Zdhhc24, a palmitoyl-transferase, plays a crucial role in palmitoylation processes. Palmitoylation is a post-translational modification that can influence protein function, localization, and stability. Zdhhc24 is involved in important biological pathways such as the regulation of the AKT pathway and antiviral innate immunity [1,2].

In the context of high-fat diet-induced liver tumorigenesis, Zdhhc24 knockout mice were used. The findings showed that Zdhhc24, along with Zdhhc17, palmitoylates AKT. A high-fat diet promotes AKT kinase activity through this palmitoylation, which in turn promotes non-alcoholic steatohepatitis (NASH) and liver cancer. In antiviral innate immunity, Zdhhc24 catalyzes the palmitoylation of mitochondrial antiviral signaling protein (MAVS), enhancing the TBK1-IRF3-interferon (IFN) pathway and leading to antiviral immune responses, especially under conditions of palmitic acid (PA) stimulation or in high-fat-diet-fed mouse models [1,2].

In conclusion, Zdhhc24 is essential for palmitoylation events that regulate the AKT pathway in liver-related diseases and MAVS-mediated antiviral innate immunity. The use of Zdhhc24 knockout mouse models has significantly contributed to understanding its role in these disease-related biological processes, providing insights into potential therapeutic strategies for liver tumorigenesis and antiviral treatments.