Zdhhc11, a member of the DHHC palmitoyl transferase family, is involved in palmitoylation, an important post-translational protein modification. It participates in various biological processes, including innate immune responses, lipid droplet homeostasis, and NF-κB signaling pathways. Zdhhc11 is also associated with the growth of several types of cancers, such as Burkitt lymphoma, Hodgkin lymphoma, and diffuse large B-cell lymphoma, as well as colorectal cancer [1,2,4,5].

Zdhhc11 knockout mice have been used to study its function. In Zdhhc11-deficient mice, NF-κB activity stimulated by IL-1β, LPS, and DNA virus infection was impaired, and serum IL6 levels were lower upon LPS and D-galactosamine treatment or HSV-1 infection compared to control mice. This indicates that Zdhhc11 positively regulates NF-κB signaling by enhancing TRAF6 oligomerization [1]. In another study, Zdhhc11-/-mice exhibited lower serum cytokine levels and higher lethality after HSV-1 infection, suggesting its importance in mediating MITA-dependent innate immune responses against DNA viruses [3].

In conclusion, Zdhhc11 plays a crucial role in multiple biological processes. Through gene-knockout mouse models, its functions in innate immune responses and NF-κB signaling have been revealed. These findings are relevant to understanding diseases related to abnormal immune responses and cancer development, providing insights into potential therapeutic strategies targeting Zdhhc11.