Gpr34, a G-protein-coupled receptor of Lysophosphatidylserine (LysoPS), is a key player in multiple biological processes. It is involved in immune cell function, tissue repair, and is associated with various diseases. The pathways it influences include PI3K-AKT and ERK signaling. Genetic models, like Gpr34-deficient mice, have been crucial in understanding its functions [1,2,3,4,5,6,7,8,9,10].

In the context of tissue repair, Gpr34-deficient mice exhibited compromised activation of type 3 innate lymphoid cells (ILC3s) and reduced tissue repair during colon injury, indicating that Gpr34 in ILC3s is essential for sensing apoptotic neutrophils and triggering tissue repair [2]. In neurodegenerative diseases, Gpr34 knockdown in APP/PS1 mice relieved cognitive deficits and suppressed neuroinflammation, suggesting its contribution to Alzheimer's disease pathogenesis [10]. In cancer, genetic deletion of Gpr34 in ILC1s enhanced their antitumor activity, highlighting Gpr34 as a metabolic immune checkpoint [4].

In conclusion, Gpr34 plays diverse and important roles in biological processes such as tissue repair, neuroinflammation, and antitumor immunity. Studies using Gpr34-deficient mouse models have significantly advanced our understanding of its functions in diseases like colon injury-related disorders, Alzheimer's disease, and cancer, offering potential therapeutic targets for these conditions.