Prokr2, encoding for a G-protein-coupled receptor, can bind PROK1 and PROK2. It is involved in the PROK2-PROKR2 signaling pathway, which is crucial for multiple biological processes. Its function is essential in processes like the migration of GnRH neurons, the development of the olfactory bulb, and has implications in various endocrine-related pathways [1,4]. Genetic models, such as knockout (KO) mouse models, have been valuable in understanding its function.

Mice lacking Prokr2 show abnormal olfactory bulb formation and defects in GnRH neuron migration [1]. In terms of human diseases, patients with mutations in PROKR2 typically present hypogonadotropic hypogonadism, anosmia/hyposmia or Kallmann Syndrome. Functional studies on PROKR2 mutations in isolated hypogonadotropic hypogonadism (IHH) patients suggest that disruption of the Gαq signaling pathway, rather than the MAPK/ERK pathway, is primarily responsible for PROKR2-related IHH [2]. Additionally, in patients with pituitary disorders, ranging from isolated growth hormone deficiency to septo-optic dysplasia, PROKR2 mutations have been reported [1,3].

In conclusion, Prokr2 is vital for processes related to olfactory bulb development and GnRH neuron migration. The study of Prokr2 KO mouse models has significantly contributed to understanding its role in diseases such as hypogonadotropic hypogonadism and pituitary disorders. These findings enhance our understanding of the biological functions of Prokr2 and its implications in disease mechanisms.