TRIM13, a RING-type E3 ubiquitin ligase, is involved in multiple biological processes [2,4]. It participates in pathways such as antiviral innate immunity, cholesterol metabolism, autophagy, and apoptosis, which are crucial for maintaining normal cellular functions and organismal homeostasis. Genetic models, like KO mouse models, have been instrumental in studying its functions [2].

In a KO mouse model, deletion of TRIM13 protected against diet-induced atherosclerosis by rescuing cholesterol efflux and inhibiting foam cell formation, revealing its role in arterial lipid accumulation [2]. In avian species, ApdTRIM13 (duck TRIM13) mediates the autophagic degradation of MAVS, attenuating antiviral innate immunity [1]. In lung adenocarcinoma cells, overexpression of TRIM13 suppressed cell proliferation, increased apoptosis and oxidative stress, and activated autophagy via the KEAP1/NRF2 pathway [3]. In clear-cell renal cell carcinoma, up-regulation of TRIM13 decreased the migration and invasion ability of cells [4]. In non-small-cell lung carcinoma cells, TRIM13 overexpression inhibited cell proliferation and induced apoptosis through regulating the NF-κB pathway [5]. In acute myeloid leukemia, CHAF1B represses TRIM13 expression, and overexpression of TRIM13 suppresses self-renewal of leukemic cells [6]. In immune cells, TRIM13 is a negative regulator of MDA5-mediated type I interferon production [7].

In conclusion, TRIM13 plays diverse and significant roles in multiple biological processes and diseases. KO and other genetic models have been essential in uncovering these functions, especially in areas like atherosclerosis, cancer development, and antiviral immunity, providing potential therapeutic targets for related diseases.