Kif5b, a member of the kinesin family, is an important motor protein involved in microtubule-mediated intracellular transport. It contributes to key cellular processes such as intracellular trafficking, organelle dynamics, and cell division [1]. Ubiquitously expressed, it is distinct from some of its family members like KIF5A and KIF5C which have more specific tissue expressions [1].

In a Kif5b conditional knockout (CKO) mouse model where Kif5b was knocked out in CaMKIIα -Cre-expressing neurons, dendritic spine plasticity was affected. There was heightened turnover and lower stability of dendritic spines 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. Moreover, the learning-dependent localization of FMRP after fear extinction was disrupted in these cKO mice, indicating Kif5b's role in dendritic targeting of synaptic proteins underlying dendritic spine plasticity [2].

In conclusion, Kif5b is essential for intracellular transport and plays a crucial role in maintaining normal cellular functions. The Kif5b cKO mouse model has revealed its significance in dendritic spine plasticity, which may have implications for understanding neurological processes. This contributes to our knowledge of how disruptions in Kif5b function can lead to various phenotypic changes, highlighting its importance in disease-related research.