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. Genetic models, like gene knockout (KO) mouse models, have been instrumental in studying its functions. This signaling pathway is important in processes such as the migration of neurons, including GnRH neurons and olfactory bulb interneurons, and may also be related to body physiology regulation [1,2,4].

In KO mouse models, lacking Prokr2 leads to abnormal olfactory bulb formation and defects in GnRH neuron migration [1]. In patients, mutations in PROKR2 are typically associated with hypogonadotropic hypogonadism, anosmia/hyposmia or Kallmann Syndrome. Additionally, some patients with pituitary disorders, ranging from isolated growth hormone deficiency to septo-optic dysplasia, carry PROKR2 variants [1]. Functional studies on PROKR2 mutations in isolated hypogonadotropic hypogonadism patients indicate that disruption of the Gαq signaling pathway may be the primary cause of PROKR2-related IHH [3].

In conclusion, Prokr2 is essential for neuron migration processes, especially those related to the olfactory bulb and GnRH neurons. The study of Prokr2 KO mouse models has significantly contributed to understanding its role in diseases such as hypogonadotropic hypogonadism and pituitary disorders. These insights into Prokr2 function may help in further understanding the mechanisms of related diseases and potentially developing new treatment strategies.