, France.
Géraldine Schlecht-LoufUniversité Paris-Saclay, Inserm, Inflammation, Microbiome and Immunosurveillance, 92140, Clamart, France.ORCID http://orcid.org/0000-0002-7924-5371
Francoise BachelerieUniversité Paris-Saclay, Inserm, Inflammation, Microbiome and Immunosurveillance, 92140, Clamart, France.
Dagmar SchützInstitute of Pharmacology and Toxicology, Jena University Hospital, 07747, Jena, Germany.
Ralf StummInstitute of Pharmacology and Toxicology, Jena University Hospital, 07747, Jena, Germany.ORCID http://orcid.org/0000-0002-9458-5526
Martine J SmitAmsterdam Institute for Molecules Medicines and Systems, Division of Medicinal Chemistry, Faculty of Sciences, VU University Amsterdam, 1081, HV, Amsterdam, The Netherlands.
Nathalie C GuérineauInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.
Séverine Chaumont-DubelInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France.ORCID http://orcid.org/0000-0001-6860-6891
Philippe MarinInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, Montpellier, France. philippe.marin@igf.cnrs.fr.ORCID http://orcid.org/0000-0002-5977-7274
Centre National de la Recherche Scientifique · FRInserm · FRJena University Hospital · DEAIMM Therapeutics (Netherlands) · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The atypical chemokine receptor 3 (ACKR3) plays a pivotal role in directing the migration of various cellular populations and its over-expression in tumors promotes cell proliferation and invasiveness. The intracellular signaling pathways transducing ACKR3-dependent effects remain poorly characterized, an issue we addressed by identifying the interactome of ACKR3. Here, we report that recombinant ACKR3 expressed in HEK293T cells recruits the gap junction protein Connexin 43 (Cx43). Cx43 and ACKR3 are co-expressed in mouse brain astrocytes and human glioblastoma cells and form a complex in embryonic mouse brain. Functional in vitro studies show enhanced ACKR3 interaction with Cx43 upon ACKR3 agonist stimulation. Furthermore, ACKR3 activation promotes β-arrestin2- and dynamin-dependent Cx43 internalization to inhibit gap junctional intercellular communication in primary astrocytes. These results demonstrate a functional link between ACKR3 and gap junctions that might be of pathophysiological relevance.

Indexed as

AnimalsAstrocytesCell CommunicationCell ProliferationConnexin 43ConnexinsGap JunctionsGene Knock-In TechniquesGlioblastomaHEK293 CellsHumansMiceMice, Inbred C57BLMice, KnockoutProtein Interaction Domains and MotifsReceptors, CXCRACKR3 protein, humanConnexin 43ConnexinsGJA1 protein, humanReceptors, CXCR

Identifiers

PMID32978390
PMCPMC7519114
OpenAlexW3088783706

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.