Zdhhc17, a member of the zinc finger DHHC-domain containing (ZDHHC) family, is an S-acyltransferase crucial for S-palmitoylation, a post-translational modification. This process impacts protein localization, stability, and function, and is involved in various cellular pathways [1].

In high-fat diet-induced liver tumorigenesis, Zdhhc17 knockout mice helped reveal that Zdhhc17 palmitoylates AKT, promoting its activation, thus driving NASH and liver cancer development [2]. In polycystic ovary syndrome (PCOS), Zdhhc17 depletion in granulosa cells decreased HSP90α palmitoylation, hampering androgen to estrogen conversion, suggesting its role in PCOS pathophysiology [3]. In glioblastoma, Zdhhc17 knockout-related studies showed that palmitoylation mediated by Zdhhc17 preserves Oct4A from lysosome degradation, maintaining GSC tumorigenicity and stemness [4]. Also, in nervous system development, loss-of-function of Zdhhc17 in zebrafish led to motor dysfunction due to defective axonal outgrowth of spinal motor neurons [5].

In conclusion, Zdhhc17 plays essential roles in multiple biological processes and disease conditions. Through gene knockout models in different organisms, its functions in processes like liver tumorigenesis, PCOS, glioblastoma development, and nervous system development have been elucidated, highlighting its potential as a therapeutic target in related diseases.