Molecular insights into ligand recognition and receptor activation of GPR15

In response to the chemokine-like peptide GPR15L, G protein-coupled receptor 15 (GPR15) is crucial for immune cell trafficking and inflammatory diseases. However, understanding of its physiology and pathology is hindered by lack of molecular details of the interaction between GPR15 and the full-length GPR15L. Here, we report the structure of GPR15 bound to the full-length GPR15L and G<sub>i3</sub> protein. Combined with mutagenesis data, this structure reveals key interactions that define ligand recognition and a subpocket that governs GPR15L selectivity and receptor activation. Molecular dynamics simulations suggest that sulfation modifications in the N-terminal region of GPR15 may play a role in stabilizing the binding between GPR15 and the core region of GPR15L. Furthermore, molecular docking of some potential small-molecule antagonists suggests a conserved molecular pattern of these ligands inhibiting receptor activation. These findings provide essential insight into functional modulation of GPR15 and would facilitate development of therapeutic strategies for treatment of inflammation and immune diseases.

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Publication Details

Journal
iScience
Published
2025-11-05
DOI
https://doi.org/10.1016/j.isci.2025.113935
Primary Topic
Receptor Mechanisms and Signaling
Type
article
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article

Molecular insights into ligand recognition and receptor activation of GPR15

Qiang Zhao, Cuiying Yi, Xiaojing Chu, Qiuxiang Tan et al.
iScience
Receptor Mechanisms and Signaling
article

Molecular insights into ligand recognition and receptor activation of GPR15

Qiang Zhao, Cuiying Yi, Xiaojing Chu, Qiuxiang Tan, Beili Wu, Shutian Chen, Shuo Han, Xu Han, Limin Ma, Yiming Zhang
article en

Abstract

In response to the chemokine-like peptide GPR15L, G protein-coupled receptor 15 (GPR15) is crucial for immune cell trafficking and inflammatory diseases. However, understanding of its physiology and pathology is hindered by lack of molecular details of the interaction between GPR15 and the full-length GPR15L. Here, we report the structure of GPR15 bound to the full-length GPR15L and G<sub>i3</sub> protein. Combined with mutagenesis data, this structure reveals key interactions that define ligand recognition and a subpocket that governs GPR15L selectivity and receptor activation. Molecular dynamics simulations suggest that sulfation modifications in the N-terminal region of GPR15 may play a role in stabilizing the binding between GPR15 and the core region of GPR15L. Furthermore, molecular docking of some potential small-molecule antagonists suggests a conserved molecular pattern of these ligands inhibiting receptor activation. These findings provide essential insight into functional modulation of GPR15 and would facilitate development of therapeutic strategies for treatment of inflammation and immune diseases.

iScienceVol. 28(12)
Chinese Academy of Sciences (CN), ShanghaiTech University (CN), Shanghai Institute of Materia Medica (CN), Institute for Advanced Study (DE), University of Chinese Academy of Sciences (CN)
Openalex Percentile: Top 71%
Receptor Mechanisms and Signaling
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