Trim2, also known as CMT2R or RNF86, is a member of the TRIM superfamily and functions as an E3 ubiquitin ligase. It is involved in multiple biological processes such as neuroprotection, antiviral responses, and plays diverse roles in cell evolution including intracellular signaling, apoptosis, and carcinogenesis [1].

Trim2-knockout mice (Trim2A/A) develop ataxia associated with loss of cerebellar Purkinje cells and a peripheral neuropathy, indicating that loss of Trim2 in these neurons has cell-autonomous effects on their axons [3]. Knocking out Trim2 in Vero E6 cells inhibits porcine epidemic diarrhea virus replication [2]. In a model of inflammation-induced angiogenesis, Trim2 -/- mice showed less adventitial macrophage infiltration and reduced adventitial proliferating neovessels, while in a hypoxia-mediated angiogenesis model, there were no differences in blood flow reperfusion between Trim2 -/- and wild-type mice [4].

In conclusion, Trim2 is a multifunctional gene involved in various biological processes and diseases. Gene-knockout mouse models have revealed its role in neurological diseases, viral infections, and angiogenesis. Understanding Trim2's functions can provide insights into the mechanisms of these diseases and potential therapeutic targets.