Zdhhc11, a member of the DHHC palmitoyl transferase family, is involved in palmitoylation, an important post-translational protein modification. This process is implicated in various biological processes, including immune responses, lipid metabolism, and tumor-related pathways [1,2,4,5,6,7,8].

In terms of immune-related functions, Zdhhc11 knockout mice showed lower serum cytokine levels and higher lethality after HSV-1 infection, indicating its role in DNA virus-triggered innate immune responses as it facilitates the recruitment of IRF3 to MITA [4]. In NF-κB signaling, Zdhhc11 deficiency impaired NF-κB activity stimulated by IL-1β, LPS, and DNA virus infection, and Zdhhc11 knockout mice had a lower level of serum IL6 upon LPS and D-galactosamine or HSV-1 infection, suggesting its positive regulation of NF-κB activation by enhancing TRAF6 oligomerization [2].

In lipid metabolism, elimination of Zdhhc11 in mice enlarged lipid droplets, showing its role in regulating lipid droplet catabolism by modifying ATGL [5].

In cancer, knockdown of circZDHHC11, a transcript of the Zdhhc11 gene, strongly inhibited Burkitt lymphoma growth, and knockdown of MYC, MYB and ZDHHC11 decreased the growth of Hodgkin lymphoma and diffuse large B-cell lymphoma cells [3,6]. Also, in colorectal cancer, siRNA-mediated knockdown of ZDHHC11 suppressed cell growth [7].

In conclusion, Zdhhc11 plays essential roles in innate immune responses, lipid metabolism, and tumor-related biological processes. Studies using Zdhhc11 knockout mouse models have significantly contributed to understanding its functions in diseases such as viral infections and various cancers, providing insights into potential therapeutic targets for these conditions.