Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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.
Claudia V Perez AlmeriaAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-7312-8529
Omolade OtunAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.
Thomas D LammeAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.ORCID http://orcid.org/0009-0005-2168-9809
Lotte Di NiroAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.ORCID http://orcid.org/0009-0008-9553-0667
Caitrin CruddenAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-7786-112X
Jan Paul BebelmanAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.
Noureldine YoussefInstitute for Molecular Cell Biology, CMB - Center for Molecular Biomedicine, University Hospital Jena, Friedrich-Schiller-University Jena, Jena, Germany.ORCID http://orcid.org/0000-0001-8958-1646
Lejla MusliAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.
Shawn JenjakDepartment of Biochemistry, Medical College of Wisconsin, Milwaukee, WI, USA.
Vladimir BobkovAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0002-5414-8188
Julia DrubeInstitute for Molecular Cell Biology, CMB - Center for Molecular Biomedicine, University Hospital Jena, Friedrich-Schiller-University Jena, Jena, Germany.ORCID http://orcid.org/0000-0001-6188-2279
Carsten HoffmannInstitute for Molecular Cell Biology, CMB - Center for Molecular Biomedicine, University Hospital Jena, Friedrich-Schiller-University Jena, Jena, Germany.ORCID http://orcid.org/0000-0003-0884-9300
Marco SideriusAmsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0003-3630-4228
Raimond Heukers *Amsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0003-4498-7751
Christopher T Schafer *Amsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands.ORCID http://orcid.org/0000-0001-9907-295X
Martine J Smit *Amsterdam Institute for Molecular and Life Sciences (AIMMS), Department of Chemistry & Pharmaceutical Sciences, Division of Medicinal Chemistry, Faculty of Science, Vrije Universiteit, Amsterdam, the Netherlands. mj.smit@vu.nl.ORCID http://orcid.org/0000-0003-2713-0238
Funding
Structural Basis for Chemokine FunctionR37AI058072 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI Brian F Volkman · 2020 to 2026
$2.8M
European Commission (EC) H2020-MSCA grant agreement 860229NIAID NIH HHS R37 AI058072U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R37AI058072
6 · The paper itself
Abstract
Stimulation of atypical chemokine receptor 3 (ACKR3) by chemokines does not activate G proteins but recruits arrestin. It is a chemokine scavenger that indirectly influences responses by restricting the availability of CXCL12, an agonist shared with the canonical receptor CXCR4. ACKR3 is upregulated in numerous disorders. Due to limited insights in chemokine-activated ACKR3 signaling, it is unclear how ACKR3 contributes to pathological phenotypes. One explanation may be that constitutive activity of ACKR3 drives non-canonical signaling through a basal receptor state. Here we characterize the constitutive responses of ACKR3 using inverse agonistic nanobodies to suppress its basal activity. These tools promote an inactive receptor conformation which decreased arrestin engagement and inhibited constitutive internalization. Basal non-chemotactic, cancer cell motility was also suppressed, suggesting a role for ACKR3 in this process. The basal receptor activity in pathophysiology may provide an alternate therapeutic approach for targeting ACKR3.
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.
Constitutive activity of an atypical chemokine receptor revealed by inverse agonistic nanobodies. · full record | Socratic