Kif4, a member of the Kinesin-4 kinesin family, has a highly conserved structure with an N-terminal motor region, coiled-coil region, and C-terminal loading region. It plays crucial roles in multiple cellular processes such as DNA repair, DNA replication, mitosis, and meiosis. Kif4 is also involved in various signaling pathways like the PARP1 signaling pathway [3]. It is essential for maintaining genetic stability and is associated with many biological processes, making it a significant gene for understanding cellular function [3].

In mouse oocytes, Kif4 knockdown leads to defective midzone formation and longer spindles, revealing its role in anaphase during meiosis [2]. Kif4-mutant mice exhibit mild developmental delay with a lower seizure threshold, and the mutation causes aberrant morphology in dendrites and spines of hippocampal pyramidal neurons through the PARP1-TrkB-KCC2 pathway, indicating its role in regulating seizure susceptibility [1]. In CRC cells, inhibiting Kif4 can reverse its promotion of cell proliferation, invasion, and migration, as well as its activation of the Hedgehog pathway and inhibition of autophagy [4].

In conclusion, Kif4 is essential for multiple biological processes including cell division and DNA-related functions. Gene-knockout or conditional-knockout mouse models have revealed its significant roles in diseases such as epilepsy and colorectal cancer, providing potential therapeutic targets for these diseases.