Evidence map›Paper›PMID 39466725›Full record

ArticlePLoS biology2024

Structure of G protein-coupled receptor GPR1 bound to full-length chemerin adipokine reveals a chemokine-like reverse binding mode.

Aijun Liu, Yezhou Liu, Geng Chen, Wenping Lyu, Fang Ye, Junlin Wang, Qiwen Liao, Lizhe Zhu, Yang Du, Richard D Ye

Abstract read
In one paragraph

Article in PLoS biology, 2024. 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. Review
  3. Multiscale Computational Dissection of CCRL2-Mediated Chemerin Presentation.Journal of chemical information and modeling · 2025
    Article
  4. Article
  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

10 authors.

Aijun LiuKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Yezhou LiuKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Geng ChenKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Wenping LyuWarshel Institute for Computational Biology, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Fang YeKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Junlin WangKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Qiwen LiaoKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Lizhe ZhuWarshel Institute for Computational Biology, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Yang DuKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
Richard D YeKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.ORCID 0000-0002-2164-5620

Funding

National Natural Science Foundation of China 82402140Science, Technology and Innovation Commission of Shenzhen Municipality GXWD20201231105722002-20200831175432002Shenzhen Science and Technology Program RCBS20221008093330067
6 · The paper itself

Abstract

Chemerin is an adipokine with chemotactic activity to a subset of leukocytes. Chemerin binds to 3 G protein-coupled receptors, including chemokine-like receptor 1 (CMKLR1), G protein-coupled receptor 1 (GPR1), and C-C chemokine receptor-like 2 (CCRL2). Here, we report that GPR1 is capable of Gi signaling when stimulated with full-length chemerin or its C-terminal nonapeptide (C9, YFPGQFAFS). We present high-resolution cryo-EM structures of Gi-coupled GPR1 bound to full-length chemerin and to the C9 peptide, respectively. C9 insertion into the transmembrane (TM) binding pocket is both necessary and sufficient for GPR1 signaling, whereas the full-length chemerin uses its bulky N-terminal core for interaction with a β-strand located at the N-terminus of GPR1. This interaction involves multiple β-strands of full-length chemerin, forming a β-sheet that serves as a "lid" for the TM binding pocket and is energetically expensive to remove as indicated by molecular dynamics simulations with free energy landscape analysis. Combining results from functional assays, our structural model explains why C9 is an activating peptide at GPR1 and how the full-length chemerin uses a "two-site" model for enhanced interaction with GPR1.

Indexed as

ChemokinesReceptors, G-Protein-CoupledAdipokinesAnimalsBinding SitesCryoelectron MicroscopyHEK293 CellsHumansIntercellular Signaling Peptides and ProteinsProtein BindingReceptors, CCRReceptors, ChemokineSignal TransductionAdipokinesChemokinesGPR1 protein, humanIntercellular Signaling Peptides and ProteinsRARRES2 protein, humanReceptors, CCRReceptors, ChemokineReceptors, G-Protein-Coupled

Identifiers

PMID39466725
PMCPMC11515964

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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.