Evidence map›Paper›PMID 40155369›Full record

ArticleNature communications2025

Structural visualization of small molecule recognition by CXCR3 uncovers dual-agonism in the CXCR3-CXCR7 system.

Shirsha Saha, Fumiya K Sano, Saloni Sharma, Manisankar Ganguly, Annu Dalal, Sudha Mishra, Divyanshu Tiwari, Hiroaki Akasaka, Takaaki A Kobayashi, Nabarun Roy and 7 more

Abstract read
In one paragraph

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Structure basis for C-C chemokine receptor 4 modulation by orthosteric and allosteric antagonists.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Elucidating biased signaling in class A GPCRs.Trends in pharmacological sciences · 2025
    Review
  5. Review
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

17 authors.

Shirsha Saha *Department of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India.
Fumiya K Sano *Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0002-8965-788X
Saloni Sharma *Department of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India.ORCID http://orcid.org/0009-0005-9109-9054
Manisankar GangulyDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India.
Annu DalalDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India.
Sudha MishraDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India.
Divyanshu TiwariDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India.
Hiroaki AkasakaDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0003-2118-0912
Takaaki A KobayashiDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0009-0007-4740-006X
Nabarun RoyDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India.
Nashrah ZaidiDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India.
Yuzuru ItohDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.ORCID http://orcid.org/0000-0001-7802-5572
Rob LeursAmsterdam Institute for Molecules, Medicines, and Systems (AIMMS), Division of Medicinal Chemistry, Faculty of Sciences, VU University Amsterdam, Amsterdam, The Netherlands.ORCID http://orcid.org/0000-0003-1354-2848
Ramanuj BanerjeeDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India. ramanujb@iitk.ac.in.ORCID http://orcid.org/0000-0002-7751-2317
Wataru ShihoyaDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan. wtrshh9@gmail.com.ORCID http://orcid.org/0000-0003-4813-5740
Osamu NurekiDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan. nureki@bs.s.u-tokyo.ac.jp.ORCID http://orcid.org/0000-0003-1813-7008
Arun K ShuklaDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur, India. arshukla@iitk.ac.in.ORCID http://orcid.org/0000-0003-2910-8288

Funding

DBT India Alliance (Wellcome Trust/DBT India Alliance) IA/S/20/1/504916DBT-Wellcome Trust India Alliance IA/S/20/1/504916DST | Science and Engineering Research Board (SERB) IPA/2020/000405DST | Science and Engineering Research Board (SERB) SPR/2020/000408Indian Council of Medical Research (ICMR) F.NO.52/15/2020/BIO/BMSJapan Agency for Medical Research and Development (AMED) JP22ama121002Japan Agency for Medical Research and Development (AMED) JP22ama121012MEXT | Japan Society for the Promotion of Science (JSPS) 21H05037MEXT | Japan Society for the Promotion of Science (JSPS) 22H02751MEXT | Japan Society for the Promotion of Science (JSPS) 22K19371MEXT | Japan Society for the Promotion of Science (JSPS) 23KJ0491Wellcome Trust
6 · The paper itself

Abstract

Chemokine receptors are critically involved in multiple physiological and pathophysiological processes related to immune response mechanisms. Most chemokine receptors are prototypical GPCRs although some also exhibit naturally-encoded signaling-bias toward β-arrestins (βarrs). C-X-C type chemokine receptors, namely CXCR3 and CXCR7, constitute a pair wherein the former is a prototypical GPCR while the latter exhibits selective coupling to βarrs despite sharing a common natural agonist: CXCL11. Moreover, CXCR3 and CXCR7 also recognize small molecule agonists suggesting a modular orthosteric ligand binding pocket. Here, we determine cryo-EM structures of CXCR3 in an Apo-state and in complex with small molecule agonists biased toward G-proteins or βarrs. These structural snapshots uncover an allosteric network bridging the ligand-binding pocket to intracellular side, driving the transducer-coupling bias at this receptor. Furthermore, structural topology of the orthosteric binding pocket also allows us to discover and validate that selected small molecule agonists of CXCR3 display robust agonism at CXCR7. Collectively, our study offers molecular insights into signaling-bias and dual agonism in the CXCR3-CXCR7 system with therapeutic implications.

Indexed as

Receptors, CXCRReceptors, CXCR3Small Molecule LibrariesBinding SitesCryoelectron MicroscopyHEK293 CellsHumansLigandsProtein BindingSignal TransductionACKR3 protein, humanCXCR3 protein, humanLigandsReceptors, CXCRReceptors, CXCR3Small Molecule Libraries

Identifiers

PMID40155369
PMCPMC11953467

What OpenQuestion holds

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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.