Disease relevance of GPR103

• Altogether, these results suggest that osteopenia in GPR103-/- mice may be mediated directly by the loss of GPR103 expression in bone [1].

High impact information on GPR103

• QRFP binds and activates the human GPR103, as well as mouse GPR103A and GPR103B, with nanomolar affinities in transfected cells [2].
• Dexamethasone, a known inhibitor of osteoblast growth and inducer of osteoblast differentiation, inhibited GPR103 expression in human osteoblast primary cultures [1].
• Microcomputed tomography confirmed the reduction in trabecular bone and connective tissue densities in GPR103 knockout animals [1].
• Histological analysis revealed that GPR103-/- mice exhibited a thinned osteochondral growth plate, a thickening of trabecular branches, and a reduction in osteoclast number, suggestive of an early arrest of osteochondral bone formation [1].
• GPR103 shared identities with the neuropeptide FF 2, neuropeptide Y2 and galanin GalR1 receptors (34-38% in the TM regions) [3].

Anatomical context of GPR103

• GPR103 mRNA signals were detected in the cortex, pituitary, thalamus, hypothalamus, basal forebrain, midbrain and pons [3].
• Reverse transcription-PCR analysis showed that GPR103 was expressed in human skull, mouse spine, and several osteoblast cell lines [1].

References