ArticleMolecular pharmacology2025
Identification and molecular characterization of missense mutations in orphan G protein-coupled receptor GPR61 occurring in severe obesity.
Article in Molecular pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Recent developments in GPCR signalling in appetite regulation.Bioscience reports · 2026Review
- Structure-based screening and a conformational biosensor identify a GPR183 inverse agonist and an activation switch.Nature communications · 2026Article
- Orphan GPCRs in diabetes mellitus: metabolic control, inflammation, and drug development.Frontiers in endocrinology · 2026Review
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Authors and funding
3 authors.
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Abstract
Severe obesity is a complex chronic metabolic condition with a body mass index over 40 and can be caused, for example, by dysregulated G protein-coupled receptors (GPCRs) signaling. The orphan GPCR GPR61 had been linked to the regulation of metabolism and, here, we identify 34 mutations in the GPR61 gene which are present with much higher frequency in severe obesity samples from the UK10K obesity screen compared to the normal population. Furthermore, the cumulative sum of GPR61 mutations was found to be higher compared to the highly mutated and well-established target, melanocortin 4 receptor. Some GPR61 mutations presented an impact on ligand-independent GPR61-induced cAMP production. Specifically, R236C
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