Rnf144a, a member of the RING-in-between RING (RBR) E3 ubiquitin ligase family, plays diverse roles in biological processes. It is involved in pathways related to innate immune responses, autophagy, and cell proliferation, and has implications in diseases like cancer [1,3,4]. Genetic models, such as gene knockout (KO) mouse models, are valuable for studying its functions.

Rnf144a-deficient mice show increased susceptibility to carcinogen-induced bladder tumorigenesis due to stabilization of PD-L1, DNA-PKcs, and BMI1 [2]. In L. monocytogenes infection, rnf144a deficiency protects mice from infection with inhibited innate immune responses, as RNF144A promotes Lm infection by inhibiting autophagy through BECN1 degradation [3]. In ovarian cancer, downregulated RNF144A expression is associated with poor patient survival, and overexpression of RNF144A inhibits ovarian tumor growth by inducing LIN28B degradation [5].

In conclusion, Rnf144a has crucial functions in innate immunity, autophagy, and cancer development. KO mouse models have revealed its role in promoting DNA virus-or cytosolic DNA-triggered innate immune responses, inhibiting autophagy during L. monocytogenes infection, and suppressing tumorigenesis in bladder and ovarian cancers. Understanding Rnf144a's functions can potentially provide new strategies for treating related diseases.