TAFA2, also known as FAM19A2, is a cytokine specifically expressed in the central nervous system. It plays a vital role in multiple biological processes. In neurons, it functions as a neurotrophic factor essential for neuronal survival. It activates the cAMP/PKA/CREB/BCL2 signaling pathway by binding to ADGRL1 to suppress apoptosis [2]. In skeletal (stromal) stem cells, TAFA2 induces their migration through the activation of the Rac1-p38 signaling pathway, which is relevant for regenerative medicine applications [1].

Tafa-2 knockout mice were generated to investigate its in vivo function. The mutant mice showed impairments in spatial learning, memory, and abnormal anxiety-and depression-like behaviors. Further examination revealed that Tafa-2 deficiency led to severe neuronal reduction and increased apoptosis in the brain via downregulation of the PI3K/Akt and MAPK/Erk pathways [3].

In conclusion, TAFA2 is crucial for neuronal survival and neurobiological functions as demonstrated by knockout mouse models. It also has potential implications in regenerative medicine related to stem cell migration. These findings from model-based research provide insights into understanding related biological processes and possible therapeutic targets for neurological and regenerative-related diseases.