Kif5b, a member of the kinesin family, is an ubiquitous protein. Kinesins are motor proteins involved in microtubule-mediated intracellular transport, contributing to key cellular processes such as intracellular trafficking, organelle dynamics, and cell division [1].

In a conditional knockout (CKO) mouse model where Kif5b was knocked out in CaMKIIα -Cre-expressing neurons, heightened turnover and lower stability of dendritic spines were observed in layer 2/3 pyramidal neurons, along with reduced acquisition of spine postsynaptic density protein 95 in the mouse cortex. Also, the preceding transport of RNA-binding protein fragile X mental retardation protein (FMRP) to newly formed spines, which occurs in control mice, was abolished in KIF5B cKO mice. This indicates Kif5b is involved in the dendritic targeting of synaptic proteins underlying dendritic spine plasticity [2]. Dominant negative variants in KIF5B identified in four individuals with osteogenesis imperfecta, when modeled in C. elegans, led to abnormal body length and motility phenotypes, defective mitochondria transport, and disrupted intracellular trafficking in human cells, along with down-regulation of the mTOR signaling pathway [3].

In conclusion, Kif5b plays crucial roles in intracellular transport and in maintaining normal cellular and developmental processes. Model-based research, especially the Kif5b CKO mouse model and the C. elegans model with Kif5b -related variants, has revealed its significance in dendritic spine plasticity and skeletal development, providing insights into related disease mechanisms [2,3].