Structural basis of oligomerization-modulated activation and autoinhibition of orphan receptor GPR3

G protein-coupled receptor 3 (GPR3) is a class A orphan receptor characterized by high constitutive activity in the G<sub>s</sub> signaling pathway. GPR3 has been implicated in Alzheimer's disease and the regulation of thermogenesis in human adipocytes, yet the molecular mechanisms underlying its self-activation and potential endogenous modulators remain unclear. In this study, we present cryo-electron microscopy (cryo-EM) structures of GPR3 in different oligomerization states, both in the absence and presence of G protein. Notably, in addition to the monomeric form of GPR3, our findings reveal a functional GPR3 dimer with an extensive dimer interface-a feature rarely observed in class A GPCRs. Moreover, oligomerization appears to be linked to a unique autoinhibition mechanism involving intracellular loops, which may regulate GPR3 signaling. Collectively, these results provide new insights into the oligomerization-modulated activation of orphan GPCRs, advancing our understanding of their signaling properties.

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Publication Details

Journal
Cell Reports
Published
2025-03-31
DOI
https://doi.org/10.1016/j.celrep.2025.115478
Citations
6
Primary Topic
Receptor Mechanisms and Signaling
Type
article
Field-Weighted Citation Impact
4.84
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article

Structural basis of oligomerization-modulated activation and autoinhibition of orphan receptor GPR3

Lijie Wu, Tian Hua, Hongqing Tu, Yanan Yu et al.
6 citations
Cell Reports
Receptor Mechanisms and Signaling
4.84
article

Structural basis of oligomerization-modulated activation and autoinhibition of orphan receptor GPR3

Lijie Wu, Tian Hua, Hongqing Tu, Yanan Yu, Hao Chang, Xiaoting Li, Na Chen, Wei L. Shen, Junlin Liu
article en
6 citations

Abstract

G protein-coupled receptor 3 (GPR3) is a class A orphan receptor characterized by high constitutive activity in the G<sub>s</sub> signaling pathway. GPR3 has been implicated in Alzheimer's disease and the regulation of thermogenesis in human adipocytes, yet the molecular mechanisms underlying its self-activation and potential endogenous modulators remain unclear. In this study, we present cryo-electron microscopy (cryo-EM) structures of GPR3 in different oligomerization states, both in the absence and presence of G protein. Notably, in addition to the monomeric form of GPR3, our findings reveal a functional GPR3 dimer with an extensive dimer interface-a feature rarely observed in class A GPCRs. Moreover, oligomerization appears to be linked to a unique autoinhibition mechanism involving intracellular loops, which may regulate GPR3 signaling. Collectively, these results provide new insights into the oligomerization-modulated activation of orphan GPCRs, advancing our understanding of their signaling properties.

Cell ReportsVol. 44(4)
ShanghaiTech University (CN)
Zero hunger
Openalex Percentile: Top 5%
Receptor Mechanisms and Signaling
4.84
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Structural basis of oligomerization-modulated activation and autoinhibition of orphan receptor GPR3 — Lijie Wu, Tian Hua, et al. · Cell Reports (2025) | TGRS Research Map | TGRS