Fbxl19, a member of the Skp1-Cullin-1-F-box family of E3 ubiquitin ligase, is involved in a variety of biological processes. It can regulate cell proliferation, migration, and differentiation, and is associated with pathways like the ubiquitin-proteasome pathway. Genetic models are valuable for studying its function [2,3,4].

In the context of diseases, FBXL19 targeted STK11 degradation enhances cigarette smoke-induced airway epithelial cell cytotoxicity, as CSE enhances STK11 protein degradation in airway epithelial cells via the FBXL19-mediated ubiquitin-proteasomal pathway [1]. In endothelial cells, overexpression of FBXL19 protects the heart from influenza A infection by enhancing antiviral immunity and reducing cellular senescence programs [2]. In hepatocellular carcinoma, FBXL19 is upregulated and promotes malignant behaviors by activating MAPK signalling, and its knockdown inhibits HCC cell proliferation, migration, invasion, and induces G0/G1 phase cell cycle arrest [3]. In Streptococcus pneumoniae-induced lung injury in immature mice, FBXL19 overexpression alleviates lung injury by inducing ubiquitination and degradation of FOXM1 [5].

In summary, Fbxl19 plays crucial roles in multiple disease-related biological processes. Studies using gene-related models, such as those in airway epithelial cells, endothelial cells, hepatocellular carcinoma cells, and in immature mice with lung injury, have revealed its significance in diseases like cigarette-smoke-induced cytotoxicity, influenza A-related cardiac damage, hepatocellular carcinoma, and Streptococcus pneumoniae-induced lung injury.