Gga3, also known as Golgi-associated, γ adaptin ear containing, ADP-ribosylation factor-binding protein 3, is involved in multiple cellular processes. It plays a role in the recycling and signaling of G protein-coupled receptors (GPCRs), such as regulating the recycling and signaling of the PGD2 receptor DP1 through a Rab4-dependent mechanism [2]. It also participates in the anterograde trafficking of nascent GPCRs, like modulating the cell surface export of α2-adrenergic receptors [3]. Additionally, it is involved in the endocytic recycling of receptor tyrosine kinases, for example, mediating the endocytic recycling of TrkA to promote sustained Akt phosphorylation and cell survival [5].

In Gga3 gene-deleted C57BL/6J mice, fasting blood glucose levels are elevated, indicating its potential role in glucose metabolism [1]. Gga3 deletion and a GGA3 rare variant associated with late-onset Alzheimer's disease trigger BACE1 accumulation in axonal swellings, suggesting its significance in Alzheimer's disease pathogenesis [4].

In conclusion, Gga3 is a multifunctional protein involved in receptor trafficking, cell survival, and glucose metabolism. Studies using Gga3-deleted mouse models have revealed its importance in glucose-related physiological processes and Alzheimer's disease, providing valuable insights into the underlying biological mechanisms and potential disease-related pathways.