Nmur1, the neuromedin U receptor 1, is a G-protein-coupled receptor. Neuromedin U (NMU) binding to NMUR1 activates downstream signaling, which is involved in multiple biological processes such as mucosal immunity, allergic inflammation, and bone remodeling. The study of Nmur1-related functions often relies on genetic models like knockout (KO) mouse models to understand its roles in vivo [3,4,5,6].

In mice, a subset of small intestine eosinophils expresses NMUR1. Fate-mapping analyses show local microenvironment programming of its expression in these eosinophils, and inflammation further enhances it. Genetic perturbation experiments reveal that NMU-mediated activation of eosinophils via NMUR1 promotes goblet cell differentiation, highlighting its role in epithelial cell differentiation and barrier immunity in the small intestine [1]. In ILC2-driven allergic lung inflammation, Nmur1 is preferentially expressed by ILC2s at steady state and after IL-25 stimulation. Loss of NMU-NMUR1 signaling reduces ILC2 frequency and effector function, and alters transcriptional programs following allergen challenge, suggesting its importance in allergic inflammation at mucosal surfaces [2]. In bone remodeling, knockdown of Nmur1 in MC3T3-E1 cells in vitro shows it is required for NMU-dependent signaling in these cells, but global knockout of Nmur1 in 12-week-old male mice shows no change in trabecular bone volume, indicating it may not be essential for NMU-mediated bone remodeling in vivo [3].

In conclusion, Nmur1 is crucial for regulating mucosal immunity, allergic inflammation, and potentially bone remodeling. KO mouse models have been instrumental in uncovering these functions, highlighting its significance in understanding immune-related and bone-related disease mechanisms.