Kif3c, a motor protein of the kinesin superfamily, is highly expressed in the central nervous system and is associated with membrane vesicles in neurons [6]. It can form a heteromeric kinesin with Kif3A [6,7]. Kif3c is involved in multiple biological processes and associated with pathways such as PI3K/AKT/mTOR [2,3,4,5]. It plays a role in cell proliferation, migration, invasion, and apoptosis, thus having importance in normal biological functions and disease-related processes [3,4,5]. Genetic models like mouse models are valuable for studying its functions.

In a knock-in mouse model, double mutations in Zfp513 (equivalent to human ZNF513) and Kif3c led to gingival hyperplasia phenotypes, while single mutations in either Zfp513 or Kif3c alone did not result in clear phenotypes of gingival fibromatosis. This shows that Kif3c, in combination with ZNF513, is involved in regulating gingival fibroblast proliferation, migration, and fibrosis response via the PI3K/AKT/mTOR and Ras/Raf/MEK/ERK pathways [1].

In conclusion, Kif3c is crucial for normal cellular functions related to cell movement and growth. Its role in diseases, such as hereditary gingival fibromatosis, glioma, and various cancers, has been revealed through model-based research. The study of Kif3c using mouse models provides insights into its functions in specific disease conditions, offering potential targets for treatment and a better understanding of disease mechanisms.