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G-protein Coupled Receptors01:21

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Updated: Jan 24, 2026

Crystal Structure of the N-terminal Domain of Ryanodine Receptor from Plutella xylostella
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Modelling G protein-biased agonism using GLP-1 receptor C-terminal mutations.

Hanh Duyen Tran1, Yiming Zuo1, Carissa Wong1

  • 1Section of Endocrinology, Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, Imperial College London, Du Cane Road, W12 0NN, United Kingdom.

Molecular Metabolism
|January 22, 2026
PubMed
Summary
This summary is machine-generated.

Modifying the glucagon-like peptide-1 receptor (GLP-1R) by reducing phosphorylation enhances G protein signaling. This approach supports using biased agonism to improve GLP-1R agonist efficacy for type 2 diabetes and obesity treatments.

Keywords:
Biased agonismGLP-1 receptorβ-arrestin

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Area of Science:

  • Pharmacology
  • Molecular Biology
  • Endocrinology

Background:

  • The glucagon-like peptide-1 receptor (GLP-1R) is a key target for type 2 diabetes and obesity.
  • Biased agonists, favoring G protein over β-arrestin signaling, show clinical efficacy.
  • Previous studies faced challenges due to ligand property variations.

Purpose of the Study:

  • To investigate G protein-biased GLP-1R agonism using receptor mutations instead of modified ligands.
  • To mimic G protein-biased signaling by inhibiting GLP-1R C-tail phosphorylation.

Main Methods:

  • Mutated human and mouse GLP-1R C-tails (serine to alanine) to inhibit phosphorylation.
  • Assessed β-arrestin recruitment, internalisation, and Gαs activation in HEK293 cells and pancreatic β-cells.
  • Compared wild-type and mutant receptors using native GLP-1 and biased ligands (ExF1, ExD3).

Main Results:

  • Reduced C-terminal phosphorylation decreased GLP-1R internalisation and β-arrestin recruitment.
  • Phosphodeficient GLP-1R exhibited preferential Gαs activation and increased cAMP generation.
  • Specific phosphorylation sites differentially regulated β-arrestin recruitment, internalisation, and cAMP production.

Conclusions:

  • Genetic modifications reducing β-arrestin recruitment and internalisation can enhance GLP-1R signaling.
  • This provides evidence supporting G protein bias as a strategy to improve GLP-1R agonist efficacy.
  • The findings offer a novel approach to developing more effective GLP-1R-based therapeutics.